Podcasts about herceptin

Richard was diagnosed with breast cancer in 2015, and Stuart was diagnosed in 2005 and now lives with secondary breast cancer. They are both involved with the Men's VMU, an online group aimed at supporting men with a breast cancer diagnosis, promoting research into breast cancer in men, and raising awareness of the signs and symptoms. Only around 400 men are diagnosed with breast cancer in the UK each year. Richard and Stuart talk about how their diagnoses took them by surprise, and share their work in the Men's VMU trying to get the message to as many people as possible. Find out more about the Men's VMU. Find out more about Breast Cancer Now's support service Someone Like Me. If you'd like to find out more about Breast Cancer Now's support services, visit the Breast Cancer Now website or phone our free helpline on 0808 800 6000 (UK only). You can subscribe to this podcast on Spotify, Apple Podcasts, or wherever you get your podcasts. Every episode is available to watch or listen to on the Breast Cancer Now website. Key Topics: 2:15 Richard's breast cancer diagnosis 5:38 Stuart's breast cancer diagnosis 7:56 Campaigning to receive Herceptin as a man 13:13 Stuart's secondary breast cancer diagnosis 15:51 Looking out for the signs and symptoms of secondary breast cancer 16:32 Living with secondary breast cancer 20:32 The Men's VMU – support for men with breast cancer 24:22 The use of tamoxifen in men 27:58 The "pinkness" and femininity of breast cancer 31:44 The erosion of male identity after a breast cancer diagnosis 36:10 How the Men's VMU encourages talking about difficult topics 37:11 Find out more about the Men's VMU 37:49 Someone Like Me service from Breast Cancer Now 39:01 The accessibility of resources and support to men with breast cancer 43:51 The importance of family support 45:39 Richard and Stuart's tips for a man just diagnosed 46:39 Getting involved with fundraising and awareness events 47:57 What it means to Richard and Stuart to live well 51:01 How to get in touch with the Men's VMU

View the Show Notes Page for This Episode Become a Member to Receive Exclusive Content Sign Up to Receive Peter's Weekly Newsletter Susan Desmond-Hellmann is a physician and scientist whose remarkable career has spanned clinical medicine, oncology, biotech innovation, and global health leadership. In this episode, Susan shares insights from her journey training in internal medicine during the early AIDS crisis, treating HIV-related cancers in Uganda, and developing groundbreaking cancer therapies like Herceptin and Avastin. She reflects on her leadership roles at UCSF and the Bill and Melinda Gates Foundation, offering lessons on guiding large-scale health initiatives, navigating uncertainty, and fostering scientific innovation. The conversation explores the promise of precision medicine, the integration of patient care and policy, and the evolving role of artificial intelligence in transforming diagnostics, drug development, and global access to care. We discuss: Susan's medical training, the start of the AIDS epidemic, and the transformative experiences that shaped her career [3:00]; Susan's experience working on the frontlines of the HIV/AIDS crisis in Uganda [12:30]; Susan's time working in general oncology and her transition to biotech where she helped develop taxol—a top-selling cancer drug [26:30]; Genentech's origins, and its groundbreaking use of recombinant DNA to develop biologic drugs [33:45]; Susan's move to Genentech, and her pivotal role in the development and success of Herceptin as a groundbreaking therapy in targeted oncology [44:00]; The rise of antibody-based cancer therapies: the development of Rituxan and Avastin [52:15]; The step-by-step drug development process and the scientific and strategic challenges involved [1:01:30]; The ethical and economic controversy surrounding Avastin's high cost and limited survival benefit [1:12:30]; Susan's tenure as chancellor at UCSF: leading during a financially strained period, and her strategic approach to fundraising and institutional development [1:14:45]; What Susan learned as CEO of the Bill and Melinda Gates Foundation: strategic processes and decision-making frameworks [1:26:00]; Susan's philosophy of leadership and how she sought to build an empowering, values-driven culture at the Gates Foundation [1:35:15]; The erosion of public trust in science during COVID, the communication failures around controversial treatments like ivermectin, and the need for better public health engagement and transparency [1:39:30]; The role of AI in transforming medicine: from drug development to cancer detection and beyond [1:53:00]; and More. Connect With Peter on Twitter, Instagram, Facebook and YouTube

In this episode of the Better Than Before Breast Cancer podcast, we're diving into how common post-treatment medications—like Tamoxifen, Aromatase Inhibitors (Letrozole, Anastrozole, Exemestane), Herceptin, Fulvestrant, and Bisphosphonates (like Fosamax and Reclast)—can deplete critical nutrients your body needs to feel good and stay strong. Have you ever wondered if the medications you're taking after breast cancer treatment could be affecting your energy, mood, or even your bone health? You're not imagining things. You'll learn: Which nutrients are most commonly depleted by these medications (like magnesium, vitamin D, calcium, B12, and CoQ10) The symptoms that may be tied to nutrient deficiencies (think fatigue, brain fog, joint pain, and more) How some medications may increase cholesterol levels or raise your risk of fatty liver Why supporting your body with the right foods and lifestyle habits can make all the difference Plus, I'll share simple, whole-food nutrition strategies and daily lifestyle tips that can help you feel more energized, support your bones, balance your mood, and reduce long-term side effects—without adding overwhelm. Whether you're taking medications now or just want to be prepared, this episode is packed with practical, supportive guidance to help you stay nourished and in tune with your healing body.   Resources and Studies Mentioned: Tamoxifen and Metabolic Risks Aromatase Inhibitors and Bone Health Bisphosphonates and Bone Metabolism Fulvestrant and Bone Health Herceptin and CoQ10 Support Metformin and Vitamin B12 Deficiency   Subscribe, listen, and share to help other women embrace joy as their right and not just a reward.  

For years, breast cancer has been classified as either HER2-positive or HER2-negative, determining whether a patient could receive HER2-targeted therapies like trastuzumab (Herceptin). However, a growing body of research suggests a middle category—HER2-low breast cancer—which has led to important changes in how clinicians approach treatment. A recent review published in Oncotarget, titled “Evolving Concepts in HER2-Low Breast Cancer: Genomic Insights, Definitions, and Treatment Paradigms,” explores what this means for both patients and clinicians​. Full blog - https://www.oncotarget.org/2025/02/12/her2-low-breast-cancer-a-new-understanding/ Paper DOI - https://doi.org/10.18632/oncotarget.28680 Correspondence to - Andrew A. Davis - aadavis@wustl.edu Video short - https://www.youtube.com/watch?v=dn54UrHCUNQ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28680 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, breast cancer, HER2-low, genomics About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

You are going to have some bad days, and that's okay, but the good days have to outweigh the bad ones. You have to put your mind into beating breast cancer. -Theresa Jay In honor of Breast Cancer Awareness month, we're profiling inspiring survivors with incredible stories to tell. My friendship with today's guest began in 2006 when I donated my wedding dress to her charity. Theresa Jay is the Founder of the Pink Rose Foundation www.pinkrose.org which provides scholarships to college-bound students who have lost a parent to breast cancer. To date, the charity has awarded over 100,000 dollars in scholarships. Diagnosed at only 41 with stage 3B metastatic breast cancer, there was a time when she thought she might not live to see her son and daughter grow up and go off to college, but here she is today, a 25-year survivor. Determined to play an active role in her treatment and recovery, Theresa became her own best advocate. Her mastectomy was performed after four grueling rounds of chemotherapy and when her pathology revealed 17 active lymph nodes, she asked her care team for stem cell therapy and enrollment in a clinical trial for a drug called Herceptin. Says Theresa: Even if the clinical trial and all the other treatments didn't work , I felt that it was my responsibility to be a part of breast cancer research for the next generation of women.” 18 months of treatments exhausted her in mind, body and soul, but during that time in her life, Theresa refused to give up or give in. “My love for my children propelled me through the toughest days. I just couldn't see anyone else raising my children. I got dressed every day, regardless of how badly I felt, and I put my makeup on. You look good, you feel better”. When her treatments were finally over, Theresa went right back to work as an engineer and launched the Pink Rose Foundation. In this interview, she's got a lot of wisdom to share including advice for someone who is just getting started on her breast cancer journey: Take a day and cry. Process it. And then, the next day, wake up and decide you are going to WIN.” For 22 minutes with a survivor who beat the odds, just hit that download button. #breastcancer #metastaticbreastcancer #breastcancerawarenessmonth #courage #hope #grateful.

A number of breast cancer treatments, including chemotherapy and some targeted therapy medicines, like Herceptin (trastuzumab), can cause oral side effects, including mouth sores, dry mouth and infections. Dr. Sollecito explains why these side effects happen and how they're treated. Listen to the episode to hear Dr. Sollecito explain: why it's a good idea to see a dentist before starting chemotherapy the type of dental check-up schedule someone receiving breast cancer treatment should consider what to do if you develop a cavity or need a root canal during treatment

Ronald Martell is a serial entrepreneur and biopharma veteran whose record includes the launch of Herceptin. He continues his mission to bring new drugs to patients with unmet medical needs. The CEO of Jasper Therapeutics explains his ambitions for his company's new antibody therapy and for the future of the industry.

A print and runway model, Christine Handy withstood a lumpectomy, two mastectomies and a MRSA infection, plus a chemotherapy regimen featuring Herceptin and taxol to survive HER2+ breast cancer.  That inspired her to write a book, “Walk Beside Me,” and to produce a film, “Hello, Beautiful.”

The most enthralling conversation I've ever had with anyone on cancer. It's with Charlie Swanton who is a senior group leader at the Francis Crick Institute, the Royal Society Napier Professor in Cancer and medical oncologist at University College London, co-director of Cancer Research UK.Video snippet from our conversation. Full videos of all Ground Truths podcasts can be seen on YouTube here. The audios are also available on Apple and Spotify.Transcript with audio links and many external linksEric Topol (00:07):Well, hello, this is Eric Topol with Ground Truths, and I am really fortunate today to connect us with Charlie Swanton, who is if not the most prolific researcher in the space of oncology and medicine, and he's right up there. Charlie is a physician scientist who is an oncologist at Francis Crick and he heads up the lung cancer area there. So Charlie, welcome.Charles Swanton (00:40):Thank you, Eric. Nice to meet you.Learning from a FailureEric Topol (00:43):Well, it really is a treat because I've been reading your papers and they're diverse. They're not just on cancer. Could be connecting things like air pollution, it could be Covid, it could be AI, all sorts of things. And it's really quite extraordinary. So I thought I'd start out with a really interesting short paper you wrote towards the end of last year to give a sense about you. It was called Turning a failing PhD around. And that's good because it's kind of historical anchoring. Before we get into some of your latest contributions, maybe can you tell us about that story about what you went through with your PhD?Charles Swanton (01:26):Yeah, well thank you, Eric. I got into research quite early. I did what you in the US would call the MD PhD program. So in my twenties I started a PhD in a molecular biology lab at what was then called the Imperial Cancer Research Fund, which was the sort of the mecca for DNA tumor viruses, if you like. It was really the place to go if you wanted to study how DNA tumor viruses worked, and many of the components of the cell cycle were discovered there in the 80s and 90s. Of course, Paul Nurse was the director of the institute at the time who discovered cdc2, the archetypal regulator of the cell cycle that led to his Nobel Prize. So it was a very exciting place to work, but my PhD wasn't going terribly well. And sort of 18, 19 months into my PhD, I was summoned for my midterm reports and it was not materializing rapidly enough.(02:25):And I sat down with my graduate student supervisors who were very kind, very generous, but basically said, Charlie, this isn't going well, is it? You've got two choices. You can either go back to medical school or change PhD projects. What do you want to do? And I said, well, I can't go back to medical school because I'm now two years behind. So instead I think what I'll do is I'll change PhD projects. And they asked me what I'd like to do. And back then we didn't know how p21, the CDK inhibitor bound to cyclin D, and I said, that's what I want to understand how these proteins interact biochemically. And they said, how are you going to do that? And I said, I'm not too sure, but maybe we'll try yeast two-hybrid screen and a mutagenesis screen. And that didn't work either. And in the end, something remarkable happened.(03:14):My PhD boss, Nic Jones, who's a great guy, still is, retired though now, but a phenomenal scientist. He put me in touch with a colleague who actually works next door to me now at the Francis Crick Institute called Neil McDonald, a structural biologist. And they had just solved, well, the community had just solved the structure. Pavletich just solved the structure of cyclin A CDK2. And so, Neil could show me this beautiful image of the crystal structure in 3D of cyclin A, and we could mirror cyclin D onto it and find the surface residue. So I spent the whole of my summer holiday mutating every surface exposed acid on cyclin D to an alanine until I found one that failed to interact with p21, but could still bind the CDK. And that little breakthrough, very little breakthrough led to this discovery that I had where the viral cyclins encoded by Kaposi sarcoma herpes virus, very similar to cyclin D, except in this one region that I had found interactive with a CDK inhibitor protein p21.(04:17):And so, I asked my boss, what do you think about the possibility this cyclin could have evolved from cyclin D but now mutated its surface residues in a specific area so that it can't be inhibited by any of the control proteins in the mammalian cell cycle? He said, it's a great idea, Charlie, give it a shot. And it worked. And then six months later, we got a Nature paper. And that for me was like, I cannot tell you how exciting, not the Nature paper so much as the discovery that you were the first person in the world to ever see this beautiful aspect of evolutionary biology at play and how this cyclin had adapted to just drive the cell cycle without being inhibited. For me, just, I mean, it was like a dream come true, and I never experienced anything like it before, and I guess it's sizes the equivalent to me of a class A drug. You get such a buzz out of it and over the years you sort of long for that to happen again. And occasionally it does, and it's just a wonderful profession.Eric Topol (05:20):Well, I thought that it was such a great story because here you were about to fail. I mean literally fail, and you really were able to turn it around and it should give hope to everybody working in science out there that they could just be right around the corner from a significant discovery.Charles Swanton (05:36):I think what doesn't break you makes you stronger. You just got to plow on if you love it enough, you'll find a way forward eventually, I hope.Tracing the Evolution of Cancer (TRACERx)Eric Topol (05:44):Yeah, no question about that. Now, some of your recent contributions, I mean, it's just amazing to me. I just try to keep up with the literature just keeping up with you.Charles Swanton (05:58):Eric, it's sweet of you. The first thing to say is it's not just me. This is a big community of lung cancer researchers we have thanks to Cancer Research UK funded around TRACERx and the lung cancer center. Every one of my papers has three corresponding authors, multiple co-first authors that all contribute in this multidisciplinary team to the sort of series of small incremental discoveries. And it's absolutely not just me. I've got an amazing team of scientists who I work with and learn from, so it's sweet to give me the credit.Eric Topol (06:30):I think what you're saying is really important. It is a team, but I think what I see through it all is that you're an inspiration to the team. You pull people together from all over the world on these projects and it's pretty extraordinary, so that's what I would say.Charles Swanton (06:49):The lung community, Eric, the lung cancer community is just unbelievably conducive to collaboration and advancing understanding of the disease together. It's just such a privilege to be working in this field. I know that sounds terribly corny, but it is true. I don't think I recall a single email to anybody where I've asked if we can collaborate where they've said, no, everybody wants to help. Everybody wants to work together on this challenge. It's just such an amazing field to be working in.Eric Topol (07:19):Yeah. Well I was going to ask you about that. And of course you could have restricted your efforts or focused on different cancers. What made you land in lung cancer? Not that that's only part of what you're working on, but that being the main thing, what drew you to that area?Charles Swanton (07:39):So I think the answer to your question is back in 2008 when I was looking for a niche, back then it was lung cancer was just on the brink of becoming an exciting place to work, but back then nobody wanted to work in that field. So there was a chair position in thoracic oncology and precision medicine open at University College London Hospital that had been open, as I understand it for two years. And I don't think anybody had applied. So I applied and because I was the only one, I got it and the rest is history.(08:16):And of course that was right at the time when the IPASS draft from Tony Mok was published and was just a bit after when the poster child of EGFR TKIs and EGFR mutant lung cancer had finally proven that if you segregate that population of patients with EGFR activating mutation, they do incredibly well on an EGFR inhibitor. And that was sort of the solid tumor poster child along with Herceptin of precision medicine, I think. And you saw the data at ASCO this week of Lorlatinib in re-arranged lung cancer. Patients are living way beyond five years now, and people are actually talking about this disease being more like CML. I mean, it's extraordinary the progress that's been made in the last two decades in my short career.Eric Topol (09:02):Actually, I do want to have you put that in perspective because it's really important what you just mentioned. I was going to ask you about this ASCO study with the AKT subgroup. So the cancer landscape of the lung has changed so much from what used to be a disease of cigarette smoking to now one of, I guess adenocarcinoma, non-small cell carcinoma, not related to cigarettes. We're going to talk about air pollution in a minute. This group that had, as you say, 60 month, five year plus survival versus what the standard therapy was a year plus is so extraordinary. But is that just a small subgroup within small cell lung cancer?Charles Swanton (09:48):Yes, it is, unfortunately. It's just a small subgroup. In our practice, probably less than 1% of all presentations often in never smokers, often in female, never smokers. So it is still in the UK at least a minority subset of adenocarcinomas, but it's still, as you rightly say, a minority of patients that we can make a big difference to with a drug that's pretty well tolerated, crosses the blood-brain barrier and prevents central nervous system relapse and progression. It really is an extraordinary breakthrough, I think. But that said, we're also seeing advances in smoking associated lung cancer with a high mutational burden with checkpoint inhibitor therapy, particularly in the neoadjuvant setting now prior to surgery. That's really, really impressive indeed. And adjuvant checkpoint inhibitor therapies as well as in the metastatic setting are absolutely improving survival times and outcomes now in a way that we couldn't have dreamt of 15 years ago. We've got much more than just platinum-based chemo is basically the bottom line now.Revving Up ImmunotherapyEric Topol (10:56):Right, right. Well that actually gets a natural question about immunotherapy also is one of the moving parts actually just amazing to me how that's really, it's almost like we're just scratching the surface of immunotherapy now with checkpoint inhibitors because the more we get the immune system revved up, the more we're seeing results, whether it's with vaccines or CAR-T, I mean it seems like we're just at the early stages of getting the immune system where it needs to be to tackle the cancer. What's your thought about that?Charles Swanton (11:32):I think you're absolutely right. We are, we're at the beginning of a very long journey thanks to Jim Allison and Honjo. We've got CTLA4 and PD-1/PDL-1 axis to target that's made a dramatic difference across multiple solid tumor types including melanoma and lung cancer. But undoubtedly, there are other targets we've seen LAG-3 and melanoma and then we're seeing new ways, as you rightly put it to mobilize the immune system to target cancers. And that can be done through vaccine based approaches where you stimulate the immune system against the patient's specific mutations in their cancer or adoptive T-cell therapies where you take the T-cells out of the tumor, you prime them against the mutations found in the tumor, you expand them and then give them back to the patient. And colleagues in the US, Steve Rosenberg and John Haanen in the Netherlands have done a remarkable job there in the context of melanoma, we're not a million miles away from European approvals and academic initiated manufacturing of T-cells for patients in national health systems like in the Netherlands.(12:50):John Haanen's work is remarkable in that regard. And then there are really spectacular ways of altering T-cells to be able to either migrate to the tumor or to target specific tumor antigens. You mentioned CAR-T cell therapies in the context of acute leukemia, really extraordinary developments there. And myeloma and diffuse large B-cell lymphoma as well as even in solid tumors are showing efficacy. And I really am very excited about the future of what we call biological therapies, be it vaccines, an antibody drug conjugates and T-cell therapies. I think cancer is a constantly adapting evolutionary force to be reckoned with what better system to combat it than our evolving immune system. It strikes me as being a future solution to many of these refractory cancers we still find difficult to treat.Eric Topol (13:48):Yeah, your point is an interesting parallel how the SARS-CoV-2 virus is constantly mutating and becoming more evasive as is the tumor in a person and the fact that we can try to amp up the immune system with these various means that you just were reviewing. You mentioned the other category that's very hot right now, which is the antibody drug conjugates. Could you explain a bit about how they work and why you think this is an important part of the future for cancer?Antibody-Drug ConjugatesCharles Swanton (14:26):That's a great question. So one of the challenges with chemotherapy, as you know, is the normal tissue toxicity. So for instance, neutropenia, hair loss, bowel dysfunction, diarrhea, epithelial damage, essentially as you know, cytotoxics affect rapidly dividing tissues, so bone marrow, epithelial tissues. And because until relatively recently we had no way of targeting chemotherapy patients experienced side effects associated with them. So over the last decade or so, pioneers in this field have brought together this idea of biological therapies linked with chemotherapy through a biological linker. And so one poster chart of that would be the drug T-DXd, which is essentially Herceptin linked to a chemotherapy drug. And this is just the most extraordinary drug that obviously binds the HER2 receptor, but brings the chemotherapy and proximity of the tumor. The idea being the more drug you can get into the tumor and the less you're releasing into normal tissue, the more on tumor cytotoxicity you'll have and the less off tumor on target normal tissue side effects you'll have. And to a large extent, that's being shown to be the case. That doesn't mean they're completely toxicity free, they're not. And one of the side effects associated with these drugs is pneumonitis.(16:03):But that said, the efficacy is simply extraordinary. And for example, we're having to rewrite the rule books if you like, I think. I mean I'm not a breast cancer physician, I used to be a long time ago, but back in the past in the early 2000s, there was HER2 positive breast cancer and that's it. Now they're talking about HER2 low, HER2 ultra-low, all of which seem to in their own way be sensitive to T-DXd, albeit to a lower extent than HER2 positive disease. But the point is that there doesn't seem to be HER2 completely zero tumor group in breast cancer. And even the HER2-0 seem to benefit from T-DXd to an extent. And the question is why? And I think what people are thinking now is it's a combination of very low cell service expression of HER2 that's undetectable by conventional methods like immunohistochemistry, but also something exquisitely specific about the way in which HER2 is mobilized on the membrane and taken back into the cell. That seems to be specific to the breast cancer cell but not normal tissue. So in other words, the antibody drug conjugate binds the tumor cell, it's thought the whole receptor's internalized into the endosome, and that's where the toxicity then happens. And it's something to do with the endosomal trafficking with the low level expression and internalization of the receptor. That may well be the reason why these HER2 low tumors are so sensitive to this beautiful technology.Eric Topol (17:38):Now I mean it is an amazing technology in all these years where we just were basically indiscriminately trying to kill cells and hoping that the cancer would succumb. And now you're finding whether you want to call it a carry or vector or Trojan horse, whatever you want to call it, but do you see that analogy of the HER2 receptor that's going to be seen across the board in other cancers?Charles Swanton (18:02):That's the big question, Eric. I think, and have we just lucked out with T-DXd, will we find other T-DXd like ADCs targeting other proteins? I mean there are a lot of ADCs being developed against a lot of different cell surface proteins, and I think the jury's still out. I'm confident we will, but we have to bear in mind that biology is a fickle friend and there may be something here related to the internalization of the receptor in breast cancer that makes this disease so exquisitely sensitive. So I think we just don't know yet. I'm reasonably confident that we will find other targets that are as profoundly sensitive as HER2 positive breast cancer, but time will tell.Cancer, A Systemic DiseaseEric Topol (18:49):Right. Now along these lines, well the recent paper that you had in Cell, called embracing cancer complexity, which we've talking about a bit, in fact it's kind of those two words go together awfully well, but hallmarks of systemic disease, this was a masterful review, as you say with the team that you led. But can you tell us about what's your main perspective about this systemic disease? I mean obviously there's been the cancer is like cardiovascular and cancers like this or that, but here you really brought it together with systemic illness. What can you say about that?Charles Swanton (19:42):Well, thanks for the question first of all, Eric. So a lot of this comes from some of my medical experience of treating cancer and thinking to myself over the years, molecular biology has had a major footprint on advances in treating the disease undoubtedly. But there are still aspects of medicine where molecular biology has had very little impact, and often that is in areas of suffering in patients with advanced disease and cancer related to things like cancer cachexia, thrombophilia. What is the reason why patients die blood clots? What is the reason patients die of cancer at all? Even a simple question like that, we don't always know the answer to, on death certificates, we write metastatic disease as a cause of cancer death, but we have patients who die with often limited disease burden and no obvious proximal cause of death sometimes. And that's very perplexing, and we need to understand that process better.(20:41):And we need to understand aspects like cancer pain, for example, circadian rhythms affect biological sensitivity of cancer cells to drugs and what have you. Thinking about cancer rather than just sort of a single group of chaotically proliferating cells to a vision of cancer interacting both locally within a microenvironment but more distantly across organs and how organs communicate with the cancer through neuronal networks, for example, I think is going to be the next big challenge by setting the field over the next decade or two. And I think then thinking about more broadly what I mean by embracing complexity, I think some of that relates to the limitations of the model systems we use, trying to understand inter-organ crosstalk, some of the things you cover in your beautiful Twitter reviews. (←Ground Truths link) I remember recently you highlighted four publications that looked at central nervous system, immune cell crosstalk or central nervous system microbiome crosstalk. It's this sort of long range interaction between organs, between the central nervous system and the immune system and the cancer that I'm hugely interested in because I really think there are vital clues there that will unlock new targets that will enable us to control cancers more effectively if we just understood these complex networks better and had more sophisticated animal model systems to be able to interpret these interactions.Eric Topol (22:11):No, it's so important what you're bringing out, the mysteries that still we have to deal with cancer, why patients have all these issues or dying without really knowing what's happened no less, as you say, these new connects that are being discovered at a remarkable pace, as you mentioned, that ground truths. And also, for example, when I spoke with Michelle Monje, she's amazing on the cancer, where hijacking the brain cells and just pretty extraordinary things. Now that gets me to another line of work of yours. I mean there are many, but the issue of evolution of the tumor, and if you could put that in context, a hot area that's helping us elucidate these mechanisms is known as spatial omics or spatial biology. This whole idea of being able to get the spatial temporal progression through single cell sequencing and single cell nuclei, all the single cell omics. So if you could kind of take us through what have we learned with this technique and spatial omics that now has changed or illuminated our understanding of how cancer evolves?Charles Swanton (23:37):Yeah, great question. Well, I mean I think it helps us sort of rewind a bit and think about evolution in general. Genetic selection brought about by diverse environments and environmental pressures that force evolution, genetic evolution, and speciation down certain evolutionary roots. And I think one can think about cancers in a similar way. They start from a single cell and we can trace the evolutionary paths of cancers by single cell analysis as well as bulk sequencing of spatially separated tumor regions to be able to reconstruct their subclones. And that's taught us to some extent, what are the early events in tumor evolution? What are the biological mechanisms driving branched evolution? How does genome instability begin in tumors? And we found through TRACERx work, whole genome doubling is a major route through to driving chromosome instability along with mutagenic enzymes like APOBEC that drive both mutations and chromosomal instability.(24:44):And then that leads to a sort of adaptive radiation in a sense, not dissimilar to I guess the Cambrian explosion of evolutionary opportunity upon which natural selection can act. And that's when you start to see the hallmarks of immune evasion like loss of HLA, the immune recognition molecules that bind the neoantigens or even loss of the neoantigens altogether or mutation of beta 2 microglobulin that allow the tumor cells to now evolve below the radar, so to speak. But you allude to the sort of spatial technologies that allow us to start to interpret the microenvironments as well. And that then tells us what the evolutionary pressures are upon the tumor. And we're learning from those spatial technologies that these environments are incredibly diverse, actually interestingly seem to be converging on one important aspect I'd like to talk to you a little bit more about, which is the myeloid axis, which is these neutrophils, macrophages, et cetera, that seem to be associated with poor outcome and that will perhaps talk about pollution in a minute.(25:51):But I think they're creating a sort of chronic inflammatory response that allows these early nascent tumor cells to start to initiate into frankly tumor invasive cells and start to grow. And so, what we're seeing from these spatial technologies in lung cancer is that T-cells, predatory T-cells, force tumors to lose their HLA molecules and what have you to evade the immune system. But for reasons we don't understand, high neutrophil infiltration seems to be associated with poor outcome, poor metastasis free survival. And actually, those same neutrophils we've recently found actually even tracked to the metastasis sites of metastasis. So it's almost like this sort of symbiosis between the myeloid cells and the tumor cells in their biology and growth and progression of the tumor cells.Eric Topol (26:46):Yeah, I mean this white cell story, this seems to be getting legs and is relatively new, was this cracked because of the ability to do this type of work to in the past everything was, oh, it's cancer's heterogeneous and now we're getting pinpoint definition of what's going on.Charles Swanton (27:04):I think it's certainly contributed, but it's like everything in science, Eric, when you look back, there's evidence in the literature for pretty much everything we've ever discovered. You just need to put the pieces together. And I mean one example would be the neutrophil lymphocyte ratio in the blood as a hallmark of outcome in cancers and to checkpoint inhibitor blockade, maybe this begins to explain it, high neutrophils, immune suppressive environment, high neutrophils, high macrophages, high immune suppression, less benefit from checkpoint inhibitor therapy, whereas you want lymphocyte. So I think there are biomedical medical insights that help inform the biology we do in the lab that have been known for decades or more. And certainly the myeloid M2 axis in macrophages and what have you was known about way before these spatial technologies really came to fruition, I think.The Impact of Air PollutionEric Topol (28:01):Yeah. Well you touched on this about air pollution and that's another dimension of the work that you and your team have done. As you well know, there was a recent global burden of disease paper in the Lancet, which has now said that air pollution with particulate matter 2.5 less is the leading cause of the burden of disease in the world now.Charles Swanton (28:32):What did you think of that, Eric?Eric Topol (28:34):I mean, I was blown away. Totally blown away. And this is an era you've really worked on. So can you put it in perspective?Charles Swanton (28:42):Yeah. So we got into this because patients of mine, and many of my colleagues would ask the same question, I've never smoked doctor, I'm healthy. I'm in my mid 50s though they're often female and I've got lung cancer. Why is that doctor? I've had a good diet, I exercise, et cetera. And we didn't really have a very good answer for that, and I don't want to pretend for a minute we solved the whole problem. I think hopefully we've contributed to a little bit of understanding of why this may happen. But that aside, we knew that there were risk factors associated with lung cancer that included air pollution, radon exposure, of course, germline genetics, we mustn't forget very important germline variation. And I think there is evidence that all of them are associated with lung cancer risk in different ways. But we wanted to look at air pollution, particularly because there was an awful lot of evidence, several meta-analysis of over half a million individuals showing very convincingly with highly significant results that increasing PM 2.5 micron particulate levels were associated with increased risk of lung cancer.(29:59):To put that into perspective, where you are on the west coast of the US, it's relatively unpolluted. You would be talking about maybe five micrograms per meter cubed of PM2.5 in a place like San Diego or Western California, assuming there aren't any forest fires of course. And we estimate that that would translate to about, we think it's about one extra case of never smoking lung cancer per hundred thousand of the population per year per one microgram per meter cube rise in the pollution levels. So if you go to Beijing for example, on a bad day, the air pollution levels could be upwards of a hundred micrograms per meter cubed because there are so many coal fired power stations in China partly. And there I think the risk is considerably higher. And that's certainly what we've seen in the meta-analyses in our limited and relatively crude epidemiological analyses to be the case.(30:59):So I think the association was pretty certain, we were very confident from people's prior publications  this was important. But of course, association is not causation. So we took a number of animal models and showed that you could promote lung cancer formation in four different oncogene driven lung cancer models. And then the question is how, does air pollution stimulate mutations, which is what I initially thought it would do or something else. It turns out we don't see a significant increase in exogenous like C to A carcinogenic mutations. So that made us put our thinking caps on. And I said to you earlier, often all these discoveries have been made before. Well, Berenblum in 1947, first postulated that actually tumors are initiated through a two-step process, which we now know involves a sort of pre initiated cell with a mutation in that in itself is not sufficient to cause cancer.(31:58):But on top of that you need an inflammatory stimulus. So the question was then, well, okay, is inflammation working here? And we found that there was an interleukin-1 beta axis. And what happens is that the macrophages come into the lung on pollution exposure, engulf phagocytose the air pollutants, and we think what's happening is the air pollutants are puncturing membranes in the lung. That's what we think is happening. And interleukin-1 beta preformed IL-1 beta is being released into the extracellular matrix and then stimulating pre-initiated cells stem cells like the AT2 cells with an activating EGFR mutation to form a tumor. But the EGFR mutation alone is not sufficient to form tumors. It's only when you have the interleukin-1 beta and the activated mutation that a tumor can start.(32:49):And we found that if we sequence normal lung tissue in a healthy adult 60-year-old adult, we will find about half of biopsies will have an activating KRAS mutation in normal tissue, and about 15% will have an activating mutation in EGFR in histologically normal tissue with nerve and of cancer. In fact, my friend and colleague who's a co-author on the paper, James DeGregori, who you should speak to in Colorado, fascinating evolutionary cancer biologists estimates that in a healthy 60-year-old, there are a hundred billion cells in your body that harbor an oncogenic mutation. So that tells you that at the cellular level, cancer is an incredibly rare event and almost never happens. I mean, our lifetime risk of cancer is perhaps one in two. You covered that beautiful pancreas paper recently where they estimated that there may be 80 to 100 KRAS mutations in a normal adult pancreas, and yet our lifetime risk of pancreas cancer is one in 70. So this tells you that oncogenic mutations are rarely sufficient to drive cancer, so something else must be happening. And in the context of air pollution associated lung cancer, we think that's inflammation driven by these white cells, these myeloid cells, the macrophages.Cancer BiomarkersEric Topol (34:06):No, it makes a lot of sense. And this, you mentioned the pancreas paper and also what's going in the lung, and it seems like we have this burden of all you need is a tipping point and air pollution seems to qualify, and you seem to be really in the process of icing the mechanism. And like I would've thought it was just mutagenic and it's not so simple, right? But that gets me to this is such an important aspect of cancer, the fact that we harbor these kind of preconditions. And would you think that cancer takes decades to actually manifest most cancers, or do we really have an opportunity here to be able to track whether it's through blood or other biomarkers? Another area you've worked on a lot whereby let's say you could define people at risk for polygenic risk scores or various cancers or genome sequencing for predisposition genes, whatever, and you could monitor in the future over the course of those high-risk people, whether they were starting to manifest microscopic malignancy. Do you have any thoughts about how long it takes for the average person to actually manifest a typical cancer?Charles Swanton (35:28):That's a cracking question, and the answer is we've got some clues in various cancers. Peter Campbell would be a good person to speak to. He estimates that some of the earliest steps in renal cancer can occur in adolescence. We've had patients who gave up smoking 30 or so years ago where we can still see the clonal smoking mutations in the trunk of the tumor's evolutionary tree. So the initial footprints of the cancer are made 30 years before the cancer presents. That driver mutation itself may also be a KRAS mutation in a smoking cigarette context, G12C mutation. And those mutations can precede the diagnosis of the disease by decades. So the earliest steps in cancer evolution can occur, we think can precede diagnoses by a long time. So to your point, your question which is, is there an opportunity to intervene? I'm hugely optimistic about this actually, this idea of molecular cancer prevention.An Anti-Inflammatory Drug Reduces Fatal Cancer and Lung Cancer(36:41):How can we use data coming out of various studies in the pancreas, mesothelioma, lung, et cetera to understand the inflammatory responses? I don't think we can do very much about the mutations. The mutations unfortunately are a natural consequence of aging. You and I just sitting here talking for an hour will have accumulated multiple mutations in our bodies over that period, I'm afraid and there's no escaping it. And right now there's not much we can do to eradicate those mutant clones. So if we take that as almost an intractable problem, measuring them is hard enough, eradicating them is even harder. And then we go back to Berenblum in 1947 who said, you need an inflammatory stimulus. Well, could we do something about the inflammation and dampen down the inflammation? And of course, this is why we got so excited about IL-1 beta because of the CANTOS trial, which you may remember in 2017 from Ridker and colleagues showed that anti IL-1 beta used as a mechanism of preventing cardiovascular events was associated with a really impressive dose dependent reduction in new lung cancer primaries.(37:49):Really a beautiful example of cancer prevention in action. And that data weren't just a coincidence. The FDA mandated Novartis to collect the solid tumor data and the P-values are 0.001. I mean it's very highly significant dose dependent reduction in lung cancer incidents associated with anti IL-1 beta. So I think that's really the first clue in my mind that something can be done about this problem. And actually they had five years of follow-up, Eric. So that's something about that intervening period where you can treat and then over time see a reduction in new lung cancers forming. So I definitely think there's a window of opportunity here.Eric Topol (38:31):Well, what you're bringing up is fascinating here because this trial, which was a cardiology trial to try to reduce heart attacks, finds a reduction in cancer, and it's been lost. It's been buried. I mean, no one's using this therapy to prevent cancer between ratcheting up the immune system or decreasing inflammation. We have opportunities that we're not even attempting. Are there any trials that are trying to do this sort of thing?Charles Swanton (39:02):So this is the fundamental problem. Nobody wants to invest in prevention because essentially you are dealing with well individuals. It's like the vaccine challenge all over again. And the problem is you never know who you are benefiting. There's no economic model for it. So pharma just won't touch prevention with a barge pole right now. And that's the problem. There's no economic model for it. And yet the community, all my academic colleagues are crying out saying, this has got to be possible. This has got to be possible. So CRUK are putting together a group of like-minded individuals to see if we can do something here and we're gradually making progress, but it is tough.Eric Topol (39:43):And it's interesting that you bring that up because for GRAIL, one of the multicenter cancer early detection companies, they raised billions of dollars. And in fact, their largest trial is ongoing in the UK, but they haven't really focused on high-risk people. They just took anybody over age 50 or that sort of thing. But that's the only foray to try to reboot how we or make an early microscopic diagnosis of cancer and track people differently. And there's an opportunity there. You've written quite a bit on you and colleagues of the blood markers being able to find a cancer where well before, in fact, I was going to ask you about that is, do you think there's people that are not just having all these mutations every minute, every hour, but that are starting to have the early seeds of cancer, but because their immune system then subsequently kicks in that they basically kind of quash it for that period of time?Charles Swanton (40:47):Yeah, I do think that, I mean, the very fact that we see these sort of footprints in the tumor genome of immune evasion tells you that the immune system's having a very profound predatory effect on evolving tumors. So I do think it's very likely that there are tumors occurring that are suppressed by the immune system. There is a clear signature, a signal of negative selection in tumors where clones have been purified during their evolution by the immune system. So I think there's pretty strong evidence for that now. Obviously, it's very difficult to prove something existed when it doesn't now exist, but there absolutely is evidence for that. I think it raises the interesting question of immune system recognizes mutations and our bodies are replete with mutations as we were just discussing. Why is it that we're not just a sort of epithelial lining of autoimmunity with T-cells and immune cells everywhere? And I think what the clever thing about the immune system is it's evolved to target antigens only when they get above a certain burden. Otherwise, I think our epithelial lining, our skin, our guts, all of our tissues will be just full of T-cells eating away our normal clones.(42:09):These have to get to a certain size for antigen to be presented at a certain level for the immune system to recognize it. And it's only then that you get the immune predation occurring.Forever Chemicals and Microplastics Eric Topol (42:20):Yeah, well, I mean this is opportunities galore here. I also wanted to extend the air pollution story a bit. Obviously, we talked about particulate matter and there's ozone and nitric NO2, and there's all sorts of other air pollutants, but then there's also in the air and water these forever chemicals PFAS for abbreviation, and they seem to be incriminated like air pollution. Can you comment about that?Charles Swanton (42:55):Well, I can comment only insofar as to say I'm worried about the situation. Indeed, I'm worried about microplastics actually, and you actually cover that story as well in the New England Journal, the association of microplastics with plaque rupture and atheroma. And indeed, just as in parenthesis, I wanted to just quickly say we currently think the same mechanisms that are driving lung cancer are probably responsible for atheroma and possibly even neurodegenerative disease. And essentially it all comes down to the macrophages and the microglia becoming clogged up with these pollutants or environmental particulars and releasing chronic inflammatory mediators that ultimately lead to disease. And IL-1 beta being one of those in atheroma and probably IL-6 and TNF in neurodegenerative disease and what have you. But I think this issue that you rightly bring up of what is in our environment and how does it cause pathology is really something that epidemiologists have spent a lot of time focusing on.(43:56):But actually in terms of trying to move from association to causation, we've been, I would argue a little bit slow biologically in trying to understand these issues. And I think that is a concern. I mean, to give you an example, Allan Balmain, who works at UCSF quite close to you, published a paper in 2020 showing that 17 out of 20 environmental carcinogens IARC carcinogens class one carcinogens cause tumors in rodent models without driving mutations. So if you take that to a logical conclusion, in my mind, what worries me is that many of the sort of carcinogen assays are based on driving mutagenesis genome instability. But if many carcinogen aren't driving DNA mutagenesis but are still driving cancer, how are they doing it? And do we actually have the right assays to interpret safety of new chemical matter that's being introduced into our environment, these long-lived particles that we're breathing in plastics, pollutants, you name it, until we have the right biological assays, deeming something to be safe I think is tricky.Eric Topol (45:11):Absolutely. And I share your concerns on the nanoplastic microplastic story, as you well know, not only have they been seen in arteries that are inflamed and in blood clots and in various tissues, have they been seen so far or even looked for within tumor tissue?Charles Swanton (45:33):Good question. I'm not sure they have. I need to check. What I can tell you is we've been doing some experiments in the lab with fluorescent microplastics, 2.5 micron microplastics given inhaled microplastics. We find them in every mouse organ a week after. And these pollutants even get through into the brain through the olfactory bulb we think.Charles Swanton (45:57):Permeate every tissue, Eric.Eric Topol (45:59):Yeah, no, this is scary because here we are, we have these potentially ingenious ways to prevent cancer in the future, but we're chasing our tails by not doing anything to deal with our environment.Charles Swanton (46:11):I think that's right. I totally agree. Yeah.Eric Topol (46:15):So I mean, I can talk to you for the rest of the day, but I do want to end up with a topic that we have mutual interest in, which is AI. And also along with that, when you mentioned about aging, I'd like to get your views on these two, how do you see AI fitting into the future of cancer? And then the more general topic is, can we actually at some point modulate the biologic aging process with or without help with from AI? So those are two very dense questions, but maybe you can take us through them.Charles Swanton (46:57):How long have we got?Eric Topol (46:59):Just however long you have.A.I. and CancerCharles Swanton (47:02):AI and cancer. Well, AI and medicine actually in general, whether it's biomedical research or medical care, has just infinite potential. And I'm very, very excited about it. I think what excites me about AI is it's almost the infinite possibilities to work across scale. Some of the challenges we raised in the Cell review that you mentioned, tackling, embracing complexity are perfectly suited for an AI problem. Nonlinear data working, for instance in our fields with CT imaging, MRI imaging, clinical outcome data, blood parameters, genomics, transcriptomes and proteomes and trying to relate this all into something that's understandable that relates to risk of disease or potential identification of a new drug target, for example. There are numerous publications that you and others have covered that allude to the incredible possibilities there that are leading to, for instance, the new identification of drug targets. I mean, Eli Van Allen's published some beautiful work here and in the context of prostate cancer with MDM4 and FGF receptor molecules being intimately related to disease biology.(48:18):But then it's not just that, not just drug target identification, it's also going all the way through to the clinic through drug discovery. It's how you get these small molecules to interact with oncogenic proteins and to inhibit them. And there are some really spectacular developments going on in, for instance, time resolved cryo-electron microscopy, where in combination with modeling and quantum computing and what have you, you can start to find pockets emerging in mutant proteins, but not the wild type ones that are druggable. And then you can use sort of synthetic AI driven libraries to find small molecules that will be predicted to bind these transiently emerging pockets. So it's almost like AI is primed to help at every stage in scientific investigation from the bench all the way through to the bedside. And there are examples all the way through there in the literature that you and others have covered in the last few years. So I could not be more excited about that.Eric Topol (49:29):I couldn't agree with you more. And I think when we get to multimodal AI at the individual level across all their risks for conditions in their future, I hope someday will fulfill that fantasy of primary prevention. And that is getting me to this point that I touched on because I do think they interact to some degree AI and then will we ever be able to have an impact on aging? Most people conflate this because what we've been talking about throughout the hour has been age-related diseases, that is cancer, for example, and cardiovascular and neurodegenerative, which is different than changing aging per se, body wide aging. Do you think we'll ever changed body wide aging?Charles Swanton (50:18):Wow, what a question. Well, if you'd asked me 10 years ago, 15 years ago, do you think we'll ever cure melanoma in my lifetime, I'd have said definitely not. And now look where we are. Half of patients with melanoma, advanced melanoma, even with brain metastasis curd with combination checkpoint therapy. So I never say never in biology anymore. It always comes back to bite you and prove you wrong. So I think it's perfectly possible.Charles Swanton (50:49):We have ways to slow down the aging process. I guess the question is what will be the consequences of that?Eric Topol (50:55):That's what I was going to ask you, because all these things like epigenetic reprogramming and senolytic drugs, and they seem to at least pose some risk for cancer.Charles Swanton (51:09):That's the problem. This is an evolutionary phenomenon. It's a sort of biological response to the onslaught of these malignant cells that are potentially occurring every day in our normal tissue. And so, by tackling one problem, do we create another? And I think that's going to be the big challenge over the next 50 years.Eric Topol (51:31):Yeah, and I think your point about the multi-decade challenge, because if you can promote healthy aging without any risk of cancer, that would be great. But if the tradeoff is close, it's not going to be very favorable. That seems to be the main liability of modulation aging through many of the, there's many shots on goal here, of course, as you well know. But they do seem to pose that risk in general.Charles Swanton (51:58):I think that's right. I think the other thing is, I still find, I don't know if you agree with me, but it is an immense conundrum. What is the underlying molecular basis for somatic aging, for aging of normal tissues? And it may be multifactorial, it may not be just one answer to that question. And different tissues may age in different ways. I don't know. It's a fascinating area of biology, but I think it really needs to be studied more because as you say, it underpins all of these diseases we've been talking about today, cardiovascular, neurodegeneration, cancer, you name it. We absolutely have to understand this. And actually, the more I work in cancer, the more I feel like actually what I'm working on is aging.(52:48):And this is something that James DeGregori and I have discussed a lot. There's an observation that in medicine around patients with alpha-1 antitrypsin deficiency who are at higher risk of lung cancer, but they're also at high risk of COPD, and we know the associations of chronic obstructive pulmonary disease with lung cancer risk. And one of the theories that James had, and I think this is a beautiful idea, actually, is as our tissues age, and COPD is a reflection of aging, to some extent gone wrong. And as our tissues age, they become less good at controlling the expansion of these premalignant clones, harboring, harboring oncogenic mutations in normal tissue. And as those premalignant clones expand, the substrate for evolution also expands. So there's more likely to be a second and third hit genetically. So it may be by disrupting the extracellular matrices through inflammation that triggers COPD through alpha-1 antitrypsin deficiency or smoking, et cetera, you are less effectively controlling these emergent clones that just expand with age, which I think is a fascinating idea actually.Eric Topol (54:01):It really is. Well, I want to tell you, Charlie, this has been the most fascinating, exhilarating discussion I've ever had on cancer. I mean, really, I am indebted to you because not just all the work you've done, but your ability to really express it, articulate it in a way that hopefully everyone can understand who's listening or reading the transcript. So we'll keep following what you're doing because you're doing a lot of stuff. I can't thank you enough for joining me today, and you've given me lots of things to think about. I hope the people that are listening or reading feel the same way. I mean, this has been so mind bending in many respects. We're indebted to you.Charles Swanton (54:49):Well, we all love reading your Twitter feeds. Keep them coming. It helps us keep a broader view of medicine and biological research, not just cancer, which is why I love it so much.******************************************The Ground Truths newsletters and podcasts are all free, open-access, without ads.Please share this post/podcast with your friends and network if you found it informativeVoluntary paid subscriptions all go to support Scripps Research. Many thanks for that—they greatly helped fund our summer internship programs for 2023 and 2024.Thanks to my producer Jessica Nguyen and Sinjun Balabanoff tor audio and video support at Scripps Research.Note: you can select preferences to receive emails about newsletters, podcasts, or all I don't want to bother you with an email for content that you're not interested in. Get full access to Ground Truths at erictopol.substack.com/subscribe

The Bill & Melinda Gates Foundation, with an endowment of over $50 billion, is one of the largest and most influential philanthropic organizations in the world. With a focus on addressing global health, poverty, and education, its initiatives have led to the reduction of malaria mortality by 60% over the past two decades, the near eradication of polio, increased educational opportunities of millions of students, and improved sanitation conditions for millions of people in developing countries. For six years, oncologist Sue Desmond-Hellmann, MD, MPH was the CEO of this organization. Prior to that, she served as Chancellor of the University of California at San Francisco, as well as President of Product Development at Genentech, where she oversaw the development of Herceptin, Avastin, Rituxan, and other blockbuster cancer drugs that are now staples in the arsenal of many medical oncologists.The topics of our discussion in this episode are as varied as Dr. Desmond-Hellman's career. We discuss, among other things, how seeing the work of her pharmacist father encouraged her to pursue a career in medicine, how her early experiences treating HIV patients in Uganda spurred her to tackle global health challenges, how she discovered a passion for product development in the pharmaceutical industry, how she reconciles the ethical quandaries of developing medications that can cause serious adverse effects and that can sometimes cost hundreds of thousands of dollars per dose, what her mission while at the Gates Foundation was, and her perspectives on the role of artificial intelligence and human health and well-being, now that she has joined the board of directors of OpenAI, the company behind ChatGPT.In this episode, you will hear about: 2:50 - How working in her father's pharmacy led Dr. Desmond-Hellmann to a career in medicine4:56 - A brief summary of Dr. Desmond-Hellmann's multifaceted career trajectory15:36 - What the day to day work of pharmaceutical drug development looks like 18:30 - The challenging ethical concerns that surround drug approvals especially as it pertains to safety concerns23:44 - Dr. Desmond-Hellmann's experiences in Uganda that forever transformed her views on poverty 27:55 - The aims of the Gates Foundation 30:47 - How Dr. Desmond-Hellmann views her work both in the non-profit and the for-profit sectors 37:15 - Dr. Desmond-Hellmann's mission when she took on a leading role at The Gates Foundation 38:38 - How Dr. Desmond-Hellmann thinks about shaping the future of AI as she takes a seat on the board of OpenAI45:14 - Dr. Desmond-Hellmann's advice for medical trainees and clinicians on how to navigate the many opportunities available to them along their career pathDr. Sue Desmond-Hellmann can be found on Twitter/X @suedhellmann.Visit our website www.TheDoctorsArt.com where you can find transcripts of all episodes.If you enjoyed this episode, please subscribe, rate, and review our show, available for free on Spotify, Apple Podcasts, or wherever you get your podcasts. If you know of a doctor, patient, or anyone working in health care who would love to explore meaning in medicine with us on the show, feel free to leave a suggestion in the comments or send an email to info@thedoctorsart.com.Copyright The Doctor's Art Podcast 2024

We pick up from last week inc. the latest data on the mind-body axis, off-licence meds, autophagy, gut health, and dental health. Always consult your doctor for advice.

In today's episode of Keeping Abreast with Dr. Jenn, I am thrilled to be joined by Carla Patullo, an award-winning musician and film composer who shares her profound journey through breast cancer. Diagnosed in 2019, Carla's story is one of resilience, self-advocacy, and the transformative power of music. We delve into her initial hesitation to prioritize her health amidst a demanding career, the critical importance of listening to our bodies, and her advocacy to receive the medical attention she needed.In this episode you'll:Learn the importance of self-advocacy in navigating the healthcare system.Discover how Carla's breast cancer diagnosis led her to overhaul her lifestyle and prioritize self-care.Understand the critical role of supportive healthcare teams in inspiring hope and positive change.Gain insight into the transformative power of gratitude and setting boundaries post-treatment.Hear about the impact of Herceptin on HER2-positive breast cancerEpisode Timeline:01:19 Guest Introduction: Carla Patullo02:34 Carla's Initial Health Journey and Diagnosis08:47 The Importance of Self-Advocacy in Healthcare14:15 Finding the Right Medical Support17:32 Transition from Survivor Mentality to Living with Hope21:50 Carla's New Album and Healing Through Music26:08 The Role of Herceptin in HER2-Positive Breast Cancer32:27 Embracing Gratitude and Setting Boundaries Post-Treatment35:46 Carla's New Approach to Life: Prioritizing Self-Care and Nature41:15 Dr. Jenn's Insights on Primary Food and Nourishment45:03 Carla's Evolving Creative Process and Morning Routines52:30 Reflections on Carla's Album "She Hals" and Its Impact58:55 Closing Remarks and Encouragement to ListenersCarla Patullo is an acclaimed musician and film composer whose work has earned awards and accolades. Diagnosed with breast cancer in 2019, her journey has deeply influenced her music and outlook on life. Carla's latest album incorporates elements of healing and explores themes of trauma, movement, and stillness, with a focus on holistic well-being. Her resilience and creativity continue to inspire and empower others on their health journeys.Connect with Carla:Website: https://www.carlapatullo.com/aboutTo talk to a member of Dr. Jenn's team and learn more about working privately with RHMD, visit: https://jennsimmons.simplero.com/page/377266?kuid=327aca17-5135-44cf-9210-c0b77a56e26d&kref=vOKy0sAiorrKTo get your copy of Dr. Jenn's book, The Smart Woman's Guide to Breast Cancer, visit: https://tinyurl.com/SmartWomansBreastCancerGuideJoin the Facebook group: Facebook: https://www.facebook.com/groups/keepingabreastwdrjennConnect with Dr. Jenn:Website: https://www.realhealthmd.com/Facebook: https://www.facebook.com/DrJennSimmonsInstagram: https://www.instagram.com/drjennsimmons/YouTube: https://www.youtube.com/@dr.jennsimmons

Synopsis: In this episode of Biotech2050, Dr. Ted Love, former CEO of Global Blood Therapeutics and Current Chairman of BIO, shares insights on sickle cell breakthroughs, transitioning from academia to research, navigating a tight funding environment, and protecting an innovative ecosystem to benefit patients. Biography: Dr. Ted Love is the chair of the Board of Directors at the Biotechnology Innovation Organization (BIO), a position he assumed in June 2023. A long-time BIO Board Member, Dr. Love has focused on championing access to care, standing up for science, and improving the narrative around the biopharma industry. Dr. Love previously served as president and chief executive officer of Global Blood Therapeutics (GBT). During his tenure at GBT, Dr. Love led the company from a pre-clinical start-up, through the accelerated approval and launch of Oxbryta®, and into a global commercial company with an advanced pipeline of innovative therapies focused on sickle cell disease. Prior to GBT, Dr. Love was executive vice president, research and development and technical operations, at Onyx Pharmaceuticals, Inc., where he played an instrumental role in the accelerated approval of Kyprolis® for multiple myeloma, and the subsequent purchase of Onyx by Amgen. Previously, Dr. Love served as president, chief executive officer and chairman of Nuvelo, Inc., and as senior vice president, development, at Theravance, Inc. Dr. Love began his biotech career at Genentech in 1992, where he held several senior management positions in clinical science and product development, and ultimately as chairman of Genentech's Product Development Committee. As vice president, product development, Dr. Love oversaw the development strategy and execution leading to approvals of Rituxan®, Herceptin®, Xolair®, TNKase®, Raptiva® and Avastin®. Prior to Genentech, Dr. Love was a member of the Department of Cardiology at the Massachusetts General Hospital. Dr. Love currently serves on the boards of directors of Royalty Pharma and Structure Therapeutics. Dr. Love holds a B.A. in molecular biology from Haverford College and an M.D. from Yale Medical School. He completed a residency in internal medicine and a fellowship in cardiology at the Massachusetts General Hospital.

Dr. Ghaleb Husseini, AUS Professor in Chemical and Biological Engineering, joins the Morning Majlis Show to elaborate on the process of Herceptin-targeted nanocarriers and how it can fight cancer cells whilst being safe. Dr. Husseini also explains the future of cancer treatments and the next steps required for this treatment to become a fully approved method. Listen to #Pulse95Radio in the UAE by tuning in on your radio (95.00 FM) or online on our website: www.pulse95radio.com ************************ Follow us on Social. www.facebook.com/pulse95radio www.twitter.com/pulse95radio www.instagram.com/pulse95radio www.youtube.com/pulse95radio

In a conversation with CancerNetwork®, Amy Tiersten, MD, spoke about how findings from the phase 1/2 ASPIRE trial (NCT03304080) may support anastrozole (Arimidex) plus palbociclib (Ibrance), trastuzumab (Herceptin), and pertuzumab (Perjeta) as a first-line treatment for patients with hormone receptor (HR)–positive, HER2-positive metastatic breast cancer. Data presented at the 2023 San Antonio Breast Cancer Symposium (SABCS)highlighted a clinical benefit rate of 97% (95% CI, 83%-100%; P

The last week was a busy one for us here at CURE® and across the oncology space in general. There were two major meetings we covered: the San Antonio Breast Cancer Symposium and the American Society of Hematology Annual Meeting.  The San Antonio Breast Cancer Symposium — also known as SABCS — features breast cancer research conducted around the globe. We had editors on the ground in San Antonio, as well as back in our office covering the meeting. Here are some highlights from SABCS.  And, to view all of our conference coverage, be sure to check out curetoday.com/conference Kadcyla Is the ‘First Therapy to Show Improved Survival' in a Breast Cancer Subset For in patients with HER2-positive early breast cancer that still had remaining invasive disease after undergoing neoadjuvant therapy Kadcyla outperformed Herceptin when it came to overall survival, which is the time until death of any cause, and invasive disease-free survival, which is the time patients live without experience metastases or invasive disease.  The findings, which come out of the KATHERINE trial, mark the “first therapy to show an improved survival after post-surgical therapy in patients with HER2-positive early breast cancer and residual invasive disease after neoadjuvant therapy,” according to study author, Dr. Sibylle Loibl, who presented the findings at SABCS.  More specifically, at the 8.4-year follow-up mark, 70.1% of patients in the Kadcyla group and 62% in the Herceptin group were still alive. Also at that point, 32.2% given Kadcyla did not develop invasive disease, compared with 19.7% of patients in the Herceptin group.  Keytruda, Chemo Show Early-Stage Breast Cancer Event-Free Survival Benefits Findings from phase 3 KEYNOTE-522 trial showed that presurgical Keytruda plus chemotherapy, followed by postsurgical Keytruda led to improved event-free survival — that's time a patient lives without complications from their disease — in patients with high-risk, early-stage triple-negative breast cancer.  At a median follow-up of 63.1 months, the five-year event-free survival rate was 81.3% with neoadjuvant Keytruda/chemotherapy followed by adjuvant Keytruda compared with 72.3% in those who received placebo/chemotherapy and then placebo. These findings, according to Dr. Peter Schmid, further support the use of this Keytruda regimen as the standard of care for this patient population.  Tecentriq Plus Perjeta, Herceptin, Chemo Does Not Improve pCR in HER2+ Breast Cancer Another phase 3 trial — the APTneo Michelangelo — showed that adding Tecentriq and Herceptin to Perjeta and chemotherapy actually did not lead to a statistically significant improvement in pathologic complete response (that's the disappearance of cancer) when given in the presurgical setting for patients with HER2-positive breast cancer.  The study found that while Tecentriq and Herceptin-containing regimens did lead to a higher number of pathologic complete responses, these difference between the two treatment groups was not statistically significant, meaning that the researchers could not definitively say that one therapy was the result of better outcomes.  No Racial Difference in Recurrence-Free Survival in HR+, HER2- Breast Cancer While research has shown that Black and White patients with HR-positive, HER2-negative breast cancer tend to have different survival outcomes, research presented at SABCS found that three-year recurrence-free survival is actually comparable between the two groups.   “More aggressive treatment can improve outcomes for (patients with HR-positive, basal-type tumors), as demonstrated by improved (overall survival) in (those who) achieved pathologic complete response,” study investigators stated in the poster. “These data highlight the importance of genomic testing to help optimize treatment and reduce outcome disparities in Black women.”

In a recent discussion with CancerNetwork®, Joleen Hubbard, MD, research collaborator with Mayo Clinic and deputy director for clinical research at Allina Health Cancer Institute in Minneapolis, Minnesota, discussed new opportunities for patients with colorectal cancer (CRC).   In the discussion, Hubbard highlighted the potential of trastuzumab deruxtecan-nxki (Enhertu; T-DXd) in patients with HER2-expressing metastatic CRC based on studies including the phase 2 DESTINY-CRC01 trial (NCT03384940), which assessed the efficacy and safety of the agent in those who progressed after 2 or more prior regimens.1  These trials may play a role in continuing HER2 inhibition downstream after the FDA approval of trastuzumab (Herceptin) plus tucatinib (Tukysa) in patients with metastatic HER2-positive CRC.2   Hubbard also discussed the phase 3 MOUNTAINEER-03 study (NCT03043313) and its effects in the CRC space.3 This trial assessed the safety and efficacy of frontline tucatinib and trastuzumab in patients with treatment-refractory, RAS wild-type, HER2-positive metastatic CRC. Primary endpoints for this analysis showed a clinically meaningful overall response rate of 38.1% and a median duration of response of 12.4 months. Additionally, the treatment combination was well tolerated.   She said she is “optimistic” that moving HER2-directed therapy to the first-line setting, as seen in the MOUNTAINEER-03 study, may help outcomes for patients with metastatic CRC.  “It's a very exciting space,” Hubbard said. “Because it's only 5% to 8% of patients [who have CRC], it may not get as much attention, but there's 150,000 new cases of [CRC] diagnosed each year. So, 5% to 8% of that is a large number of patients [whom] we need to be looking at, studying, and potentially impact with these treatments.”  References  Yoshino T, Di Bartolomeo M, Raghav K, et al. Final results of DESTINY-CRC01 investigating trastuzumab deruxtecan in patients with HER2-expressing metastatic colorectal cancer. Nat Commun. 2023;14(1):1-13. doi:10.1038/s41467-023-38032-4   Seagen announces FDA accelerated approval of Tukysa (tucatinib) in combination with trastuzumab for people with previously treated RAS wild-type, HER2-positive metastatic colorectal cancer. News release. FDA. January 19, 2023. Accessed December 6, 2023. https://bwnews.pr/3Xpzbqn  Bekaii-Saab TS, Van Cutsem E, Tabernero J, et al. MOUNTAINEER-03: phase 3 study of tucatinib, trastuzumab, and mFOLFOX6 as first-line treatment in HER2+ metastatic colorectal cancer—Trial in progress. J Clin Oncol. Published online January 24, 2023. doi:10.1200/jco.2023.41.4_suppl.tps261 

It is our second week of 95bFM's election coverage, and this week's focus is health. Rosetta spoke to Adele Gautier, Research and Strategic Programmes Manager at Breast Cancer Foundation New Zealand, about Pharmac's decision to replace Herceptin with Herzuma, but not to widen eligibility for multiple rounds of treatment for patients with advanced breast cancer. For our weekly catch up with the ACT Party, producer Rawan spoke to SImon Court about some of ACT's health policies, including their proposed review of Pharmac, their promise to subsidise more elective surgeries as well as establish Mental Health and Addiction NZ. For our bi-weekly segment of Tomorrow's World where Rawan and Leilani explore current events around science, technology and the environment, Rawan looked into the increase of youth vaping and The Labour Party's proposed policies surrounding the topic. Rawan spoke to Otago public health expert Janet Hoek and The Health Coalition's Leitu Tufunga. Finally, Rosetta spoke to Co-Chair of the Health Coalition's Alcohol Panel, Karen Wright, about The Sale and Supply of Alcohol Amendment (Community Participation) Bill, and reducing alcohol-related harm in Aotearoa.  

Last Wednesday, Pharmac confirmed it would be replacing treatment Herceptin (brand name for the drug Trastuzumab) with Herzuma, another version of the drug which is equally as effective but at a lower cost. Pharmac has decided not to provide more retreatment opportunities for patients with advanced HER2-positive breast cancer, but Breast Cancer Foundation New Zealand is urging them to reconsider. Rosetta spoke to Adele Gautier, Research and Strategic Programmes Manager for BCFNZ about the decision, and what more needs to be done to increase retreatment options in Aotearoa.

The ‘vote for me' bribe policies continue. National was promising yesterday to pay for 13 cancer treatments not currently available to patients in New Zealand. They're available in Australia, not in New Zealand. The New Zealand Cancer Control Agency recently identified 13 treatments for lung, bowel, kidney and head and neck cancers that provide significant clinical benefits - and they are funded in Australia, not in New Zealand. National says it will allocate $280 million in ring-fenced funding to Pharmac over four years to pay for these therapies. They say it's a better use of taxpayers' money than paying the $5 prescription fees for everyone, including those who can afford to pay for it themselves. National's not throwing everybody under the bus re prescriptions though - they say superannuitants and those on low incomes will receive free prescriptions, as I understand it, a lot of people receive them free anyway if they fall into certain categories. The total amount any family will pay for prescriptions in a year will be capped at $100, and that's how they're going to fund cancer treatments. People who can afford prescriptions will pay for them. Those who can't - won't.   On the Mike Hosking Breakfast, Medical oncologist Dr Chris Jackson wasn't entirely enthusiastic, I think it's fair to say. He believes there are a number of fishhooks in the policy of telling Pharmac what it should be funding.  Dr Jackson also said they'd rather see the funding go towards the  nurses, the doctors, the personnel who need to see these patients before you start talking about drug funding. And probably worth noting, he is married to a Labour minister, Rachel Brooking. But, I'm quite sure, even within your own family, spouses are entitled to different views.  In this case, he was like, I don't think it's a good idea to politicise it. The money should have gone to more doctors, more nurses and more radiologists. Except, Pharmac has been politicised before - remember Herceptin?   So to Dr Jackson's point, drugs can and do get politicised all the time. If you have an organised and eloquent group of campaigners, they will be able to achieve more to get their drug of choice funded than those who don't have the resources. Than those who don't have the lobby group, who don't have the organisational ability and access to publicity that others do. They just have to sit and wait patiently for their drug to come up on the Pharmac list. Personally, I'd rather pay a maximum of $100 a year on my prescriptions than have to sell the house or, heaven forbid, set up and Give-a-little page to keep a loved one alive.See omnystudio.com/listener for privacy information.

This week I'm Still Here welcomes Lori Lober, who has been living with metastatic breast cancer for twenty three years. Lori started on #Herceptin in clinical trials and is still on it today. Her story is inspirational. Listen as she shares her journey with us. You can find Lori, and her books on social media by searching Lori Lober.  I'm Still Here is hosted by Heather and Larry Jose. Heather was diagnosed with Stage IV (Metastatic) Breast Cancer in 1998 at age 26. Heather has lived with metastatic breast cancer for over 20 years and is often contacted by women asking for help with their diagnosis and transition to life with mets. IG: @heatherjose FB: Heather Jose I'm Still Here lyrics written by @Sanjay, our awesome son! #breastcancer #metastaticbreastcancer #stageIVneedsmore #breastcancerawareness #heatherjose #metavivor #livingwithmets #fearofrecurrence #canceradvocate #livingwithcancer #cancersucks #metastaticcancersurvivor#breastcancerpodcast

"Take control of your health and be an advocate: you can beat the odds and outlive cancer." Here's what I cover with Penny Casselman in this episode: What does the experience of being diagnosed with cancer look like for someone who has already lost their mother to the same disease?How can genetic testing help inform and shape a treatment plan for cancer?What choices did Penny Casselman make to ensure she was on the right side of the ground and to reduce her risk of cancer reoccurrence? Penny Casselman is a 45-year-old advocate for her own health who has outlived her mother's metastatic breast cancer. She is a doer who has undergone a radical hysterectomy, bilateral mastectomy, chemotherapy, and a year of Herceptin, as well as a Zometa infusion to lower her risk of recurrence.

Natasha adjusts to post-treatment daily life, continuing with hormone blockers and finally seeing a mental health professional. While working with less fortunate patients who don't have mittens or cold caps, Natasha looks back with gratitude on how privileged her treatment experience was.At work, she finds herself pushing patients much harder to advocate for themselves around symptom management and advises them not to accept puking and feeling like crap the whole time.Cold weather leads to cold feet which leads to worrying about the onset of neuropathy. She experiences a constellation of odd side effects including tingling, arrhythmia, jacked up taste buds, hot flashes that may or may not mean anything and wonders about the cause. Is it from the hormone blockers? Menopause? Aftereffects of chemo? In this final episode of Season 2, she finally gets in to see a therapist and wishes it had been possible from the beginning. Going back and listening to episodes of the podcast reminds her how far she's come and although she'll always be terrified, it has opened her heart in a way she's thankful for and there is a way it's made her softer. Thank you to all who have listened to Natasha's story. We hope her real-time story has helped you and welcome your notes, thoughts, and feedback. We'll be back soon with some special episodes, including a long awaited Kristen update and some incredible special guests. To stay in touch with what we're doing, the newsletter is the best place to get real time updates. Subscribe at at https://breastcancerstories.substack.com/subscribe If you have just been diagnosed, and are interested in telling your story from beginning to end on our podcast, send us a note on our website at breastcancerstoriespodcast.comYour support is crucial to continuing our mission, which is simply to help those with breast cancer and the people who love them through the shock of diagnosis and treatment. To support the show, you can donate directly on the website through PayPal at https://www.breastcancerstoriespodcast.com/donate or become a premium subscriber of our newsletter at https://breastcancerstories.substack.com/subscribe **About Breast Cancer Stories**Breast Cancer Stories follows Natasha Curry, a palliative care nurse practitioner at San Francisco General Hospital, through her experience of going from being a nurse to a patient after being diagnosed with breast cancer. Natasha was in Malawi on a Doctors Without Borders mission in 2021 when her husband of 25 years announced in a text message that he was leaving. She returned home, fell into bed for a few weeks, and eventually pulled herself together and went back to work. A few months later when she discovered an almond-sized lump in her armpit, she did everything she tells her patients not to do and dismissed it, or wrote it off as a “fat lump."Months went by before Natasha finally got a mammogram, but radiology saw nothing in either breast. It was the armpit lump that caught their attention. Next step was an ultrasound, where the lump was clearly visible. One painful biopsy later, Natasha found out she had cancer; in one life-changing moment, the nurse became the patient.This podcast is about what happens when you have breast cancer, told in real time. Host and Executive Producer: Eva SheieCo-Host: Kristen VenglerEditor and Audio Engineer: Daniel CroeserTheme Music: Them Highs and Lows, [Bird of Figment](https://music.apple.com/us/artist/bird-of-figment/1434663902)Story Editor: Mary Ellen ClarksonAssistant Producer: Hannah BurkhartCover Art Designer: Shawn HiattBreast Cancer Stories is a production of [The Axis.](https://www.theaxis.io/)PROUDLY MADE IN AUSTIN, TEXAS

Show Summary:"I started working at her second ovarian cancer recurrence, and there's more metastasis. She cried and said, 'My cancer came back because I had chocolate cake at my daughter's birthday.' That was a pivotal moment in my practice, so I said, 'I think it's more important that you focus on the joy of your daughter's birthday and that you enjoyed that chocolate cake."Confirming a cancer diagnosis can feel like a death sentence. The fear surrounding it, on top of pity and well-meaning suggestions from family and friends, adds to the confusion and stress of the situation.That is why navigating a clear path to healing can be challenging, and finding a cancer care plan that is compassionate and humane is a breath of fresh air in nursing the patient back to vibrant health.Our guest, Dr. Bianca Di Giulio, L.Ac., is a Doctor of Acupuncture and Chinese Medicine. Co-authoring a book on Integrative Oncology with her husband, they established two clinics in the Bay Area, California, where the medical paradigms and practices of the East and West are married for a safe, holistic and natural way of healing.Beat the Big C with a plan. Listen to Episode 51 of the Gutsy Health Podcast to learn more! Exceptional Highlights:Chinese Medicine is highly individualized, where aside from herbs and nutritional advice, recommendations consider a person's habits, lifestyle, and even state of mind and emotions.Acupuncture is a pivotal gateway toward integrative cancer care. Aside from empirical research based on 5000 years of Chinese Medicine, PubMed also has thousands of studies supporting it.Consuming cold food, especially in the morning, is like taking a cold bomb. It inhibits the absorption and metabolism of food and fluids, which generates the powerful chi energy in the body. Show Highlights:Integrative is a beautiful blend of multiple principles, approaches, and therapeutics to optimize health and wellness.Dr. Bianca Di Giulio 08:56Western oncology requires labs, scans, and blood work to monitor tumor progression. At the same time, it's translated into Chinese medicine principles and theories, such as asking if there's an emotional component. Slowly developed over fifteen years, Acupuncture headlines the six-week formula of her Insight Cancer Program.Dr. Bianca Di Giulio 29:01By targeting specific acupuncture points in combination with chemotherapy and radiation, the synergy among those points is where the medicine is.Chinese herbal medicine entails putting together multiple herbs that harness their synergy. Dr. Bianca Di Giulio 35:02 Astragalus, or Huáng qí, increases the white blood cells and strengthens the immune system. Danshen breaks down the cells' fibrin barrier to synthesize and potentiate the radioactive component of chemotherapy. Cordyceps offers a protective mechanism for breast cancer patients who receive Herceptin.Get 20% off your first order of Resist Nutrition Bars, a powerhouse snack for hormone and blood sugar regulation. Order yours at www.resistnutrition.comSponsor Link:www.resistnutrition.comImportant Links: Gutsy Health Podcast InstagramInsight Cancer Care WebsiteThe Wellness Principle Website

ASCO: You're listening to a podcast from Cancer.Net. This cancer information website is produced by the American Society of Clinical Oncology, known as ASCO, the voice of the world's oncology professionals. The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guests' statements on this podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Cancer research discussed in this podcast is ongoing, so data described here may change as research progresses. In this podcast, Cancer.Net Editorial Board members discuss new research in gastrointestinal and genitourinary cancers presented at this year's ESMO Congress, held September 9-13 in Paris, France. First, Dr. David Ilson discusses treatment advances in liver, colorectal, and gastric, or stomach, cancers. Dr. Ilson is an attending physician and member at Memorial Sloan Kettering Cancer Center and a professor of medicine at Weill Cornell Medical College. You can view Dr. Ilson's disclosures at Cancer.Net. Dr. Ilson: Hi, I'm Dr. David Ilson from Memorial Sloan Kettering Cancer Center in New York. I'm a GI medical oncologist, and it's my pleasure today to review some important presentations in GI cancers from the recent ESMO meeting in Paris from 2022. I have no relevant relationships to disclose for this discussion. So, important presentations were made in hepatocellular cancer, in colorectal cancer, and gastric and other cancers, and I'm going to highlight some of the key presentations from the meeting.  One of the most anxiously awaited presentations was one in hepatocellular or liver cancer. For patients that have advanced disease who are not candidates for surgery or local treatments, standard therapy now, it used to be lenvatinib and sorafenib, and that's now been replaced by the combination of an immunotherapy drug, atezolizumab combined with the drug bevacizumab. That's the new standard of care. And recently, we had a promising data for another immunotherapy combination using the drug durvalumab combined with tremelimumab. So what we saw this year was another important global study looking at the first-line use of immunotherapy in hepatocellular cancer. This trial took 794 patients with advanced hepatocellular cancer and assigned them to a standard treatment with a drug called lenvatinib. Lenvatinib and sorafenib were the old standard treatments for hepatocellular cancer. And lenvatinib alone was compared to a combination of lenvatinib and pembrolizumab, an immunotherapy drug. The primary endpoint was to see whether adding immunotherapy to lenvatinib improved survival. And this was a negative trial. It did not show an improvement in survival for adding pembrolizumab to lenvatinib over lenvatinib alone, and there was really no significant difference in the time that patients were on treatment. The response was slightly higher with the addition of pembrolizumab to lenvatinib, but again there was no survival difference. So this combination will not move forward. And again, as I said earlier, the new standard first-line treatment is atezolizumab plus bevacizumab. In colorectal cancer, probably one of the most exciting presentations was the use of immunotherapy treatments in locally advanced colon cancer. There is an important subset of colorectal cancer that has what's called an MSI-high status. MSI-high colon cancers are very responsive to immunotherapy drugs, and there has been a lot of interest in patients with localized colorectal cancer using immunotherapy drugs prior to surgery rather than conventional chemotherapy or radiation. So this important trial looked at 112 patients with localized colorectal cancer. Most of the patients were stage 3, and they all were documented to have this MSI-high status, which indicated a higher chance of response to immunotherapy. And patients received a brief course of immunotherapy, 2 doses of the drug nivolumab combined with 1 dose of ipilimumab over only 6 weeks followed by surgery. What they showed in these 112 patients who went to surgery, there was almost 100% response to this treatment. In fact, almost two-thirds of patients had no cancer found at surgery, even only after several weeks of immunotherapy. And in the 112 patients treated, there have been no recurrences in any of these patients. So it's quite remarkable that immunotherapy could induce a complete remission in two-thirds of patients, and that was only after a few weeks of exposure of the drug. So I think we're going to see more interest in using immunotherapy treatments as a potential pre-surgical treatment for colon cancer. And we could argue with such a high rate of complete remission, if we gave immunotherapy longer, maybe we could consider nonsurgical management, to just keep treating the patients with immunotherapy. This is actually the case that's now been seen in rectal cancer, a recent study presented from my institution where they treated patients with rectal cancer with immunotherapy, and we also achieved 100% remission, and none of the patients in this small study required surgery. So I think this important study, which is called the NICHE-2 trial, indicates a high degree of effectiveness of immunotherapy in MSI-high colon cancers. And certainly, it raises interest in using this as a preoperative treatment and potentially could lead to some patients getting treatment with immunotherapy alone without surgery. Then I'm going to comment a little bit about advanced metastatic colon cancer. Another important presentation was studying a new drug called fruquintinib. Fruquintinib is an oral drug that targets the VEGF pathway, which is an angiogenesis pathway in colon cancer. Standard treatment for colon cancer when it's stage 4 disease is now use of chemotherapy, like FOLFOX and FOLFIRI, drugs like bevacizumab, cetuximab, and panitumumab. And in more chemotherapy-resistant cancers, we use drugs like regorafenib and TAS-102. So this trial looked at a large group of patients, over 690 patients who had received all conventional treatments. They had progressive disease on all conventional treatments, including the late-line drugs regorafenib and TAS-102. And this was a placebo-controlled trial in which patients either received the drug fruquintinib or they received placebo plus supportive care. It was reasonable to offer a placebo in this trial because there really was no other standard treatment option for these patients. The primary endpoint of overall survival was improved with fruquintinib. Survival was improved with a reduction in the risk of death by about 30% and improvement in time on treatment. Very few patients responded to fruquintinib, so this was largely a drug that stabilized the cancer, but it did lead to modest improvements in time on treatment and modest improvements in survival. So this drug may potentially be evaluated as a new treatment option in very chemotherapy-resistant colorectal cancer. I just want to mention briefly another new class of agents for which we had data presented at the ESMO meeting. These are drugs that inhibit a mutation in their cancer called KRAS G12C. There are promising drugs that target this pathway. And there were 2 drugs that were followed up on at ESMO, one was a drug called sotorasib and another drug was adagrasib. These are drugs that target KRAS G12C mutations in colon cancer. And both of the trials that were presented used these drugs combined with drugs that target the EGFR pathways, so either panitumumab or cetuximab, and very encouraging responses were seen on these trials. The trial that looked at the combination of adagrasib plus cetuximab achieved a response in about 46% of patients, which is very encouraging. The trial that studied sotorasib, combined sotorasib with panitumumab, and they observed a 30% response, and some of these responses were durable. So the take-home message is that these drugs, adagrasib and sotorasib, are promising new agents to target KRAS G12C mutations in patients with advanced colon cancer and indicate that we may get even a higher degree of activity when we add EGFR-targeted drugs including panitumumab or cetuximab to these agents. So the other area that I want to comment on is gastric cancer. Recently, in the United States, we had a regulatory approval for the drug trastuzumab deruxtecan in patients who have HER2-positive gastric cancer that's advanced and is being treated with chemotherapy alone, HER-2-positive patients who had received previous trastuzumab or Herceptin. So trastuzumab deruxtecan is a promising drug used in patients that develop resistance to trastuzumab. So there was an update of the trial called Gastric-DESTINY02, which was a phase 2 trial of trastuzumab deruxtecan in Wwestern patients as a second-line treatment for patients with HER2-positive gastric cancer, and the updated analysis again showed a promising response in 40% of patients. The response duration was about 8 months, and patients achieved a survival of a year or more. So this updated presentation really reinforced that this is an active drug for patients with HER2-positive gastric cancer whose disease progresses on previous treatment with trastuzumab. So this was a very exciting ESMO meeting. There were a lot of other studies and important presentations, but I've tried to highlight today what I think are the most important as we move forward in trying to identify new treatments for patients. ASCO: Thank you, Dr. Ilson. Next, Dr. Sumanta (Monty) Pal and Dr. Tian Zhang discuss new research in kidney, bladder, and prostate cancers. Dr. Pal is the co-director of City of Hope's Kidney Cancer Program and is the head of the kidney and bladder cancer disease team at the institution. Dr. Zhang is an Associate Professor of Internal Medicine at UT Southwestern Medical Center and is a medical oncologist at the Harold C. Simmons Comprehensive Cancer Center. You can view disclosures for Dr. Pal and Dr. Zhang at Cancer.Net. Dr. Pal: Welcome to this Cancer.Net podcast. My name is Monty Pal. I'm a medical oncologist in the City of Hope in Los Angeles. I'm thrilled to be here today with my dear friend and colleague, Dr. Tian Zhang from UT Southwestern. Tian, mind giving us a quick intro? Dr. Zhang: Hi, Monty. Great to be here with you today. Tian Zhang at UT Southwestern in Dallas, Texas, where I'm a GU medical oncologist. I'm really excited to talk through the ESMO trials with you today. Dr. Pal: A little bit of housekeeping first. Let's go ahead and get some of our disclosures out of the way. I get travel support from CRISPR Therapeutics and from Ipsen. Tian, how about you? Dr. Zhang: Sure. I've received honoraria from Exelixis, BMS, Genentech, AstraZeneca, and Janssen, all relevant to our discussion today. Dr. Pal: Very good, very good. Well, thank you so much for joining us today. We've got a lot to talk about in about 15 minutes. The first thing that I wanted to chat about is adjuvant therapy. First of all, before we dive into the weeds here, can you just kind of tell our audience what adjuvant therapy is in broad strokes? Dr. Zhang: In kidney cancer, we think a lot about how we might prevent disease recurrence after surgery. So adjuvant treatment refers to systemic treatment that's given after a big surgery. And so in kidney cancer, that's usually after nephrectomy or removal of the kidney. Dr. Pal: Excellent, excellent. You beat me to the punchline. We are going to focus on kidney cancer, no doubt. This year at the European Society of Medical Oncology, or ESMO, meeting, which was held in early September, we actually had some really key studies presented in this space, one of which I'll disclose that I led. Studies I would say were maybe a little bit disheartening there, but nonetheless, I do think we can learn a lot from them. One of these trials was called PROSPER. This was a really interesting study that actually didn't just look at adjuvant therapy but actually looked at treatment before surgery, which we called neoadjuvant therapy. Tian, can you kind of walk us through the design of that trial really quickly? Dr. Zhang: This was a trial done in the ECOG Cooperative Group, and patients were randomized to receiving either nivolumab, which is an immune checkpoint inhibitor, before surgery, followed by a year of nivolumab after surgery, or to surgery and observation with ongoing scans. So it was really trying to look at a perioperative approach of using nivolumab. Dr. Pal: So how about this? Maybe we'll kind of discuss some of these results in amalgam, but maybe let's go through these trial designs first. The second trial that was highlighted this year at ESMO was called IMmotion010. That's one thing that I just love about these studies. They all have very clever names. I don't know what an IMmotion is, but tell us about IMmotion010 and what that trial design looked like. Dr. Zhang: Sure. So IMmotion010, again, also was an adjuvant trial for resected intermediate- and high-risk kidney cancers, randomized folks to either atezolizumab for a year or placebo for a year. And so this is in the context of having had resected kidney cancers and following folks for the treatment results, and the primary endpoint there was disease-free survival. Dr. Pal: Okay. So we've got an immune therapy called nivolumab and the PROSPER trial that was looked at before and after surgery. We've got atezolizumab, a different checkpoint inhibitor that was looked at following surgery. Tell us about the third trial. This is the last study in the space called CheckMate 914. What did that trial look at? Dr. Zhang: That one, again, also a phase 3 adjuvant trial, enrolling folks after surgery that had high-risk kidney cancer and randomized to either the combination of nivolumab with ipilimumab, both checkpoint inhibitors versus placebo. And again, this treated patients for about 6 months and also primary endpoint of disease-free survival. Dr. Pal: Now, whenever we do these studies, we always define them as being positive or negative, and that's really not meant to sort of cast any aspersions on how well the study was done or any really sentiments around the trial itself. It's really objective, and it's based on whether or not a study hits what we define ahead of the trial as being called a primary endpoint. So we actually, in these studies, looked at a primary endpoint of something called recurrence-free survival. And so that's really the proportion of patients who actually are living on without any sort of recurrence of their kidney cancer. I think it might be easy enough to sort of describe whether or not these trials hit that endpoint were positive or negative. What was the final report here on these trials, Tian? Dr. Zhang: Well, Monty, I think all 3 of these trials were, quote-unquote, "negative," and we all had high hopes for all 3 of these trials. And certainly, many, many patients participated, and we will learn eventually a lot from these trials. But none of these 3 met their prespecified primary endpoint of recurrence-free survival endpoint. Dr. Pal: So this is a little bit tricky because we did have these 3 negative studies presented at ESMO this year, but there was 1 positive trial that's adjuvant or postoperative space presented previously and then now published, actually, in the New England Journal of Medicine with an FDA approval to boot. Can you tell us about that, Tian? Dr. Zhang: Well, that one was called KEYNOTE-564 and randomized patients to either a year of pembrolizumab or placebo. And so you're absolutely right. It did show an improvement in disease-free survival comparing pembrolizumab with placebo. And so pembrolizumab is approved in this adjuvant setting after nephrectomy. Dr. Pal: And so this can be kind of a tough space because I can imagine our listeners are hearing this saying, "OK. Well, at ESMO, we've got 3 negative trials looking at postoperative therapy, and we've got 1 positive trial looking at pembrolizumab in the space." So what's one to do in this setting? What are you telling patients these days about whether or not to use adjuvant treatment for kidney cancer? Dr. Zhang: Yeah. I think it's a conversation that patients have with their oncologist after surgery, and it really depends on their own risk factors, their clinical and pathologic features at the time of resection. It depends a lot on patient preferences and their own priorities and things such as their tolerance for toxicity or how often they're coming into the treatment center. And I do think this is a time point where they have a shared decision-making that we can help our patients understand the totality of the data and then decide if a year of pembrolizumab is worthwhile or if they'd rather continue with surveillance after surgery. Dr. Pal: I totally agree with you, and I love that term “shared decision-making,” because it's never one of those situations where I walk into the clinic room and say, "Here's what you're going to do." And it's also never the situation where the patient walks into the clinic room and says, "Here's what I want." It's always this really sort of mutual process, isn't it, where you sort of look at a patient's clinical state. You look at some of the features under the microscope, but then it comes down to really, really lengthy and personal discussions around what that patient wants to get out of treatment. So I think that's very well said, Tian.  I'm going to move to actually a different setting, which is termed “metastatic disease.” So we've talked about localized kidney cancer, where the disease is sort of confined to the kidney for the most part. We talked about what we do after we remove visible evidence of disease. But there is, unfortunately, a number of patients where we can't necessarily remove all the disease burden. So we lean more heavily on what we call systemic treatments. These are treatments that enter into the bloodstream either by mouth or through the veins. And in kidney cancer, just to give you a really, really brief synopsis, there's been this huge evolution over time. When I started in the field, it was really the advent of using a single oral therapy for kidney cancer. And over the next five 5 years, we sort of saw this evolution towards using doublet therapies, which is a mix of pills and IVs or maybe IVs alone. And more recently, there's been a lot of excitement. You can probably see where this is going, right? We've looked at 1 drug, and it works. We've looked at 2 drugs, and they seem to work. Logic would perhaps suggest that maybe you could get away with using 3 drugs in concert. So, Tian, this year at ESMO, there was a really important trial called COSMIC-313 that looked at 3 drugs versus 2 drugs. Can you tell us a little bit more about the design of the study? Dr. Zhang: COSMIC-313, the large phase 3 study, which randomized more than 850 patients to either the triplet, as you're speaking of, the cabozantinib, nivolumab, and ipilimumab versus nivolumab and ipilimumab with placebo standing in for cabozantinib. And so this was a very large trial, looking particularly at progression-free survival, comparing the triplet versus the immunotherapy doublet. Dr. Pal: And then tell us about the results of this because I have to tell you. I mean, I spent a lot of time looking over this, and I struggled with the end results a little bit. We talked about the primary endpoint of studies when we were discussing adjuvant therapy. And one of the things we'd mentioned is that you decide on this beforehand. And the primary endpoint in this trial was actually the delay in cancer growth. And as you pointed out, the study met that endpoint. But how do you interpret the results overall? How are you incorporating triplet therapy now? Dr. Zhang: Sure. I think it did certainly meet the progression-free survival primary endpoint. The median was not reached for the triplet versus 11.3 months for the doublet. And so importantly, I think it was a, quote-unquote, "positive trial." But how are we using this? Well, we have not seen the overall survival data of these patients. And so when you're thinking about combining all 3 drugs in the frontline setting, I think it's really important to think about what might come after and whether these folks truly live longer with using all 3 upfront versus a sequential approach. So I think the jury is still out. It certainly met its primary endpoint, and it's quite promising. But I'm still waiting for the overall survival data to really inform or change my practice. Dr. Pal: I've got to agree with you there. One of the things that we always discussed in clinic is whether or not a particular treatment strategy is going to increase longevity. It comes up in every conversation, I would say, whenever we're thinking about approaching a new line of treatment. And I wish I could say definitively that this triplet strategy improves longevity, but to be totally fair, that data just doesn't exist yet. So it's a really difficult conversation. I agree with you. Maybe a little pause before we start incorporating triplets. So I've got to say, it was certainly a big year for kidney cancer, one of my fellows put this table together, and it really showed that this year amongst the past maybe 10 years in kidney cancer, we had more big phase 3 trials being reported as more than any year previously. But there are also some pretty key developments in other diseases that you and I treat, Tian, and one of those is bladder cancer. And a trial that I think was really quite important has the name EV-103. Tough name to remember, but it actually looked at a disease space that I think can be a bit of a challenge for us, and that's the patient who is presenting in the clinic has actually advanced bladder cancers spread to other parts of the body and is quite ill and perhaps can't receive conventional aggressive chemotherapy with a drug called cisplatin. So what did this proportion of EV-103 that was presented show us? Dr. Zhang: Well, people hear about Cohort K thrown around, and so this trial actually has had multiple cohorts. And this particular cohort came out of some really exciting data from their dose escalation studies, and also Cohort A, where patients were treated with an antibody drug conjugate, this enfortumab vedotin, or EV, with an immune checkpoint inhibitor called pembrolizumab. And in the early cohort of 40 patients, they saw a pretty high objective response rate. That means the rate of patients where tumors were shrinking. And so that was about 70% of those 40 patients had objective responses. And so they designed this Cohort K to randomize patients to either enfortumab vedotin with pembrolizumab or enfortumab vedotin on its own, which has been approved in refractory metastatic urothelial cancer but particularly for first-line cisplatin-ineligible patient population. And so they randomized about 150 patients in the setting and looked at objective responses, and I agree with you. Certainly, very promising in terms of having objective response rate of about 65% and compared with enfortumab vedotin on its own, which came in around 45%. It does seem that this combination has more activity than the monotherapy. Dr. Pal: Yeah. That's a great summary. And to the patients out there listening, when we talk about responses, we're talking about pretty deep responses here, meaning 30% or more reductions in the size of tumors. And Tian mentions that you've got 65% to 70% of patients with these responses. It really does entail a sizable reduction, not just a small decrease in the volume of tumors. And I'm telling you, just from having been in the scene for 15 years now, I mean, it's just remarkable sort of progress that we're making.  We're going to wrap up by talking about prostate cancer, and just to really describe some overarching results. So there's a setting in prostate cancer that I always find to be a bit of a challenge, and these are patients who have had surgery for their prostate cancer. So extensively no visible spread of their disease, but they start having their PSA creep up afterwards. And there was a trial that sort of addressed that. Tian, can you give us the sort of quick and dirty summary of the study? Dr. Zhang: Sure. So we call this PSA recurrence or biochemical recurrence setting. And this trial was led by Dr. Rahul Aggarwal in the Alliance Cooperative Group. But everyone who had biochemical recurrence were randomized to receiving androgen deprivation therapy alone, which is usually our standard of care; a combination of that androgen deprivation therapy with apalutamide, which is an androgen receptor blocker; or the combination of a triplet of the androgen deprivation therapy, the apalutamide, and then an abiraterone acetate, which is a blocker of steroid synthesis in the adrenal glands. And so this trial enrolled ultimately about 500 patients and randomized them 1 to 1 to 1 to these 3 cohorts. And interestingly, the combinations of either the androgen receptor, androgen deprivation therapy with apalutamide or the triplet with combined abiraterone acetate all prolonged PSA progression-free survival compared to androgen deprivation therapy alone. So I think it was a really well-done study in the cooperative groups and helps answer some questions around intensifying treatment in that biochemical recurrent space. Dr. Pal: Yeah. These cooperative groups studies, each one of them are so critical. These are just funded by our federal government, and they really offer us a chance to really ask pure questions, so really, really important study design. And maybe in 30 seconds, let's go over this last study over here. I don't want to keep our listeners on for too long, but there was a study called PROpel. Again, you got to love these study names. So this PROpel study looked at advanced prostate cancer. So again, this is prostate cancer where the disease has spread from the prostate to other organ systems. This is potentially a new paradigm for the disease. Before, we used to just basically give everybody hormone therapy in this setting. We've doubled down and given patients more advanced hormonal therapy with drugs like abiraterone that you alluded to, but now there's this potential to use targeted treatments. And maybe you can tell us a little bit about how that's been incorporated in PROpel, Tian. Dr. Zhang: Sure. Well, PROpel randomized patients to a combination of abiraterone with olaparib, which is what we call PARP inhibitor, and it blocks DNA damage repair, basically, in cancer cells. And olaparib has been approved as a single agent in more refractory, metastatic, castration-resistant prostate cancer. And so this trial randomized folks with a combination in sort of earlier lines of castration-resistant disease to either that combination or abiraterone with placebo. We saw earlier this year, actually, that the primary endpoint was improved for all comers, but I don't know if we saw some more subgroup analysis of patients with BRCA alterations and also with homologous recombination repair alterations. And I think that's very important, the fact that we saw more of an improvement in those subpopulations than those patients without the BRCA alterations or the homologous recombination repair mutations. Dr. Pal: Excellent. Excellent summary. I think that's about all that we've got time for today. New paradigms in prostate cancer and bladder cancer potentially and a massive amount of new data in kidney cancer to things going forward with clinical practice from ESMO 2022. Tian, thanks so much for joining me today, and I hope everyone listening enjoyed this as well. Dr. Zhang: Thanks, Monty. Take care. ASCO: Thank you, Dr. Pal and Dr. Zhang. You can find more research from recent scientific meetings at www.cancer.net. Cancer.Net Podcasts feature trusted, timely, and compassionate information for people with cancer, survivors, and their families and loved ones. Subscribe wherever you listen to podcasts for expert information and tips on coping with cancer, recaps of the latest research advances, and thoughtful discussions on cancer care. And check out other ASCO Podcasts to hear the latest interviews and insights from thought leaders, innovators, experts, and pioneers in oncology. Cancer.Net is supported by Conquer Cancer, the ASCO Foundation, which funds lifesaving research for every type of cancer, helping people with cancer everywhere. To help fund Cancer.Net and programs like it, donate at CONQUER.ORG/Donate.

On the eve of her first chemotherapy infusion, Natasha hauls a pile of new prescriptions home and questions why so much harm must be done to be “healthy” again. After meeting her oncologist Dr. Chen, a specialist in HER-2 positive breast cancer, the clinical trial that originally sounded promising turned out not to be a good fit, leading to a much less invasive chemo recipe consisting of Taxotere, Carboplatin, Herceptin, and Perjeta spaced three weeks apart, but thankfully no need for Taxol. To save her hair from falling out, Natasha's dad graciously volunteers to cover the cost of cold caps (thanks Neil!) but the tradeoff is additional logistics, longer appointments on the chemo days, and no guarantee that it will work. Links Support the Breast Cancer Stories podcast https://www.breastcancerstoriespodcast.com/donate Subscribe to our newsletter here: http://eepurl.com/hX12YD Other Links Support the Breast Cancer Stories podcast https://www.breastcancerstoriespodcast.com/donate Subscribe to our newsletter here: http://eepurl.com/hX12YD About Breast Cancer Stories Breast Cancer Stories follows Natasha Curry, a palliative care nurse practitioner at San Francisco General Hospital, through her experience of going from being a nurse to a patient after being diagnosed with breast cancer. Natasha was in Malawi on a Doctors Without Borders mission in 2021 when her husband of 25 years announced in a text message that he was leaving. She returned home, fell into bed for a few weeks, and eventually pulled herself together and went back to work. A few months later when she discovered an almond-sized lump in her armpit, she did everything she tells her patients not to do and dismissed it, or wrote it off as a “fat lump." Months went by before Natasha finally got a mammogram, but radiology saw nothing in either breast. It was the armpit lump that caught their attention. Next step was an ultrasound, where the lump was clearly visible. One painful biopsy later, Natasha found out she had cancer; in one life-changing moment, the nurse became the patient. This podcast is about what happens when you have breast cancer, told in real time. Host and Executive Producer: Eva Sheie Co-Host: Kristen Vengler Editor and Audio Engineer: Daniel Croeser Theme Music: Them Highs and Lows, Bird of Figment (https://music.apple.com/us/artist/bird-of-figment/1434663902) Production Assistant: Mary Ellen Clarkson Cover Art Designer: Shawn Hiatt Breast Cancer Stories is a production of The Axis. (http://www.theaxis.io/) PROUDLY MADE IN AUSTIN, TEXAS

Welcome to another episode of On the Couch with myself Henry Jennings. Today I am talking to Dr Leslie Chong, CEO and MD of Imugene (IMU).A very interesting look at an early stage biotech, where it is with trials and data, plus some words of advice on how to look at investing in biotechs in general. And a quick chat on Italian art to finish off. A great podcast and well worth a listen.Leslie has 24 years of oncology experience in Phase I – III of clinical program development, including leadership role involvement in two marketed oncology products. She was previously Senior Clinical Program Lead at Genentech, Inc., in San Francisco. Genentech is widely regarded as one of the world's most successful biotech companies with a strong oncology franchise including the best-selling breast cancer drug Herceptin.Why not sign up for a free trial? Get access to expert insights and research and become a better investor.Marcus Today DisclaimerIMPORTANTThe content included on our website, podcasts and in our emails has been prepared to provide general information only and, as such, the specific needs, investment objectives or financial situation of any particular user accessing the Marcus Today website or associated emails have not been taken into consideration. Each individual user should obtain advice from their financial planner or advisor before acting on any information provided on the Marcus Today website or associated emails so that such individual users can obtain advice applicable to their personal circumstance from their own financial advisor. Please note that stocks can go down as well as up. Past results are not indicative of future performance and returns can be negative.

In this episode, Ayesha discussed a new COVID-19 test technology that Innova Medical Group, world leader in at-home COVID-19 tests, has reached a licensing deal for with the University of Birmingham where the technology was developed. The new test is as sensitive and accurate as PCR tests and faster than lateral flow (rapid antigen) tests. Hear about the innovative new technology underlying the molecular test, and how the test is also being developed for the detection of other viruses. Ayesha also talked about the FDA approval of AstraZeneca and Daiichi Sankyo's antibody-drug conjugate (ADC) Enhertu (trastuzumab-deruxtecan) for the treatment of patients with unresectable or metastatic HER2-low breast cancer. The approval makes Enhertu the first approved drug for this indication. Find out about the trial data that led to the approval and its effectiveness in HER2-low breast cancer, which is a newer subtype of the cancer.Read the full articles here: Innova Secures Licensing Rights for U of Birmingham's New COVID-19 Test Technology RTF-EXPARAstraZeneca's Enhertu Gets FDA Approved as First Therapy for HER2-Low Breast CancerFor more life science and medical device content, visit the Xtalks Vitals homepage.Follow Us on Social MediaTwitter: @Xtalks Instagram: @Xtalks Facebook: https://www.facebook.com/Xtalks.Webinars/ LinkedIn: https://www.linkedin.com/company/xtalks-webconferences YouTube: https://www.youtube.com/c/XtalksWebinars/featured

En septiembre de 2002 relataba en un artículo el modo en que un anticuerpo monoclonal impedía el funcionamiento de una molécula que estimulaba el crecimiento del cáncer de mama. El anticuerpo se denominaba entonces Herceptin y, por diversos avatares, ha pasado a llamarse hoy Trastuzumab. Este anticuerpo monoclonal forma parte hoy del arsenal de armas terapéuticas que pueden ser utilizadas para frenar o incluso erradicar el cáncer de mama. En el mismo artículo hablaba de la generación de otro anticuerpo monoclonal que podía unir sus fuerzas con Herceptin para inhibir con mayor eficacia el crecimiento tumoral ¿Qué ha sido de esa nueva esperanza que nacía en aquellos años? ¿Se han hecho realidad? Hoy Trastuzumb, Pertuzumab y fármacos anticancerosos se utilizan en combinación para tratar el cáncer de mama.

En septiembre de 2002 relataba en un artículo el modo en que un anticuerpo monoclonal impedía el funcionamiento de una molécula que estimulaba el crecimiento del cáncer de mama. El anticuerpo se denominaba entonces Herceptin y, por diversos avatares, ha pasado a llamarse hoy Trastuzumab. Este anticuerpo monoclonal forma parte hoy del arsenal de armas terapéuticas que pueden ser utilizadas para frenar o incluso erradicar el cáncer de mama. En el mismo artículo hablaba de la generación de otro anticuerpo monoclonal que podía unir sus fuerzas con Herceptin para inhibir con mayor eficacia el crecimiento tumoral ¿Qué ha sido de esa nueva esperanza que nacía en aquellos años? ¿Se han hecho realidad? Hoy Trastuzumb, Pertuzumab y fármacos anticancerosos se utilizan en combinación para tratar el cáncer de mama.

Comprehensive, relevant and insightful conversations about health and medicine happen here… on MedStar Health Doc Talk.By the time we reach our 50's it seems most of us know someone who has been treated for breast cancer. According to the American Cancer Society, one in eight women will get a breast cancer diagnosis in their lifetime-  Nearly 275,000 women AND men are newly diagnosed with breast cancer each year. But what happens after they hear those dreaded words:  ‘You have breast cancer.'-? We're talking today with breast surgeon Dr. Maen Farha, medical director of the Breast Center at MedStar Good Samaritan Hospital to learn about the breast cancer journey.  

Welcome to this episode of Physician's Weekly  podcast. I am your host Dr Rachel Giles, from Medicom Medical Publishers in collaboration with Physician's Weekly. This week, we have 2 really interesting interviews about very different topics. I will start with the second interview. The 2022 American Society of Clinical Oncology (ASCO) Annual Meeting, was held 3 -7 June 2022 in Chicago, IL. One of the most covered topics talked in the hallways and you may have read in newspapers, was about precision treatment in aggressive breast cancer.  It all started 24 years ago, when a drug called Herceptin changed how doctors treat breast cancer. Its approval in 1998 made it possible to target the aggressive breast tumors tied to a gene called HER2. Other drugs quickly followed Herceptin and, over the years since, have substantially improved survival for people with the disease.A quarter of a century later, another shift in treatment could be on the horizon. At the American Society of Clinical Oncology meeting, researchers presented results proving that, for the first time, a targeted medicine, called trastuzumab deruxtecan (or T-Dxd for short) can help metastatic breast cancer patients whose tumors express only low levels of HER2. Because many more patients may soon be eligible for treatment with T-Dxd, we focused on a safety follow-up analysis of the randomized phase 3 DESTINY-Breast03 study reinforced the risk-benefit profile of trastuzumab deruxtecan compared with trastuzumab emtansine in patients with HER2-positive unresectable or metastatic breast cancer.  We speak with Prof. Guiseppe Curigliano (University of Milan, Italy) to learn the latest results. But first, we speak with Sonya M. Sloan, MD, better known as #OrthoDoc, has established herself as a force to be reckoned with in the male-dominated field of Orthopedic Surgery. Licensed to practice medicine in several states, she travels the country as a locum tenens physician. There's a shortage of doctors in America, and all types of facilities need locum tenens providers to relieve physician burnout, maintain patient satisfaction, and stay fully staffed during busy times, or while searching for a permanent doctor. Furthermore, locum tenens helps more people see a provider and receive care, offsetting the physician shortage in underserved areas—especially rural communities, urban areas with health professional shortages, VA hospitals, and Indian Health Service facilities. A 2021 survey indicated that 72% of healthcare facility managers are seeking locum tenens physicians. This is up from 47% in 2016 and up from 39% in 2012. Physician's Weekly senior editor Martta Kelly interviews Dr. Sloan.  Dr. Sloan is the author of  a book titled The Rules of Medicine: A Medical Professionals Guide to Success   Extra reading:  Modi S, Jacot W, Yamashita T, Sohn J, Vidal M, Tokunaga E, Tsurutani J, Ueno NT, Prat A, Chae YS, Lee KS, Niikura N, Park YH, Xu B, Wang X, Gil-Gil M, Li W, Pierga JY, Im SA, Moore HCF, Rugo HS, Yerushalmi R, Zagouri F, Gombos A, Kim SB, Liu Q, Luo T, Saura C, Schmid P, Sun T, Gambhire D, Yung L, Wang Y, Singh J, Vitazka P, Meinhardt G, Harbeck N, Cameron DA. Trastuzumab Deruxtecan in Previously Treated HER2-Low Advanced Breast Cancer. N Engl J Med. 2022 Jun 5. doi: 10.1056/NEJMoa2203690. Epub ahead of print. PMID: 35665782.

When Heidi Slansky survived Stage III breast cancer AND skin cancer, she wanted to come to the aid of female cancer survivors in the Dallas-Fort Worth area.  Inspired by slipping on boxing gloves and how they made her feel like she was truly fighting cancer, Heidi founded Cancer StrongHER.  Its mission is to help women physically and mentally by provided a forum to actively carry the fight through boxing fitness, tae kwon do, yoga and pilates.  At all times, the classes she offers are free of charge.  Those outside Dallas-Fort Worth can learn more about what Cancer StrongHER has to offer by checking out its website, www.cancerstrongher.org.

One of the underrated but true successes of precision medicine has been pharmacogenomics. Beginning in the '90s with the approval of the drug Herceptin for HER2 positive breast cancer, tailoring drugs to genotype has been one of the less controversial areas of our field and will only continue to build on the early promise of sequencing the human genome. Today we talk Michelle Whirl-Carrillo, Director of PharmGKB, a one-stop go-to for pharmacogenomics data that has been funded by the NIH since 2000.

Imagine for a second if you could have treatment which fits you better than a tailored suit. In some cases, biostatistics tools and custom medicines like gene therapy open new doors for patients. After today's pod, you'll know all the practical and impractical uses of precision medicine for patients.So what is precision medicine? Aren't doctors already supposed to customize treatments for each given patient's situation? The short answer is yes but the longer answer leaves a key gap I want to talk about. What the majority of doctors follow is evidence-based medicine. This is a time-tested process—a patient arrives to the clinic with XYZ history and suffers from XYZ complications. The provider then suggests the best clinical or surgical options based on what has worked for the disease in the past as well as what makes sense from experience in med school, residency, etc. In essence, treatment is targeted for alleviating symptoms or root causes of symptoms, which is great. Notice that potential solutions are personalized to the given disease more so than the patient directly. That distinct intent is where precision medicine begins. As you may imagine, patients with a given disorder can have wildly different reactions to similar treatment. To be clear, evidence-based medicine has way more benefits than drawbacks—precision medicine has been promoted over the last couple decades as taking care to another level. The greatest benefit patients get from precision medicine is that any treatment you take is created from your specific environment, lifestyle, and genetic makeup. For example, if someone ends up with a disease like lung cancer, there could be a customized therapy targeting the problem with that patient's genome in mind.Although genomics is a huge part of precision medicine today, especially with everything we've learned since the US's Human Genome Project finished up in the 2000s, precision medicine was in motion before then when the textbook Pharmacogenetics was published in 1962 by Dr. Werner Kalow. A helpful article on the Harvard Data Science Review dives more into the historical buildup of precision medicine, which I'll link on my Substack page at rushinagalla.substack.com. Even before the 20th century, doctors were interpreting data linked to the onset and treatment of disease to craft better options. For example, there might be a group of patients who all suffer from severe asthma. Precision medicine could in theory still occur here without going into each patient's genetic profile. In this situation, doctors could see that patients one to 100 live in cleaner-air environments than patients 101 to 150. Maybe patients 80 to 120 have other issues that make the asthma worse or better, and so on. Modelers then crunch and reformat all that unstructured data to suggest treatment for each individual. Obviously, evidence-based medicine isn't going away. If a whole region is dealing with an unusual flu outbreak, we know that making tweaks to the annual flu vaccines will do a reasonable job targeting the specific changes made by that strain of the flu itself without needing to consider every individual's situation case by case. Evidence-based care is still part of the foundation of what precision medicine does. But since in this day and age we're generating so much data and have a better understanding of our genetic code, there is more runway for precision medicine to take off such that patients may someday get one-of-one solutions to their issues.Shifting over to the genetic focus of modern precision medicine shows us that we can deal with patients who respond differently to common treatments. Some patients may need varying dosages, treatment lengths, or alternative choices because of side effects. Having 100% unique solutions for each person's medical issue is wonderful and utopian on paper. The reality of precision medicine's main playing field is cancer treatment, which is life-saving but not cheap. ~90% of precision treatments approved by the FDA in 2018 were for cancer indications. Well-known cancer therapy brand labels like Keytruda by Merck or Herceptin by Roche cost multiple hundreds of thousands a year before insurance discounts. There also could be issues between how customized the medicine is versus whether the patient actually matches up well to do the treatment. Cancer therapies are anything but short experiences—not all patients can handle extended courses even if the treatment is a perfect match for their genes. Not to mention that a skilled oncologist wouldn't be enough to oversee the treatment since there would be considerable expense involved for doing genetic sequencing and reading out results that not all doctors are trained to understand. Not all medical facilities are equipped to perform this kind of care regardless of superb personnel. It's also difficult to do a clinical trial to make better custom medicines in the first place since, by definition, uncommon diseases affect less people so clinical study recruitment becomes a separate challenge. This is part of why the biggest irony of precision medicine is that individual solutions improve only when you accumulate enough data at the population level. There is nothing inherently wrong there, but that's just where precision medicine is at for now.A recent in-depth review by the Brookings Institution think tank offers some insight on how “agile governance,” which is a policy approach for regulators to make better private and public partnership decisions for the purposes of innovation, can bring down precision medicine costs and ease logistical problems. That analysis focuses on aggregating private and public health care data, improving direct to consumer genetic testing incentives, and building international relationships between drug regulators among other possible initiatives to make precision medicine practical.Without a doubt, the medical field is still a number of years away from having consistent treatments with a capacity for individual genetic modifications serving patients at the outpatient clinic level. However, your care can still improve with better decision-making that still takes your social, genetic, and medical history into account so medicine doesn't reduce itself to just a bunch of if-then statements. Another field of medicine that shouldn't be reduced to algorithms is mental health, which is the prime subject of next week's pod. At that time, we'll learn about what mental health resources exist and how to use them well. Stay tuned and subscribe to Friendly Neighborhood Patient for the big and small pictures of healthcare. I'll catch you at the next episode. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit rushinagalla.substack.com

Rebecca is a breast cancer thriver, having been diagnosed when she was just 28. She is an actor, writer, teacher, and integrative cancer care advocate. In 2019, she founded Solis Cancer Community, where she shares weekly posts and blog articles that cover topics on integrative and whole-body healing pre- and post-cancer. 02:26: It was a big shock to everyone because my mammogram had been negative.  04:46: People don't like going to the doctor, especially when they're nervous about something.  07:25: I did Herceptin for a year.  09:14: I did a lot of research on statistics and recurrence rates.  11:35: How involved were your family and friends? 14:06: Those were two of the scariest things for sure.  15:30: Aren't you afraid that if you have a recurrence, you're going to regret not doing those treatments? 17:28: I started meditating to deal with the stress of the situation. 19:12: Cancer has changed my life in so many ways.  21:22: I didn't believe in myself for a long time. 24:01: I had a cold every three weeks. 25:37: I was waking up every hour and a half.  26:50: What is one thing you wish you had known at the beginning of your cancer journey Rebecca? 28:49: If you could only do one thing to improve health care in Canada, what would it be and why?  30:43: We see the best outcomes from a combined treatment path.  31:23: Thriver Rapid Fire Questions.  33:14: Aside from Cancer U, what is one resource you would recommend for cancer patients and caregivers?  Resources Rebecca on LinkedInRebecca's business website

Gabrielle noticed a lump while she had a shower one day. When she went for the regular mammogram, she brought this to the medical team's attention, and on further tests, it was diagnosed as Breast Cancer. She underwent chemotherapy, lumpectomy, sixteen cycles of radiation treatment and Herceptin injection as a part of the treatment. Cancer made Gabrielle empathetic, and she says it is essential to share your stories with other people as it can help them in one way or another on their journey. "Take each day as it comes."

Vroueskuilings hoop om meer befondsing van die regering te ontvang. 'n Versoek aan die Departement van Gesondheid om veiligheid by gesondheidsinstellings te verskerp. 'n Pasiënt wat direk geraak word deur die hoë prys van die kankermiddel Herceptin, deel haar verhaal met ons.

Lauren Tarpley was diagnosed with breast cancer in September 2020 at the age of 34. She started preventive treatments at the age of 30, so she went for annual mammograms every year. Her tumour was detected with the help of a mammogram, ultrasound and biopsy. She went through 6 rounds of chemotherapy, 11 rounds of Herceptin targeted immunotherapy, 25 rounds of radiation therapy and a double mastectomy. She is going through reconstruction currently. Her message to other cancer patients is to stay positive, find a sound support system and communicate. Summing up her journey, she says, " The journey of a lifetime.

Indira Kaur Ahluwalia was diagnosed with stage 4 breast cancer with bone metastasis in April 2007. She experienced a lot of pain in her hips and back of her body; later, she even had trouble walking. So after taking painkillers, later in March 2007, she discovered a thickening in her right breast. That was the time when she felt that this was not normal. She went to an oncologist, and several tests detected breast cancer. She went through 4 cycles of chemotherapy and opted for mastectomy. She is continuing with Herceptin and taking it after every 3 weeks. Her primary support system was spiritual and faith in God. Indira is an entrepreneur and executive at Federal Government in Washington, D.C. She believes that cancer has made her more vigilant, made her responsibilities very clear, and allowed her not to take gratitude for granted. Summing up her journey, she says, "I tried, and I am grateful for every experience".

Kara Frazier was only 26 years old when she was diagnosed with stage 3 breast cancer. To encourage her to keep fighting, her friend's mom gave her a pair of mini pink boxing gloves. Those gloves reminded Kara that she was strong and beautiful. Three years later, Kara passed those gloves on to another woman fighting her battle with cancer, and that was the beginning of Fighting Pretty! The mission of Fighting Pretty is to remind every woman how strong and beautiful she is, especially if she's battling cancer. At the heart of Fighting Pretty's work is the “Pretty Package”, a care package containing a scarf, a lipstick, words of inspiration, and most importantly, a pair of mini pink boxing gloves. Since 2013, Fighting Pretty has sent over 10,000 pretty packages to women battling cancer. Kara and her team's work has lifted so many women during their darkest times by providing hope, support, encouragement, and something pretty.    About Kara Fighting Pretty founder, Kara (Skaflestad) Frazier had just mourned the death of her Mema, who passed away after a long battle with breast cancer. Kara was in the shower when she performed her first self-breast exam and found a suspicious lump in her armpit area. In December of 2008, at just 26 years old, she went to her doctor and was told she was “too young to worry.” Kara pushed for a closer examination, only to find out that she did, in fact, have stage 3 breast cancer, which is considered to be an advanced and invasive stage of the disease. Kara faced a double mastectomy, eight rounds of chemotherapy, four weeks of radiation, fertility treatments, a year of Herceptin treatments. This was followed by hormone therapy that would last for a total of 10 years. Kara realized she wanted to go through this ordeal by “Fighting Pretty”—with a smile on her face, lipstick on her lips, and strength in her heart. Since becoming a 501 c(3) non-profit organization in 2013, Fighting Pretty moved from Kara's apartment in New York City to a headquarters in Portland, Oregon, with two part-time employees. In just a few years, Fighting Pretty has impacted over 10,000 women battling all types of cancer in 50 U.S. states and 16 countries globally. Plus, Fighting Pretty has received over $1 million worth of product donations from top cosmetic brands to send to women battling cancer. Kara works full time as the Marketing Manager at the OHSU Knight Cancer Institute and devotes her life to helping cancer patients through their fight. Kara now lives healthy and happily in Oregon with husband Ben, her new step-daughter Aubrey and dogs Archie and Zulu.   Connect with Kara Website https://www.fightingpretty.org Facebook https://www.facebook.com/FightingPretty/ Instagram https://www.instagram.com/fightingpretty Twitter https://twitter.com/fighting_pretty

In the second part of this Oncology, Etc. episode Drs. Patrick Loehrer (Indiana University) and David Johnson (University of Texas) continue their conversation with Dr. Susan Desmond-Hellmann, exploring the prominent leadership roles she held, from first female Chancellor at UCSF to CEO of the Bill and Melinda Gates Foundation and member of Facebook's Board of Directors. Subscribe: Apple Podcasts, Google Podcasts | Additional resources: education.asco.org | Contact Us Air Date: 11/18/21   TRANSCRIPT SPEAKER 1: The purpose of this podcast is to educate and inform. This is not a substitute for medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. PAT LOEHRER: Hi, Everybody. I'm Pat Loehrer. I'm director of the Centers of Global Health at Indiana University, Melvin and Bren Simon Comprehensive Cancer Center. DAVE JOHNSON: And I'm Dave Johnson. I'm Professor of Medicine here at UT Southwestern Medical School in Dallas, Texas. So Pat, we're back for another episode of the award winning "Oncology Et Cetera." PAT LOEHRER: Just seems like last month we were here time, you know? Time just flies. DAVE JOHNSON: Exactly. Before we get started, you were telling me about an interesting book you were reading-- something about friends or something. Can you elaborate? PAT LOEHRER: Sure, sure, yeah. This book I picked up-- actually, my wife picked it up. It's called First Friends. It's written by Gary Ginsburg. It's a really interesting book. It was-- basically talks about-- it probably has about eight or nine presidents but the importance of having a friend that guides him. And these were people that were, in many ways, unelected people that were close to the presidents that helped change the face of what we see today, and some of them are stories of really good friends and some of them are, I think, opportunistic friends. But it gives you a background of people like Madison and Lincoln and Roosevelt and Woodrow Wilson. It's actually a fun read. DAVE JOHNSON: I'll definitely put it on my reading list. It sounds like a pretty exciting one. Well, speaking of influential people, we're really excited to jump back into our interview with Dr. Helman. In our last episode, we covered her early life and career, her work in Uganda, her views on global oncology, and her experiences in private practice and industry. In the next half of our interview, we'll learn more about her incredible career and her multiple leadership roles. Let's start by hearing about her time as chancellor of UCSF. PAT LOEHRER: Let me transition a little bit. What I'd like to do is talk a little bit about your leadership. One Of the next big roles you had, you became chancellor at UCSF, correct? SPEAKER 2: Mm-hm. PAT LOEHRER: And so as Dave said, I think you were the first woman in that role. SPEAKER 2: I was. PAT LOEHRER: You were a groundbreaker from that capacity. So now instead of working for people-- obviously, I understand that there's people you work for when you're chancellor too, but tell a little bit about that transition from industry back into academics and how that felt in the role of being a leader and then maybe the responsibility of being the first female chancellor. SPEAKER 2: There were parts of being the chancellor at UCSF, I would say most parts of it, that I just thought were fantastic. I loved being back at a hospital and clinics. Just the way the hospital and clinical enterprise at UCSF works, the chancellor is the board. And so once a month, you'd have neurology or cardiology come and tell you about what had happened, quality control, things that had gone on and I would have done that all day long. I mean, it was just so interesting. It was so important to run a great clinical enterprise that getting back closer to patients and medicine I thought was fantastic. The other thing was the educational enterprise, and UCSF, as you know, has medicine, pharmacy, dentistry, nursing. I always tell people, no undergraduates, no English majors, no marching band. And the other chancellors reminded me, no athletic director, which apparently is a very good thing. So UCSF is a very special and unusual place. And I loved the science. I would show up at research seminars and things like that as often as I could. So there were so many parts of being at UCSF that I thought were just off the charts great. The hardest thing about being at UCSF-- being the first female chancellor, I think, was challenging but not in ways that you might expect. I was used to being a woman leader in medicine and biotech, which was unusual. So being the only woman in the room, being the first, wasn't new to me. But the thing that was hard on our family was there are roles for the spouse of the chancellor that fit more neatly into more of a classic female role, hosting things. There was a tea party for the wives of the faculty that the wife of the chancellor typically had. And for some reason, Nick didn't think that that suited him. We sort of laughed about that. DAVE JOHNSON: He can't make tea? SPEAKER 2: He can't make tea to save his life. And he's a strong introvert, which made it worse. I will tell you, some of the under-recognized, underreported people in life are spouses of chancellors and presidents of universities. And talk about unpaid labor-- my goodness! And so we sort of struggled with how did Nick show up, what did that look like. Because we didn't have any role models for what that looked like. I still laugh that Bill Clinton said he would be First Laddie. So when you have a pattern recognition, life is easier. And then being one of 10 chancellors at the UC system, I struggled a little bit with the UC Regents just because it felt-- I became chancellor in 2009, and we had some fiscal realities that we were dealing with. And the pace of the UC Regents and the format of the UC Regents, I actually made a proposal for UCSF to kind of break off from the other 9. And that was not well-received, got me in the newspaper. And I did not do that again. People saw it as disloyal and not very smart. But all in all, I thought then and think now that our public universities are absolutely-- they're treasures in America. And I was really proud to be a part of it and hope that I had made a contribution. DAVE JOHNSON: Speaking of leadership, what was it like to be CEO of the Bill and Melinda Gates Foundation? What caused you to step away from chancellor to philanthropy? PAT LOEHRER: It's not a step down. It's not a step down, basically. DAVE JOHNSON: It is not a step down. SPEAKER 2: So I would say a couple of things. First of all, Bill and Melinda pushed me hard to take the job. I was not looking to change. My husband worked at the Gates Foundation for a couple of years on HIV. So they knew us, and they knew Nick better than me. But they knew both of us. We awarded Melinda the University medal at UCSF. And to my great surprise and happiness, she accepted and came. I later think that she was using that as a reason to talk to me about the CEO job, but she got a twofer. And I was really compelled by the mission. Who wouldn't be? I was really compelled by the mission and the chance to get back into global health after the experience I had had in Uganda. But I'll tell you, it is the ambition of the Gate Foundation, the scope of the Gates Foundation, the resources, and the need to get something done. I tell you, it is hard work. It is really hard work-- from China to India to all of the continent of Africa and then US education. Throw that in on top of things. So I was thrilled to be a part of driving the agenda and the mission. Some really talented people who are working very hard at the Gates Foundation-- I was surprised, especially on US education, with the amount of pushback. And I worked really hard to be successful at working with Bill, who's known as a tough character and lived up to that mutation. DAVE JOHNSON: Good to know, just in case he calls Pat or me. PAT LOEHRER: Yeah, yeah, I'm not going to get a medal at UCSF either. So that's a-- DAVE JOHNSON: You never know, Pat. PAT LOEHRER: It's a non-starter. And this may not apply to you, but there's a lot of maybe disproportionate number of women who feel they suffer from this imposter syndrome. To be honest, Dave and I have talked about that. We both feel in that syndrome too. But along the way, I mean, if you think about growing up in Reno, Nevada, and suddenly now being a chancellor and head of the Gates Foundation, the National Academy of Science, was there ever this sense of the, wait a minute, you know, what's going on? Is this real? SPEAKER 2: For me, there has always been that sense. There has always been that sense, and I look at it as I hope there always will be that sense-- that the kind of need to demonstrate your value. And there's a part of the imposter syndrome that is humility and not overestimating what you can do. And so on my best days, I think that leads me to say I've got to work with really terrific people. My job is to bring out the best in others. If I lead, it's because there's a great thing we're going to accomplish, and I can help people see where we're going together. And so I definitely have had imposter syndrome. But the one thing that I probably overused and kind of grew to like too much was the thing of people underestimating me and then proving them wrong. That gets a little wearying after a while. It's like, OK, we're going to waste some time while you decide whether I'm worthy or whether I can do this. And let's not waste that time. Why don't you assign to me-- give me some confidence, and I'll live up to that. And I mentioned Art Levinson was my boss for most of the time I was at Genentech. And he had no time for imposter syndrome. He was like, look, how many promotions do you have to get before you think, OK, I can get this done? He thought that was sort of-- he just didn't have time for it. We have things to do, and he had jobs to get done. And one of the things I loved about him is he would constantly push me to say, you're capable of more than you think you are, which I think is the sign of a fantastic manager, which he was and is. And so I've tried to push myself to do that. And the thing is, like, you can do this. Come to me for help. We'll make sure you succeed, but don't underestimate yourself. And I think that's a consequence of imposter syndrome is both wasting time proving yourself and not taking on something that you think, actually, let me give that a try and stack the deck in favor of succeeding. And so I think that's the thing that-- there's a certain fierceness that I've always had that I like about myself that, like, of course we will succeed. Failure is not an option. Of course we will succeed. And I think that comes from working on things that I value a lot and care about a lot. PAT LOEHRER: You have been on a number of different boards, including Pfizer as well as Facebook. And in that capacity, you've seen a lot of leaders. Can you talk a little bit about the strengths and the weakness of various leaders as well as serving on the boards and the capacities of the different companies? SPEAKER 2: Yeah, well, first, let me say I know ASCO is actually a really good about being careful about conflicts of interest and things like that, and I am too. So when I became chancellor at UCSF and then CEO at the Gates Foundation, I avoided being on life sciences boards. And so I got asked a lot by Biotech and pharma boards to be on their boards. Initially, I joined Procter Gamble's board, where I served for, I think, about six years. And then I joined Facebook's board. And those were both fantastic experiences. And I actually joined the boards for two very different reasons. One, P&G's board, I wanted to learn about branding and consumers. And I felt like in medicine, I didn't really learn about consumers or branding as much as I needed to or might. And then Facebook's board I joined because as Dave mentioned, I was with Charles Sawyers. We wrote the precision medicine report for the National Academy. And I really love-- to this day, I love the concept of using the social network to connect people. There was sort of an infamous story or famous story-- it's actually a good story-- of patients with a certain form of myeloma who found each other on Facebook and went to Genentech and said, make a new medicine for those of us with this genetic abnormality. And we'll all enroll in a trial. And so these connections to me felt really powerful on precision medicine. And so getting to work with CEOs at Procter and Gamble, the CEO Mark Zuckerberg at Facebook, I do see the really different attributes of leaders. But when you're a board member, you see those attributes of leaders with a very different lens. What's the return to shareholders? How does the community think about them? What's the impact-- and increasingly for Facebook, what's the impact on the world? What's the impact on our social discourse and our ability to have a free and fair election? A lot of those things became much more operative on the Facebook board while I was on the board and really tough social issues that continue to this day. DAVE JOHNSON: Yeah, so we could go on for another hour, hour and a half, but I have one question to ask you which may seem a little bit silly in retrospect. But if you could look back on your youthful self at 21 or 22 knowing what you know now, with all the things that you've done during the course of your career, what advice would you give yourself? And perhaps I'll addend that by saying what advice would you give particularly to young women in the medical profession who are trying to balance that work-life balance that everyone talks about and worries about and struggles with, quite frankly. SPEAKER 2: I'll give you one thing I should have done better and one thing that I think I did well. So the advice on the one thing I should have done better, I think slow down a little bit and take a bit more time for fun and enjoyment. I was extremely worried about money when I was in college, and being number two of seven-- every summer, I worked. I remember at one point in medical school, I had three weeks off, and I got a job for those three weeks at a deli making sandwiches. And I went to college for three years, crammed it into three years so I wouldn't have to pay for the fourth year. So I just think that I could have taken on more loans. I could have done some things to just dial it down a bit because you don't get those years back. And that's such a great time of your life when you're 21, 22, something like that. So I wish I'd have just slowed down a bit and not been so driven for those seven years of university and medical school that I really just either worked or studied all the time. The thing that I feel like I did well, and I would say this to anybody who's going into medicine, is there's so many opportunities. There's so many wonderful things to do. But whoever your spouse is, whoever your partner in life is, take the time and energy to make sure that's the right person for you. I feel so blessed. Actually, my husband, who I've mentioned several times in this discussion, Nick, was my roommate in San Francisco when I was an intern, like real roommate. And we've been roommates ever since. And we're very compatible. He's one of seven kids too. It's another Catholic school kid. And we just have fun together and support each other. And there's no way I could have taken these crazy jobs or done the kinds of things I've done without Nick. So having a wonderful, supportive partner makes everything better. DAVE JOHNSON: That definitely resonates with Pat and me. We're both very blessed to have wives and spouses of, for me, it's 52 years. I can't remember, Pat. Yours is close. PAT LOEHRER: I had my first date with my wife 50 years ago, yeah. DAVE JOHNSON: Yeah. SPEAKER 2: OK, so you guys know what I'm talking about. PAT LOEHRER: Absolutely. DAVE JOHNSON: Yeah. PAT LOEHRER: Yeah. DAVE JOHNSON: Go ahead, Pat. PAT LOEHRER: I was going to ask a question that you probably may have already answered there, but Bob Woodward just came out of an interview with Colin Powell. One of the last questions he asked him was if he could reflect on that one person that was a moral compass for him. And so for you, that one person, alive or dead, that has been not the most powerful person you've met but the one that's really influenced you the most in terms of giving you direction, who would that be for you? SPEAKER 2: Probably, if I look at through line the entire time I've been alive, it would be my dad. He had the ability to look at a room and find the person who was struggling and go over to them. And I really loved that about my dad. PAT LOEHRER: I love it. DAVE JOHNSON: One last question. So we're at the top of the hour, and I know you're a very busy person. Pat and I love to read, but we're also documentary fiends and whatnot. We're interested. What have you read recently that really resonated with you? Do you have a recommendation for us? SPEAKER 2: I will say during the pandemic, I've gotten back into reading biographies, which I love. DAVE JOHNSON: Yeah. SPEAKER 2: So I did the Caro, Lyndon Baines Johnson, which, Master of the Senate is really good. But my favorite book of the last two years is The Code Breaker, Walter Isaacson's book about Jennifer Doudna. DAVE JOHNSON: Yeah. SPEAKER 2: One of the things I love about Walter Isaacson is he teaches you science through his biographies. Like, I think I understand relativity based on his Einstein biography, which is great. But The Code Breaker is really super good. DAVE JOHNSON: Yeah, we both read it. We couldn't agree with you more. PAT LOEHRER: Love it. Love it. DAVE JOHNSON: So Sue, again, it's been a real honor to have you as our guest, and we really appreciate the time you've taken. Thank you so much, and we hope you enjoy the beautiful weather in Alamo California, and I hope it does turn green and the rain continues for you. SPEAKER 2: Thank you so much. It's been my pleasure. Thank you both. DAVE JOHNSON: Take care. SPEAKER 2: Bye. DAVE JOHNSON: I want to take the moment to thank our listeners for tuning in to "Oncology Et Cetera," an ASCO educational podcast where Pat and I really will talk about anything and everything. So if you have an idea or a topic you'd like to share with us and like for us to pursue, please email us at education@asco.org. Thanks again, and keep in mind that Pat is a giant in oncology, but he's a short instructor. Thanks, everybody. SPEAKER 1: Thank you for listening to this week's-- to make us part of your weekly routine, click Subscribe. Let us know what you think by leaving a review. For more information, visit the comprehensive e-learning center at elearning.asco.org.

Part one of this two-part Oncology, Etc. episode features an inside look at the amazing career of Dr. Susan Desmond-Hellmann (spanning from early AIDS research in Kenya and drug development at Genentech, to serving as UCSF Chancellor and CEO of the Bill and Melinda Gates Foundation). Hosted by Drs. Patrick Loehrer (Indiana University) and David Johnson (University of Texas). Subscribe: Apple Podcasts, Google Podcasts | Additional resources: education.asco.org | Contact Us Air Date: 11/04/21

This week I will be sharing my journey from being diagnosed with Stage 3, HER2+ breast cancer, to healing in the top 40th percentile. This story is dedicated to the work I did along the way and what I hope for you is an inspiring story of healing. I will be sharing tips and tools that worked for me as a message of hope. I did it and so can you!   In this episode, I share:  How I handled getting diagnosed with cancer Finding a doctor that was right for me Going through chemo, radiation, and losing my hair Western and plant medicine The breast meridian grid, lymphatic drainage massages, acupuncture My healing process Finding support and asking for help Work with Jennifer 25% Off a Private Coaching Session  Sign-up for the Newsletter  Become a Member & Support the Illuminated Podcast Athletic Greens ~ Exclusive Discount  Resources From This Episode: Mederi Center - Holistic Health & Healing, Patient Care, Research, Education Texas Original Compassionate Cultivation ︱Medical Marajuana Breast Cancer Resource Center of Texas is an incredible local organization that is here to help. Whether you need rides, housework done, financial help, or emotional support ~ they're incredible and understand. There's a lot of grants and financial assistance out there if you need it! They can help you navigate through ALL and ANY of this! https://bcrc.org https://www.instagram.com/bcrcoftx/ Mederi Center HERBAL TEA MIXTURE: 3 parts I. equal parts ~ hibiscus, fennel, uva ursai, lemongrass After you buy the herbs just go on and blend them together in a jar, mix them up, and then just scoop out what you need as you fill the loose tea into the large metal tea infuser. I buy all of my herbs at The Herb Bar on Mary St off of S Congress, they also sell Chaga Mushrooms as a tea and that's also great!  Brew it long & brew it strong! In a crockpot on low for 7hrs + I find is the best way II. Slippery Elm/Marshmallow Root Either one. Marshmallow Root is a Slippery Elm. This is a cold brew.  1TBSP : Quart (mason jar) filled with distilled water and kept for 24 hrs in the fridge. Drain & store. Slippery Elm is kind of mucusy for lack of a better word and it looks weird but it's fine, strain it after 24 hrs. III. To Drink Mix them 50/50 or 75 mix/25 elm - they are both super beneficial and I wouldn't worry too much about the balance. Serve warm. Drink as much as you want. It's such a great kidney flush and if you're experiencing any UTI like symptoms it will clear it right up. It's kind of dry but you can add Stevia or Honey to take care of that. BONE BROTH   This is such an awesome way to get nutrients when you don't feel like eating and it will really help to get your vitamins and minerals. I loosely follow Dave Aspreys recipe. You can get Grass Fed Beef Marrow Bones from most any Farmers Market. Richardson Farms takes orders and you can collect from Barton. 10lbs will make 3 - 4 batches. It goes a long way. If available I will also add chicken feet, egg shells from past eggs I've eaten. I keep them in the freezer, knuckles ~ really whatever goodness I can find at the market. And vegetables only for the last 12 hrs. IT seems like a lot but it's pretty easy. After I warm it to serve I always add sea salt, pepper, cayenne, ginger, turmeric. Yum! It will definitely need salt, other than that flavor it however you like. If you have any problems finding the recipe then let me know. If you take HERCEPTIN as one of your drugs ~ You must consume OLIVE OIL and OLIVES. IT helps the Herceptin to work better. Water   Water is so vital and with everything you hear nowadays I have taken an extra precaution and installed filtered water that is all throughout the house - including laundry, shower, and bidet! There's also a PH tap at the sink to get high alkaline water.  SUPPLEMENTS/NUTRITION   When I first got diagnosed I went to see an Integrative Wellness Coach, Carl Schmidt at Lake Hills Pharmacy, he was very knowledgeable about Cancer in general and got me onto various supplements; Paw Paw & Methyl Folate were crucial. There's great, short YouTube videos about Paw Paw and how it works to fight cancer cells. It was so hard for me to eat veggies and drink my green drink and all the “healthy” stuff while on chemo and I got to the point where I was too tired to grocery shop, cook, clean, and eat. Ask for help! People want to help you and you have to stay nourished. If you take HERCEPTIN as one of your drugs ~ You must consume OLIVE OIL and OLIVES. It helps the Herceptin to work better. I worked alongside the Mederi Foundation in Oregon - there's a lot of info online. They had access to all of my info; blood work, tests, etc. and they sent tonics and all sorts and that's how I got the recipe for the tea. MIND/BODY ~ SPIRITUAL HEALTH   This is a really important time to look after your spiritual and mental health. This is tough and it sucks. You've got to come to terms with the fact that you are down - and that's not easy. While you're laying down listen to something inspirational or calming, meditating, etc., whatever suits you. It's better than drowning in crappy tv and having that vibration bring you down. I recommend Deepak Chopra Soul of Healing Affirmations, The Secret of Healing both on iTunes and it's so awesome to listen to. The Soul of Healing is also a book and a DVD; it's really incredible. Abraham Hicks is also great to listen to. I think it's important to reaffirm that you can do this! Don't ever refer to the cancer as “my”. Do not own it. It's here and you have to recognize that but that's not what you are and that's not how you should own it. You'll get so much literature and books, etc. Read when you can but don't overwhelm yourself and don't look at the word cancer in various forms all over the house. Know what I mean? https://open.spotify.com/album/3rpDTnXBdaciYySxV1ElyH?si=1IvS7Z0WS3CCFQxjnq2BJg&dl_branch=1  Soul of healing Affirmations https://open.spotify.com/album/71M7hkvO8USA2Qlagia2be?si=O1opisxaTs6VurW8wprEcg&dl_branch=1  Soul of Healing Meditations  Chopra, Deepak. The Soul of Healing Affirmations Whatever you believe in - believe in it. Pray hard and pray strong. ACUPUNTURIST & HEALER   I have an incredible acupuncturist and healer, her name is Rama Chittajallu and her number is 512.293.5388 I saw her for a couple of years before my diagnosis. She is a Reiki Master, Acupuncturist, and a Dr. Master of Chinese Medicine - this is a great addition and balance to the Western Medicine.  PETS   I had my dog registered as an Emotional Service Animal (ESA) She loves everyone and is just a really special beast and my bestie. She eases my anxiety SO much and truly is my xanax. It's super easy to certify your pet online audit's like $80. Trust me - if you've got a cool dog that goes everywhere with you, take it to the next level, you'll love it!   The Grove Wine Bar https://www.instagram.com/grovewinebar/ https://www.grovewinebar.com Connect with Jennifer Website Patreon YouTube Facebook Instagram

Dr. Jeffrey Cleland, Ph.D., Chairman, CEO and President of Ashvattha Therapeutics, a clinical stage biotech company discusses treatments that are in development to address inflammation of the brain caused by COVID. They recently announced positive interim results on its ongoing phase 2 PRANA clinical study, which showed that OP-101, a novel hydroxyl dendrimer therapeutic, has the ability to successfully cross the blood brain barrier and suppress hyperinflammation. The company is also developing a class of novel hydroxyl dendrimer therapeutics that they hope will become the future of targeted therapies and unlock new levels of patient care across oncology, ophthalmology, and inflammatory diseases. #AshvatthaTherapeutics Dr. Cleland has 30 years of industry experience in research and development, including more than a decade at Genentech, Inc. His experience in startups includes major roles in obtaining more than $450 million in capital at stages from Series A through D and exit via IPO including over $300 million in capital raised as CEO. As the founding CEO of Versartis (VSAR), he led one of top biotech IPOs of all time. After Versartis, he led the Series B financing and clinical translation of novel Johns Hopkins University technology as CEO of Graybug Vision (GRAY). He held executive management positions at BaroFold, Novacea and Targesome, and has managed directly all aspects of drug development and late-stage research. While at Genentech, Dr. Cleland served in product development and manufacturing roles. He held important leadership roles in the successful approval of two drugs, Herceptin® and Nutropin Depot®, as well as in early work on Lucentis®, Avastin®, and Kadcyla®. He holds a BS in Chemical Engineering from the University of California, Davis and a PhD in Chemical Engineering from the Massachusetts Institute of Technology. Dr. Cleland has authored more than 100 articles and four books, and holds several issued patents. He serves on the Boards of BIO, Exicure, and Zylem and has advisory roles with small emerging biotechnology companies.

Aion Therapeutic Inc's (CSE:AION) Dr. Stephen Barnhill tells Proactive that the group's proprietary and patented combinatorial mushroom preparations, AION F7 and AION F8, showed high efficacy in killing multiple types of breast cancer cells. Dr Barnhill says the preparations demonstrated direct killing of HER2+ breast cancer cells, ER+/PR+ breast cancer cells, and triple-negative breast cancer cells by direct cytotoxicity, a similar effectiveness as trastuzumab, an FDA approved monoclonal antibody treatment for HER2+ breast cancer sold under the brand name Herceptin.

Pek Lum, co-founder, and CEO of Auransa believes that a lot fewer drugs would fail in Phase 2 clinical trials if they were tested on patients predisposed to respond. The problem is finding the sub-populations of likely high-responders in advance and matching them up with promising drug compounds. That’s Auransa's specialty.The Palo Alto, CA-based drug discovery startup, formerly known as Capella Biosciences, has a pipeline of novel compounds for treating cancer and other conditions identified through machine learning analysis of genomic data and other kinds of data. It’s closest to the clinical trial stage with a DNA-binding drug for liver cancer (AU-409) and is also working on drugs for prostate cancer and for protecting the heart against chemotherapy drugs. The company says it discovered AU-409 as part of a broad evaluation of data sets on a range of close to 30 diseases. The company’s discovery process uses a platform called the SMarTR Engine that uses hypothesis-free machine learning to identify druggable targets and compounds as well as likely high-responder patients. Lum  calls it “interrogating gene expression profiles to identify patient sub-populations.” The company believes this approach can identify unexpected connections between diverse molecular pathways to disease, and that it will lead to progress in drug development for intractable conditions with poorly understood biology, including cancer and autoimmune, metabolic, infectious, and neurological diseases.Lum co-founded Auransa with Viwat Visuthikraisee in 2014 and is the chief architect behind its technology. Before Auransa, she was VP of Product, VP of Solutions, and Chief Data Scientist at Ayasdi (now SymphonyAyasdiAI), a Stanford spinout known for building hypothesis-free machine learning models to detect patterns in business data. Before that, she spent 10 years as a scientific director at Rosetta Inpharmatics, a microarray and genomics company that was acquired by Merck. She has bachelor's and master's of science degrees in biochemistry from Hokkaido University in Japan and a Ph.D. in molecular biology from the University of Washington, where she studied yeast genetics.Please rate and review MoneyBall Medicine on Apple Podcasts! Here's how to do that from an iPhone, iPad, or iPod touch:• Launch the “Podcasts” app on your device. If you can’t find this app, swipe all the way to the left on your home screen until you’re on the Search page. Tap the search field at the top and type in “Podcasts.” Apple’s Podcasts app should show up in the search results.• Tap the Podcasts app icon, and after it opens, tap the Search field at the top, or the little magnifying glass icon in the lower right corner.• Type MoneyBall Medicine into the search field and press the Search button.• In the search results, click on the MoneyBall Medicine logo.• On the next page, scroll down until you see the Ratings & Reviews section. Below that, you’ll see five purple stars.• Tap the stars to rate the show.• Scroll down a little farther. You’ll see a purple link saying “Write a Review.”• On the next screen, you’ll see the stars again. You can tap them to leave a rating if you haven’t already.• In the Title field, type a summary for your review.• In the Review field, type your review.• When you’re finished, click Send.• That’s it, you’re done. Thanks!TRANSCRIPTHarry Glorikian: I’m Harry Glorikian, and this is MoneyBall Medicine, the interview podcast where we meet researchers, entrepreneurs, and physicians who are using the power of data to improve patient health and make healthcare delivery more efficient. You can think of each episode as a new chapter in the never-ending audio version of my 2017 book, MoneyBall Medicine: Thriving in the New Data-Driven Healthcare Market. If you like the show, please do us a favor and leave a rating and review at Apple Podcasts.For every drug candidate that makes it all the way through the three phases of clinical trials to win FDA approval, there are about 20 others that fail along the way. Phase 2, where drug makers have to prove that a new drug is safer or more effective than existing treatments, is where a lot of drugs falter.But often, it’s not because the drugs don’t work. Sometimes it’s just because they weren’t tested on the right patients. Meaning, the people in the treatment group didn’t happen have the right genes or gene expression profiles to respond. If you could find enough patients who were likely high-responders and try your new drug just on them, your chances of approval might go way up. The tough part is identifying those subpopulations in advance and matching them up with promising drug compounds.That’s where a company like Auransa comes in. It’s a Palo Alto startup that has built an AI platform called the SMarTR Engine. The engine uses public datasets on gene expression to identify subtypes of molecular diseases and predict what kinds of compounds might work against specific subtypes. Auransa used the engine to discover a drug for liver cancer that’s about to enter clinical trials. And it’s licensing out other drugs it discovered for prostate cancer and for protecting the heart against the effects of cancer chemotherapy.Some of the ideas baked into the SMarTR Engine come from a sub-field of artificial intelligence called hypothesis-free machine learning. And joining us this week to explain exactly what that means is our guest Pek Lum. She’s a biochemist and molecular biologist who worked at the microarray maker Rosetta Inpharmatics and the software company Ayasdi before founding Auransa in 2014. And she says one of the real revolutions in drug development is that almost every disease can be divided up into molecular subtypes that can best be treated using targeted drugs.Harry Glorikian: Pek, welcome to the show.Pek Lum: Thank you. Pleasure to be here.Harry Glorikian: You know, I always try to ask this opening question when I start the show to give the listeners a good idea of of what your company does. But you guys are in in drug discovery. What tell us how people understand what is the basic approach that you guys have. And I'll get into the special sauce later. But what do you guys do in the drug discovery space?Pek Lum: No, that's a really great question in the sense that when we first started in about five years ago, we... I've always been in the drug discovery field in the sense that I worked for over 20 years ago at that time in a company called Rosetta Inpharmatics, which is really pushing the cutting edge of thinking about using molecular data. Right. And to solve the mysteries of biology. And I was extremely lucky to be one of the core members in when we were very small. And then that really kind of put me in the sense put me in the stage where I could think about more than just one gene. Right. Because the technology was just kind of getting really kind of I would say not rolling forward, like propelling forward, with microarrays.Harry Glorikian: Yes.Pek Lum: So I was part of the whole movement and it was really amazing to be kind of like, you know, in the show as it runs, so to speak. And so and then Merck bought us after we went public and worked for Merck and Co. for another eight years, really learning how technology, how we should apply technology, how we can apply technology, molecular data, RNA data, DNA data to a drug discovery pipeline. And really kind of figured out that there are many things that the pharmaceutical world does very well, but there are many things that it also fails in and that how can we do it better? So I've always been in the mindset of, when starting Auransa with my co-founder, How do we do it better? And not only just do it better, but do it very differently so that we can address the most, I would say critical problems. So Auransa is really a company started by us to address the problem of why drugs actually fail a lot when we go into a Phase II efficacy trial. Right. Is not like the drug is bad or toxic. And most of the time is you can find enough responders to make your clinical trial a success.Pek Lum: And that cause, I guess, drugs actually made to maybe against one target. You don't really think about the biology that much at the beginning or the biology responders. So Auransa was really created to think about first, the heterogeneity of the disease and the heterogeneity of patient response. So we start from looking at molecular data of the disease from the get go. We take RNA, is really the RNA world is coming back with the vaccines.Harry Glorikian: Right.Pek Lum: And the RNA has always been fascinating because it tells you about the activity of the cell, of a normal cell versus a disease cell. So we use RNA transcriptomes right, transcriptomics to study the biology and the heterogeneity. So our algorithms, there are many algorithms, one of the first algorithms of the engine is really to look at the biology of heterogeneity, whether we can subdivide a disease into more homogeneous categories before doing anything.Harry Glorikian: Right. Yeah, I remember when, because when I was at Applied Biosystems, I remember Applied Biosystems, Affymetrix and then Stephen Friend starting this and like, you know, it was all starting back then. And I want to say we sort of had an idea of what we were doing, but compared to now, it's like, wow, how naive we were back then compared to how much this whole space has evolved. And it's interesting you mention, you know, RNA and its activity because in a couple of weeks, I'm actually going to be talking to a spatial genomics company so that you get a better idea from a visual standpoint of which cells are actually activating and which aren't.Harry Glorikian: But so, you've got an interesting professional career, and I say that because you were working at a big data analytics company for a while that was utilizing an approach that was hypothesis-free machine learning, where the machine was sort of identifying unique or aspects that you should be paying attention to. Maybe that it was seeing that instead of you going in there saying, let's just look over here, you could see what the machine was seeing for you. How much can you tell us a little bit about that experience? And then how did that influence what you're doing now? Because I have to believe that they superimpose at some level.Pek Lum: Right. I think, you know, ever since my first job at Rosetta and then my subsequent jobs really kind of culminated into this into this tech, as you see today. Right. All this experience and certainly experience while being a founding member of a small team at that time of Ayasdi, which is the software company, has been also an eye-opening experience for me because we were trying to create, using a very old mathematical idea called topology, or TDA, really start to figure out whether there's maybe there's some things that can't be learned. Right. And so typical machine learning methods need a training set or a test. But there are just some things where you don't really know what the ground truth is. So how do you do that? So that's the idea of like I say, the hypothesis-free approach. And the approach that that that the tech company, the software company that we built is really around the idea that not everything can be learned. But you can actually adapt some very interesting ideas around a hypothesis-free approach and then use it in a machine learning AI framework. So I definitely have been influenced by that thinking, you know, as I as we built the software.Harry Glorikian: Right.Pek Lum: And also, when we were Rosetta, we were generating in parallel, data on thousands of genes. And often at that time we were called, "Oh, you're just going fishing," you know, but fishing is not a bad idea because you don't really know which part of the ocean you need to go to catch your Blue Marlin, for example, right?Harry Glorikian: Yeah, no, no, absolutely.Pek Lum: Fish a little bit, not the whole ocean, but, you know, to get some, I would say, boundaries. Right. So in that sense, to me, a hypothesis-free approach gives you the boundaries where you can look. So, you know, so the experience, definitely the idea that you can use methods or thinking, algorithms, that could help you in a field where you do not know the ground truth. Like patient heterogeneity, I would say nobody really can pinpoint and say, OK, I can say that, oh, this is THE subtype, these are THE markers. And therefore, I'm going to go after this. And there are many. I guess, for example, you can think of a Herceptin as a great example, right, but when you first started, you know, it was like, wow, OK, you're going to go after a target. And then the idea of really kind of subtyping breast cancer, you know, I don't know, 20, 30 years ago. Right. And we're still learning about, you know, in a patient heterogeneity and we're just beginning to scratch the surface. So for Auransa, we wanted to use a method very much like the thinking that and the idea that we had, you know, when we were when I was at Ayasdi, is that you could search with some parameters, you know, a very complex space without needing to say, this is my hypothesis. This is that one gene, because we all know that if you have a target, you know ... to have to respond you need the target. But if you have the target, it doesn't mean you're going to respond. Because things below the target or above the target are much more complex than that.Harry Glorikian: Correct. And I always feel that there's, you know, I always call them low hanging fruit. Like the first one is, OK, well, it's either luck or skill, but I got to one level. But then you start to see people that are not responding. So that means something else is going on and there's subtypes. Right. So it's funny how we always also call it "rare diseases" in these smaller population. I'm pretty convinced that at some point everything is going to be a rare disease. Right. Because of the subtypes that we're going to start to see. I mean, even we're seeing in a neurological now, or Alzheimer's. There's subtypes of Alzheimer’s. No! Really? Shocking. Amazing to me that there's subtypes. Right. We've been dealing with this for ages. And I do believe that these technologies are so good at highlighting something where a human might not have seen it, might not have understood it. You know, I was I was interviewing actually I just posted it today on imaging and agriculture. And they were saying that sometimes the machine sees things that we don't fully understand how it sees it, but it sees it and points it out, which allows us now to dig into it and be able to sort of identify what that unique feature is that the machine has pulled out. I'm not sure I want drug discovery and drugs being based on something we don't fully understand, but the machine highlighting something for us that then we can go dig into, I think is an interesting greenfield space that that we need to explore more.Pek Lum: Right. I think you're absolutely right. You know, when we first started Auransa, that was the idea that we had. And then my co-founder and I thought, what if we find like hundreds of subtypes? We're never going to be able to make a drug again a hundred subtypes. So let's hope we find a small enough number of buckets that we can say this is approximately what it looks like, to be able to be practical to find drugs against those subtypes. So when we talk about subtypes, we are talking about you're absolutely right, it's like a leaf on a tree and that we have to cut it off at one point. Enough that things that, OK, this is homogeneous enough that actually makes sense out of it. And that's where the engine, that's what the engine does. Basically, it takes data, very, very complex data, things that we could never figure that out ourselves and say this approximately five, six buckets. So we've actually not found hundreds of subtypes, otherwise we probably would not have started Auransan, because it would have been impossible. But instead, we find n of one, but maybe a five to seven subtypes at most. That is enough for us to say, the machine says, OK, it is homogeneous enough, go for this. So that's kind of where we are, where we start at Auransa. And I think that's an important concept because people often thought about precision medicine as being, oh, I'm going to make a medicine for you and you only. But actually you could learn from, say, breast cancer, and that's approximately people with estrogen-receptor-positive tumors. And then you will likely respond to a drug like Tamoxifen. And even though we know that the response rate is only about, I think maybe 30, 40 percent. Right. But that's really good. At least at this poibt. So that's where we how we think about the engine as a shining light on a homogeneous enough population that we can actually make a drug against that.Harry Glorikian: Yeah. So that sort of leads us into you have this technology that you've termed SMarTR, S-M-A-R-T-R engine. Right. What does that stand for?Pek Lum: You know, that's my one of my rare occasion where I put my marketing hat on. I don't like marketing all. And we so and you notice the Mar is big-M, little-a-r. So S is for Subpopulation. Markers. Targets. And Redefining. Because I needed it to be Smartr.Harry Glorikian: Ok, ok. So and when you like when you've described this in the papers that I've looked at it, it's a machine learning mathematical statistical approaches, highly automated and totally runs in the cloud. So can you give us a little more color on the sort of the highly automated, and why is that so important?Pek Lum: Right. It's important because it comes from my own experience of working with, like, amazingly talented implementations and data scientist at the at Merck or I know how it goes where biologists will often ask them for something and they would run their magic and they'd give us an Excel sheet or a PowerPoint. Right. It's always a one-off one of those and one of that because you know, biologists are kind of one-off. So the idea of of us building this engine is not just equipping it with algorithms. So first of all, we don't have one algorithm, a hammer looking for a nail. We have a problem to solve. The problem is how to find novel drugs, drugs that people have never thought about, for patient populations that will respond.Pek Lum: So with that in mind, we built a pipeline of algorithms that starting from thinking about heterogeneity, to understanding preclinical models that reflect the biology of human subtypes, to predicting drugs and targets for those, and getting biomarkers for the patients when we go to the clinic. And we have different algorithms for each step of the pathway. So instead of having my team do a one-off thing, we know that if we don't do good software engineering it's going to be problematic because first it's going to take a really long time. This will be kind of higgledy piggledy in Excel sheets and we might be able to solve one thing. But to do this as a platform and as a pipeline builder, it would be impossible without good engineering practices. So we wanted to put this in, like I say, in a framework where everything is connected, so where it gets to run faster and faster through better algorithms, through better software engineering. And this really kind of came from my experience to at Ayasdi, a software engineering, a software firm. And also my co-founder who is a physicist and a software engineer, that we need to have good software practices. So what we did was we built first. We don't want any servers. Everything is done on AWS and is done in modules. So we create algorithms for each part of the pipeline, of the in silico pipeline. And then we have in such a way that when we take data in, when we ingest data, that we also automate it, and then by the time it ingest data and it spits out, I would say, what subtypes of disease, what biomarkers could be used in the clinic, what targets are interesting to you, what compounds from our digital library of compounds may be effective for that. Everything is more or less connected and could be done up in the cloud and now it finishes in about 24 hours.Harry Glorikian: When do humans look at it to say hmmm, makes sense. Or maybe we need to tweak the model a little. Right. Because it's not making sense. When does that happen?Pek Lum: So we, it happens at several steps. So within our engine we actually have benchmarks in there that we run periodically. You know, for example we have about about eight to ten data sets that we have for breast cancer, thousands of patient tumors. And we know approximately that it should be discovering, and it has discovered ER+ flavored subtypes, ERBB2, HER2+ subtypes, triple negative subtypes. So that is kind of like the rails that we put into our engine as well to make sure that when we actually do tweak an algorithm, it still has its wheels. But what we do is at this point, we generate out all the in-between data, but it's kept on the cloud. And once it's up, when it outputs the the list of things, the biologists actually, I would say the biologists with a knack for computation, we look at it and I myself look at it. I love to do data analysis in my spare time when I'm not doing CEO stuff. And we can see that we will look at once it's done that it also allows you...Ok, so this is an interesting one. The engine on the cloud outputs all of this. And right now, let's say my CSO, who is not a computational person, or me, or whoever really would be kind of a big pain to kind of go up and install the stuff and look at the things, some things you can't see. So what we did as a company is to build another kind of software, which is the visualization software on top of that.Pek Lum: So we have on our other end a visualization software that we call Polo because it's exploring that basically connects everything the SMarTR engine has done into something that's visualizable. It has a URL, we go to it and let's say, for example, my CSO wants to know, OK, the last one you did on head and neck cancer, you know, how many subtypes did you find? What is the biology, what's the pathway? And it could do all of that by him just going then looking at things. Or he can actually type in his favorite gene and then see what the favorite gene actually is predicted for how it behaves across over 30 diseases, and you can do that all at his fingertips, so we have that part of the engine as well, which is not the engine. We call it Polo, which is our visualization platform.Harry Glorikian: Right. It's funny because one of the first times I interviewed Berg Pharma and they were talking about their system, I was like, if you put on a pair of VR glasses, could you see the interconnectivity and be able to look in a spatial.... I was on another planet at the time, but it was a lot of fun sort of thinking about how you could visualize how these things interact to make it easy. Because human beings I mean, you see a picture. Somehow we're able to process a picture a lot faster than all this individual data. I think it... I just slow down. I rather look at a visual if it's possible.Pek Lum: It is so important because, you know, even though the engine is extremely powerful now, takes it 24 hours to finish from data input to kind of spitting out this information that we need. Visualization and also like the interpretation and just kind of making sure kind of like the human intelligence. Can I keep an eye on things. The visualization platform is so, so important. That's why I feel like that we did the right thing in making and taking time, putting a bit of resources to make this visualization platform for our preclinical team who actually then needs to look at it and go, OK, these are the drugs that are that are predicted by the engine. Can we actually have an analog of it or does it have development legs? Does it make sense? Does the biology makes sense. And so now we're basically connected everything. So you can click on a, you can find a drug in a database and it will pop up, you know, the structure and then it will tell you, hey, this one has a furan ring. So maybe you might want to be careful about that. This one has a reactive oxygen moiety. You might want to be careful about that. As we grew the visualization platform, we got feedback from the users. So we put more and more things in there, such that now it has a little visualization module that you can go to. And if you ever want to know something, I can just, I don't have to email my data scientist at 1:00 am in the morning saying, hey, can you send me that Excel sheet that has that that particular thing on it that I want to know from two weeks ago? I can just go to Auransa's Polo, right? As long as I have wi-fi. Right. And be able to be self-sufficient and look at things and then ask them questions if things look weird or, you know, talk to my CEO and say, hey, look at this. This is actually pretty interesting. And this one gets accessed by anybody in Auransa as long as you have Wi-Fi.Harry Glorikian: So so it's software development and drug development at the same time. Right. It's interesting because I always think to myself, if we ever, like, went back and thought about how to redo pharma, you'd probably tear apart the existing big pharma. Other than maybe the marketing group, right, marketing and sales group, you tear apart the rest of it and build it completely differently from the ground up? It was funny, I was talking to someone yesterday at a financial firm, a good friend of mine, and it's her new job and she's like, my job is to fully automate the back to the back end and the middle and go from 200 people down to 30 people because we're fully automating it. I'm like, well, that sounds really cool. I'm not really thrilled about losing the other 170 people. But with today's technology, you can make some of these processes much more automated and efficient. So where do you get your data sets that you feed your programs?Pek Lum: Yeah, let me tell you this. We are asked this a lot of times. And just kind of coming back again for my background as an RNA person. Right. One thing that I think NIH and CBI did really well over 20 years ago is to say, guys, now we no longer doing a one gene thing. We have microarrays and we're going to have sequencing. There's going to be a ton of data. We need to start a national database. Right. And it will enable, for anybody that publishes, to put the data into a coherent place. And even with big projects like TCGA, they need things that could be accessed. Right. So I think it is really cool that we have this kind of, I would say, repository. That unfortunately is not used by a lot of people because, you know, everything goes in. That's a ton of heterogeneity. So when we first started the company, before we even started the company, we thought about, OK, where is it that we can get data? We could spend billions of dollars generating data on cells, pristine data, but then it would never represent what's in the clinical trials without what's out there in the human the human world, which is the wild, wild west. Right. Heterogeneity is abundant. So we thought, aha, a repository like, you know, like GEO, the Gene Expression Omnibus, right, and ANBO or TCGA allows this kind of heterogeneity to come in and allows us the opportunity to actually use the algorithms which actually have algorithms that we look for. We actually use to look for heterogeneity and put them into homogeneity. These kind of data sets. So we love the public data sets. So because it's free, is generated by a ton of money. It is just sitting there and it's got heterogeneity like nobody's business. Like you could find a cohort of patients that came from India, a cohort of patients that came from North Carolina, and group of patients that came from Singapore and from different places in the US and different platforms. So because the algorithms at first that studied heterogeneity is actually, I would say, platform independent, platform agnostic, we don't use things that are done 20 years ago. They were done yesterday. And what we do is we look at each one of them individually and then we look for recurrent biological signals. So that's the idea behind looking for true signals, because people always say, you go fishing, you may be getting junk out. Right?Pek Lum: So let's say, for example, we go to, the engine points to a spot in the sea, in the ocean, and five people go, then you're always fishing out the same thing, the Blue Marlin, then you know that there is something there. So what we do is we take each data set, runs it through an engine and say these are the subtypes that I find. It does the same thing again in another data set and say these are the things that I find. And then it looks for recurrence signals, which is if you are a artifact that came from this one lab over here, or some kind of something that is unique to this other code over there, you can never find it to be recurrent. And that's a very weird, systematic bias, you know, so so because of that, we are able to then very quickly, I would say, get the wheat and throw away the chaff. Right. And basically by just looking by the engine, looking at looking for recurring signals. So public data sets is like a a treasure trove for Auransa because we can use it.Harry Glorikian: So you guys use your engine to I think you identified something unexpected, a correlation between plant-derived flavonoid compound and the heart. I think it was, you found that it helps mitigate toxic effects in a chemotherapy drug, you know. Can you say more about how the system figured that out, because that sounds not necessarily like a brand-new opportunity, but identifying something that works in a different way than what we thought originally.Pek Lum: Right, exactly. So in our digital library, let me explain a little bit about that. We have collected probably close to half a million gene expression profiles. So it's all RNA gene expression based, representing about 22,000 unique compounds. And these are things that we might generate ourselves or they are in the public domain. So any compound that has seen a live cell is fair game to our algorithms. So basically you put a compound, could be Merck's compound, could be a tool compound, could be a natural compound, could be a compound from somewhere. And it's put on a cell and gene expression was captured. And those are the profiles or the signatures that we gather. And then the idea is that, because remember, we have this part of the engine where we say we're going to take the biology and study it and then we're going to match it or we're going to look for compounds or targets. When you knock it down, who's gene expression actually goes the opposite way of the the disease. Now, this is a concept that is not new, right. In the sense that over 20 years ago, I think Rosetta probably was one of the first companies that say, look, if you have a compound that affects the living cell and it affects biology in a way that is the opposite of your disease, it's a good thing. Right thing. So that's the concept. But, you know, the idea then is to do this in such a way that you don't have to test thousands of compounds.Harry Glorikian: Right.Pek Lum: That is accurate enough for you to test a handful. And that's what we do. And by putting the heterogeneity concept together with this is something extremely novel and extremely important for the engine. And so with this kind of toxicity is actually an interesting story. We have a bunch of friends who are spun off a company from Stanford and they were building cardiomyocytes from IPS cells to print stem cells. And they wanted to do work with us, saying that why do we work together on a cool project? We were just starting out together and we thought about this project where it is a highly unmet medical need, even though chemotherapy works extremely well. Anthracyclines, it actually takes heart, takes a toll. There is toxicity and is it's a known fact. And there's only one drug in the market and a very old drug in the market today. And there is not much attention paid to this very critical aspect. So we thought we can marry the engine. At that time were starting up with oncology. We still we still are in oncology, and they were in cardiomyocytes. So we decided to tackle this extremely difficult biology where we say, what is a how does chemotherapy affect heart cells and what does the toxicity look like? So the engine took all kinds of data sets, heart failure data sets, its key stroke and cells that's been treated with anthracyclines. So a ton of data and look for homogeneity and signals of the of the toxicity.Pek Lum: So this is a little bit different from the disease biology, but it is studying toxicity. And we then ask the engine to find compounds that we have in our digital library, that says that what is the, I would say the biology of these compounds when they hit a living cell that goes the opposite way of the toxicity. And that's how we found, actually we gave the company probably about seven, I forget, maybe seven to 10 compounds to test. The one thing that's really great about our engine is that you don't have to test thousands of compounds and it's not a screen because you screened it in silico. And then it would choose a small number of compounds, usually not usually fewer than 30. And then we able to test and get at least a handful of those that are worth looking into and have what they call development legs. So this I would say this IPSC cardiomyocyte system is actually quite complex. You can imagine that to screen a drug that protects against, say, doxorubicin is going to be a pretty complicated screen that can probably very, very hard to do in a high throughput screen because you have to hit it with docs and then you have to hit it with the compounds you want to test and see whether it protects against a readout that is quite complex, like the beating heart.Pek Lum: And so we give them about, I think, seven to 10 and actually four of them came out to be positive. Pretty amazing. Out of the four, one of them, the engine, noticed that it belonged to a family of other compounds that looked like it. So so that was really another hint for the the developers to say, oh, the developers I mean, drug developers to say, this is interesting. So we tested then a whole bunch of compounds that look like it. And then one of them became the lead compound that we actually licensed to a a pharma company in China to develop it for the Chinese market first. We still have the worldwide rights to that. So that's how we tackled toxicity. And I think you might have read about another project with Genentech, actually, Roche. We have a poster together. And that is also the same idea, that if you can do that for cardio tox, perhaps you can do it for other kinds of toxicity. And one of them is actually GI tox, which is a very common toxicity. Some of them are rate limiting, you might have to pull a drug from clinical trials because there's too much GI tox or it could be rate limiting to that. So we are tackling the idea that you can use to use machine, our engine, to create drugs for an adjuvant for a disease, a life-saving drug that otherwise could not be used properly, for example. So that's kind of one way that we have to use the engine just starting from this little project that we did with the spin out, basically.Pek Lum: So basically, you're sort of, the engine is going in two directions. One is to identify new things, but one is to, I dare say, repurpose something for something that wasn't expected or wasn't known.Pek Lum: That is right. Because it doesn't really know. It doesn't read papers and know is it's a repurposed drug or something. You just put in it basically, you know, the gene expression profiles or patterns of all kinds of drugs. And then from there, as a company, we decided on two things. We want to be practical, right. And then we want to find novel things, things that, and it doesn't matter where that comes from, as long as the drug could be used to do something novel or something that nobody has ever thought of or it could help save lives, we go for it. However, you know, we could find something. We were lucky to find something like this flavanol that has never been in humans before. So it still qualifies as an NCE, actually, and because it's just a natural compound. So so in that sense, I would say maybe is not repurposing, but it's repositioning. I don't know from it being a natural compound to being something maybe useful for heart protection. Pek Lum: Now for our liver cancer compound, it is a total, totally brand-new compound. The initial compound that the engine found is actually a very, very old drug. But it was just a completely different thing and definitely not suitable for cancer patients the way it is delivered.Harry Glorikian: This is the AU 409?Pek Lum: Correct? Entirely new entity. New composition of matter. But the engine gave us the first lead, the first hit, and told us that we analyzed over a thousand liver tumors and probably over a thousand normal controls, found actually three subtypes, two of them the main subtypes and very interesting biology. And the engine predicted this compound that it thinks will work on both big subtypes. We thought this is interesting. But we look at the compound. You know, it's been in humans. It's been used. It's an old drug. But it could never be given to a cancer patient. And so and so our team, our preclinical development team basically took that and say, can we actually make this into a cancer drug? So we evaluated that and thought, yes, we can. So we can basically, we analogged it. It becomes a new chemical. Now it's water-soluble. We want to be given as a pill once a day for liver cancer patients. So so that's how we kind of, as each of the drug programs move forward, we make a decision, the humans make a decision, after the leadds us to that and say can we make it into a drug that can be given to patients?Harry Glorikian: So where does that program stand now? I mean, where is it in its process or its in its lifecycle?Pek Lum: Yeah, it's actually we are GMP manufacturing right now. It's already gone through a pre-IND meeting, so it's very exciting for us and it's got a superior toxicity profile. We think it's very well tolerated, let's put it that way. It could be very well tolerated. And it's it's at the the stage where we are in the GMP manufacturing phase, thinking about how to make that product and so on.Harry Glorikian: So that that begs the question of do you see the company as a standalone pharma company? Do you see it as a drug discovery partner that that works with somebody else? I'm you know, it's interesting because I've talked to other groups and they start out one place and then they they migrate someplace else. Right. Because they want the bigger opportunities. And so I'm wondering where you guys are.Pek Lum: Yeah, we've always wanted to be, I say we describe ourselves as a technology company, deep tech company with the killer app. And the killer app is drug discovery and development especially. And we've always thought about our company as a platform company, and we were never shy about partnering with others from the get go. So with our O18 our team, which is a cardioprotection drug, we out-licensed that really early, and it's found a home and now is being developed. And then we moved on to our liver cancer product, which we brought a little bit further. Now it's in GMP manufacturing. And we're actually looking for partners for that. And we have a prostate cancer compound in lead optimization that will probably pan out as well. So we see ourselves as being partners. Either we co-develop, or we out-license it and maybe one day, hopefully not too far in the future, we might bring one or two of our favorite ones into later stage clinical trials. But we are not shy about partnering at different stages. So we are going to be opportunistic because we really have a lot to offer. And also one thing that we've been talking to other partners, entrepreneurs, is that using our engine to form actually other companies, to really make sure the engine gets used and properly leveraged for other things that Auransa may not do because we just can't do everything.Harry Glorikian: No, that's impossible. And the conversation I have with entrepreneurs all the time, yes, I know you can do it all, but can we just pick one thing and get it across the finish line? And it also dramatically changes valuation, being able to get what I have people that tell me, you know, one of these days I have to see one of these A.I. systems get something out. And I always tell them, like, if you wait that long, you'll be too late.Harry Glorikian: So here's an interesting question, though. And jumping back to almost the beginning. The company was named Capella. And you change the name to Auransa.Pek Lum: That's right.Harry Glorikian: And so what's the story behind that? Gosh, you know.Harry Glorikian: When somebody woke up one morning and said, I don't like that name.Pek Lum: It's actually pretty funny. So we so we like to go to the Palo Alto foothills and watch the stars with the kids. And then one day we saw Capella. From afar, you look at it, it's actually one star. You look at closer, it's two stars. Then closer, it's four stars. It's pretty remarkable. And I thought, OK, we should name it Capella Biosciences. Thinking we are the only ones on the planet that are named. So we got Capella Biosciences and then probably, we never actually had a website yet. So we were just kind of chugging along early days and then we realized that there was a Capella Bioscience across the pond in the U.K. We said what? How can somebody be named Capella Bioscience without an S? So I actually called up the company and said, “Hey, we are like your twin across the pond. We're doing something a little different, actually completely different. But you are Capella Bioscience and I am Capella Biosciences. What should we do?” And they're like, “Well, we like the name.” We're like, “Well, we like it too.” So we kind of waited for a while. And but in the meantime, I started to think about a new name in case we need to change it. And then we realized that one day we were trying to buy a table, one of those cool tables that you can use as a ping pong table that also doubles as a as a conference room table. So we called up this New York City company and they said, oh, yeah, when are you going to launch the rockets into space. We're like what? So apparently, there's a Capella Space.Harry Glorikian: Yeah, OK.Pek Lum: Well, that's the last straw, because we get people tweeting about using our Twitter handle for something else. And so it's just a mess. So we've been thinking about this other name, and I thought this is a good name. Au means gold. And ansa is actually Latin for opportunity, which we found out. So we're like oh, golden opportunity. Golden answer. That kind of fits into the platform idea. Auransa sounds feminine. I like it. I'm female CEO. And I can get auransa.com. Nobody has Auransa. So that is how Auransa came to be.Harry Glorikian: Well, you got to love the…I love the Latin dictionary when I'm going through there and when I'm looking for names for a company, I've done that a number of times, so. Well, I can only wish you incredible success in your journey and what you're doing, it's such a fascinating area. I mean, I always have this dream that one day everybody is going to share all this data and we're going to move even faster. But I'm not holding my breath on that one when it comes to private companies. But it was great to talk to you. And I hope that we can continue the conversation in the future and watch the watch the progression of the company.Pek Lum: Thank you, Harry. This has been really fun.Harry Glorikian: That’s it for this week’s show. We’ve made more than 50 episodes of MoneyBall Medicine, and you can find all of them at glorikian.com under the tab “Podcast.” You can follow me on Twitter at hglorikian. If you like the show, please do us a favor and leave a rating and review at Apple Podcasts. Thanks, and we’ll be back soon with our next interview.  

Returning guest and study author, Steve Shak, Chief Medical Officer at Exact Sciences discusses results presented at SABCS (San Antonio Breast Cancer Symposium) from the Phase 3 RxPONDER (Rx for Positive Node, Endocrine Responsive) study, one of the largest randomized, prospective clinical trials in women with node-positive, hormone receptor-positive (HR+), HER2- early-stage breast cancer. Dr. Steve Shak is the Chief Medical Officer for Exact Sciences. Joining the company in 2019 upon the closing of the Genomic Health / Exact Sciences combination, his key responsibilities include leading strategy for the company’s clinical development plans, building relationships with key leaders and institutions in the cancer community, and ensuring the voice of patients and physicians are heard at all levels of the organization. Before serving as Chief Medical Officer, he was the Co-Founder, Chief Medical Officer, and Chief Scientific Officer at Genomic Health, driving Oncotype DX assay development in breast, prostate and colon cancer. Before then, he was the Research Director and Staff Clinical Scientist at Genentech, leading the clinical team in the development of the targeted breast cancer drug Herceptin®, and the research team in the discovery of the cystic fibrosis drug Pulmozyme®. He also taught as an Assistant Professor of Medicine and Pharmacology at New York University School of Medicine. Dr. Shak received his medical degree from New York University School of Medicine and his formal post-doctoral training at Bellevue Hospital and the University of California, San Francisco. He has a bachelor’s degree from Amherst College in Massachusetts.

Hey guys! Marce Lamontagne here.  Thank you so much for joining me in my first episode of Breast Cancer and the Unknown.  In todays episode I want to tell you a little about myself and my journey that brought me to create this podcast and what I am hoping you as a listener will get out of it.  When I was first diagnosed in 2016, my brother who is a pretty well known podcaster URGED me to start a podcast.  I was like, “Yeah, yeah, I'll do it”, but the fear of the unknowns of starting a podcast and putting myself out there, really gave me hesitation.  So months pas,  then years, and I thought at some point he would stop bugging me, but he didn't! So when covid hit I thought, “Marce…if there is anytime to start a podcast now is the time.  There are so many people out there struggling with not only being newly diagnosed with Breast Cancer, but going through it during Covid with all those unknowns and fears.” I felt that if my story and others like mine could help even one person, I could get over my own fears of starting a podcast and just do it!  I mean, starting a podcast is definitely not as scary as being diagnosed with breast cancer.  So here I am, putting myself out there, I hope you enjoy it! As I said, I was diagnosed back in 2016.  I was 35 years old, a part time nurse, full time mom to a 5 year old girl (KC) and a 2 year old boy (will) and had just celebrated my 10 year anniversary with my husband when I felt a lump on my left breast. I was pretty healthy overall and had actually just finished an 8 week beachbody program.   I had  FINALLY lost the last 10 pounds of baby weight I had been carrying around!!!   I wasn't really worried but I asked my mom who is also a nurse what her thoughts were.  Since breast cancer runs in my family she recommended me setting up an apt with my PCP.  Since I alllllways listen to my mom, I made an apt for the following week and had my dr do an exam.  Although breast cancer runs strongly in my family, my doctor wasn't overally concerned. We decided to monito it and set up an apt for a follow up a month later.  when October came around I went in for my apt and my doctor said she felt the lump was the same and still was not concerned. She did however offer a mammogram to be safe, and usually I would have been like “nah- if you are not concerned neither am I” but something in my gut urged me to go ahead and set up an apt. 2 weeks later I headed in for my mammogram- not even thinking my life could drastically change, yet I walked out a completely different person.  My apt went like this- mammogram to Ultra sound which showed an enlarged lymph node, to the radiologist coming in saying they saw something worrisome and wanted to set up a biopsy.  My drive home was such a blur and when I got home THANK GOD my husband Justin was there.  He asked me how my apt went.  I immediately started crying. I remember saying… They saw something and said it was worrisome….not suspicious….worrisome…worrisome is better than suspicious right?? He gave me a big hug…Im sure not knowing what to say, but the hug I definitely needed.  I got a call the next day to set up a biopsy.  10 days later…10 days…like an eternity!! So I waited…and waited the best I could.  But by day 8 I couldn't take it anymore.   I called the Breast Center in Scarborough Maine and they were able to get me an apt to see the Nurse Practitioner Karen (my god I love Karen!)  She pulled up the mammogram and said to me- look Marce, I can tell you without even having a biopsy that you are atleast stage 2, it has spread to your lymph nodes and we will need to do chemo.  I mean if my mouth didn't hit the floor right then I would be shocked!    Fast forward through all the waiting…waiting for my biopsy results…I ended up being triple positive, waiting for second opinions, waiting for scans, genetic counseling…the works.  I mean lets be honest…this part SUCKED!! Like really SUCKED.  My head was spinning with questions…whats the treatment plan, has is spread, will I live to see my kids grow up? The waiting and fear of the Unknown was THE WORST!!! But slowly, the days past, my treatment plan turned into action, and I began my journey as a Survivor.  It wasn't easy..we know this! But atleast I was actively killing the cancer and that gave me a feeling of power and control. My treatment plan went a little something like this….4 rounds of Adrimycin and cytoxin, followed by 12 rounds of taxol and Herceptin and perjeta, Left breast mastectomy with full axillary dissection, 33 rounds of radiation and then a prophilatctic right breast mastectomy with immediate reconstruction using the DIEP flap method. I also was able to have whats called a lymphovenous bypass, which basically means after my lymph nodes were removed Dr. Singhal at Beth Isreal went in and shot some dye into my armpit and was able to reconnect two lymphatic channels to blood vessels.  This decreased my chance of having lymphedema was 33 percent down to 10 percent.  Pretty cool right?!?  Please feel free to contact me with any questions regarding my treatment plan!! I was also very lucky to have an amazing support system. Each week different friends and family members would come hang out with me during treatment and we would have a blast.  They would make fun of me after I got the benedryl and started saying random and sometimes incoherrant things.  My BFF Colleen who came to almost all my treatments (I love you girl!!)  would write up a post to put on my caring bridge page- and let me tell you, going back and reading these is pretty hilarious! I definitely recommend setting one up so that family and friends can read updates and you don't get like 100 text messages a day asking how you are doing, where you are in treatment etc.   Although I was so lucky to have such a kick ass support system, I was still a 35 year old women, newly diagnosed with cancer, knowing NO ONE my age who had been through an experience like this. I felt so alone.  That's when my oncologist recommended a young womens support group called tits and tacos…best name ever right! We would meet at a Mexican restaurant once a month and talk about our journeys and let me tell you, that group helped me stay positive during my treatment.  I love online support groups and am part of many of them, but meeting these women in person and being able to see that my fears and anxieties were not crazy and also to see how they were thriving after a cancer diagnosis  and not allowing it to take over their entire life, gave me hope that someday I would be where they were…not just surviving but thriving!!  You will hear some of these ladies stories in future episodes!!  Unfortunately that group fell by the wayside shortly after I finished treatment.  But I never forgot what that group meant to me, so when a couple of my girlfriends were diagnosed two days apart and my sister in law asked if I would chat with her firend from HS show was recently diagnosed…I said to myself…Marce…its time to get that support group up and running.  I created a private facebook group, made up some cards for my oncology office to hand out and that's how Tatas and Tapas was born! Anyone listening is welcome to check us out to see if we could be of any help to you throughout your journey!!  We do have meetups, but also have women who live out of state and just check in with questions about treatment, side effects etc.  Here I am, almost three years cancer free and felt like it was time to take a leap of faith and create this podcast.  I may have had a little push….or shove from my brother who is a pretty well known podcaster himself.  But he helped me realize that my story and others like mine can help so many women and men who are just beginning their journey. You are not alone.   We are stronger than we give ourselves credit for and we are stronger together!!  I hope you will benefit from listening to other survivor stories and consider sharing your own. There are also many resources out there that focus on supporting survivors through their journey and I will be sharing that information as well.  If you would like to share your journey or any resources that have been helpful to you,  feel free to contact me at breastcancerandtheunknown@gmail.com.  

You probably know about the gender wage gap, but have you ever thought about the gender health gap? Katie again welcomes to the podcast Priti Krishtel, co-founder and co-executive director of I-MAK, an organization using patent law to increase global access to medicines. Priti explains the ways in which women (yes, even you!) are disproportionately harmed by the high prices of drugs and healthcare, and what this means for us as we get older and need to rely more and more on the healthcare system. For example, did you know that a quarter of the twelve highest-grossing drugs in the US treat conditions that primarily affect women? This includes breast cancer drug Herceptin, which comes with a yearly price tag of over $60,000! Priti discusses the damage that high drug prices inflict on women's health, and how you (yes, even you!!) can take small steps to help lower drug prices for all.