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Dr. Shannon Westin and her guest, Dr. Breelyn Wilky, discuss the JCO article, "“Botensilimab (Fc-enhanced anti-cytotoxic lymphocyte-association protein-4 antibody) Plus Balstilimab (anti-PD-1 antibody) in Patients With Relapsed/Refractory Metastatic Sarcomas." TRANSCRIPT Shannon Westin: Hello, everyone, and welcome to another episode of JCO After Hours, the podcast where we get in depth on research that has been published in the Journal of Clinical Oncology. I am your host, Gynecologic Oncologist and Social Media Consultant Editor of the JCO, Shannon Westin. I serve here from the University of Texas MD Anderson Cancer Center. And I am so excited to welcome Dr. Breelyn Wilky. She's an Associate Professor and the Director of Sarcoma Medical Oncology in the Department of Medicine Division of Medical Oncology, and the Cheryl Bennett & McNeilly family endowed chair in Sarcoma Research, the Deputy Associate Director of Clinical research at the University of Colorado Cancer Center. Welcome. Dr. Breelyn Wilky: Thank you so much. I'm delighted to be here. Shannon Westin: And with all those titles, I'm super impressed that she was able to complete the manuscript that we're going to discuss today, which is “Botensilimab (Fc-enhanced anti-cytotoxic lymphocyte-association protein-4 antibody) Plus Balstilimab (anti-PD-1 antibody) in Patients With Relapsed/Refractory Metastatic Sarcomas.” And this was published in the JCO on January 27, 2025. And please note, our participants do not have any conflicts of interest. So this is exciting. Let's first level set. Can you review with us just the current state of sarcoma incidents, survival outcomes, that kind of thing so we all know where we're starting? Dr. Breelyn Wilky: Yes. So, you know, sarcomas are really, I like to call them the black box cancer type. And the big thing is that there's really more than a hundred different kinds of sarcomas, which collectively altogether make up only 1% of adult cancers. And so we talk about these as being bone and soft tissue tumors, but really, the heterogeneity is just incredible. You're talking maybe 10,000 to 12,000 new cases of soft tissue sarcoma per year, which is pretty rare in the grand scheme of things. And the trouble with these is that while you can cure sarcomas if you find them early and they're localized, when they metastasize and spread and are not resectable, we're looking at median overall survivals of really only 12 to 18 months, even, you know, with our best therapies that we have. So, really there's just a dire need for new treatments for this really tough group of diseases. Shannon Westin: Yeah, I agree. I'm a gynecologic oncologist, and we have our little subset of sarcomas that I know there's a little bit out of every one. So I'm really excited to pull this manuscript as one of our podcasts offerings because I think we're all seeing these patients in the clinic and certainly our listeners that have sarcoma or have family members with sarcoma, this is so good to have a real focus on a rare group of tumors that have been a little bit lumped together. Now, with that being said, I know this is such a heterogeneous population, but can you briefly overview a little bit around the standard of care for treatment of recurrent sarcomas? Dr. Breelyn Wilky: We have actually been using the same drugs really since about the 1970s, and up until very recently, nothing had really challenged doxorubicin, the old ‘red devil', like we used to call it. And this has been the mainstay of treatment for metastatic sarcomas and really used across the board. In the GYN literature, for uterine leiomyosarcoma, we did see some promising activity with the combination of doxorubicin and trabectedin coming out of the French group. But, except for that study, no combination therapy or new drug has been proven better in terms of overall survival compared to doxorubicin monotherapy, really over 40, 50 years. So it's definitely a tough situation. Now, we do have other drugs that we use, so most patients will wind up getting doxorubicin-based therapy. There's a couple of other regimens that we'll reach to, like gemcitabine docetaxel. And once you get into the specific subtypes, we have some approvals in liposarcomas and leiomyosarcomas for some other drugs. But really the median progression for survival for most of these regimens is somewhere four to six months. And response rates typically are somewhere like 10%, 15% for most of these. So it's really just a very tough field and a tough group of patients to try to make an impact for. Shannon Westin: So let's talk a little bit more kind of getting focused on what you've studied here. What's been the role of immunotherapy thus far in the treatment of sarcomas maybe prior to this particular study? Dr. Breelyn Wilky: Clearly, we all know that immune therapy has just changed cancer care forever over the last few years for so many different types of cancers and diseases like melanoma and renal cell and lung cancer have just been transformed by checkpoint inhibitors specifically directed against PD-1 or CTLA-4 or both. And so, of course, you know, sarcoma docs we're super excited to try to see if these might potentially have activity in our tumors as well. I never had seen myself in my career getting into immunotherapy until I was able to run an investigator-initiated study during my role in Miami, where we combined pembrolizumab, so PD-1 inhibitor, with axitinib which was a pan-VEGF inhibitor. And lo and behold, like I had patients that I was seeing responses when other treatments, all those chemotherapies I was just talking about had failed. And one of my first patients I treated was about a 60-year-old lady with something called cutaneous angiosarcoma. So this is a blood vessel sarcoma all over her face. And we had treated her with 10 different therapies, all the chemotherapy regimens, targeted therapies, clinical trials, and nothing was working. But I put her on a phase 1 trial with a baby dose of CTLA-4 and this woman had a complete response. And so for me, once I saw it work in even just those couple of patients, like that was nothing that we'd ever seen with our chemotherapy regimens. And so that sort of shifted my career towards really focusing on this, and this is about the time where some of the studies started to come out for sarcomas. And the take home with sarcoma is about 20% of sarcomas have this sort of immune hot physiology. So what that basically means is if you look at gene expression of immune related gene signatures, or you look for infiltrating T-cells, sort of the SWAT team of our immune system, like you can find those in the tumors. And it's sort of evidence that the immune system had some clue for that 20% of patients that this was a foreign tumor and that it should be attacking it and maybe just needed a little help. But globally, about 80% of sarcomas are these immune cold tumors, which means the immune system has no clue that these things are even a threat. And there's almost no immune activation, very, very few antigens. In other cancer types, high neoantigens or tumor antigens help the immune system work better. And so that basically goes with what we've seen with trials of PD-1 or CTLA-4 blockade. About 20% of sarcomas, with some exceptions, can respond. But really 80% across the board, you're stuck, you just can't get them to be recognized. And so that's where I think this data is so interesting is there's some signals of activity in these immune cold tumors which, at least historically with the trials we've done so far, we really haven't seen that with sort of the traditional checkpoints. Shannon Westin: So I think now this is a great time to maybe talk about the study design in general, the eligibility and just give us kind of a run through of that. Dr. Breelyn Wilky: So this trial was a phase 1 trial of a drug called botensilimab, which is a next generation CTLA-4 directed immune modulator. So what makes botensilimab different is that the CTLA-4 end is very similar to other CTLA-4 inhibitors that are out there, but it's been engineered on the back end of the molecule that binds to Fc gamma receptors to basically bind tighter with higher affinity. And what this translates to in laboratory models and increasingly now in patients is it does a better job of priming, of educating our T cells, our, again, these highly intelligent antigen specific cells, but also natural killer cells. It does a better job of sort of educating those. It helps to activate macrophages and other supporting actors in the immune response. And so the idea here is that there's evidence that botensilimab may do a better job at creating new responses in immune cold tumors. The study combined either botensilimab as monotherapy or in combination with a PD-1 inhibitor called balstilimab. And this was all comers, really a variety of tumor types. And to date I think we're close to about 500 patients with a variety of solid tumors that have been accrued to this study, this C-800-01 phase 1 trial. This paper reports on the sarcoma patients that were enrolled as part of this study. And so, again, given what I've told you about sarcomas being really immune cold, we were just so excited to have the opportunity to enroll on a next generation immune therapy for these tumors that really we were running into roadblocks trying to use immunotherapy previously. Shannon Westin: It's a very compelling idea and I'm so excited for you to tell people what you found. I think first things first, it was an early phase trial. So why don't we talk a little bit about the safety of the regimen. Was there anything that you didn't expect? Dr. Breelyn Wilky: Right. So similar to other checkpoint inhibitors, you know, the idea is that these drugs can cause immune mediated toxicities, right? So essentially you're revving up the immune system and it can sometimes get a bit confused and start attacking our normal cells, our normal organs, leading to essentially any number of toxicities of basically head to toe, something can get inflamed and you can develop a toxicity from that. So the key take homes with this particular drug with, botensilimab with balstilimab, we saw colitis was sort of the primary immune mediated toxicity and it was about a third of patients, give or take. It happens and it can be aggressive and needs to be managed aggressively. And you know, one of the things that we learned very quickly taking part in this study is how important it is that as soon as patients start to get diarrhea, immunosuppression gets on board. So steroids, early use of TNF alpha blockade, so infliximab for example, if we jumped on it quickly and we recognized it and we got the patients treated, it would resolve fairly quickly and even some patients could remain on treatment. So I think that was sort of the first take home is “Okay if you get colitis, you treat it fast, you treat it early and you can still have patients not only recover, which essentially everybody recovered from this colitis and then being able to continue on treatment and still have their anti-tumor responses.” So that's the first point. The second thing that was really interesting is part of the engineering of botensilimab on the back end of the molecule, it's been designed to decrease complement binding and it's thought that that triggers some of these other toxicities that we've seen with prior CTLA-4 inhibitors like pneumonitis or hypophysitis. We actually don't see that with botensilimab. So there's sort of this selective toxicity that may reflect the design of the molecule. But overall the treatment was, we didn't see any new safety signals that were outside of what we would expect in class. And colitis was sort of the dominant thing that we had to be ready for and ready to manage. Shannon Westin: We've been doing it for a while now, so we kind of know what to do and we can act quickly and really try to mitigate and avoid some of the major toxicities. So that's great that that was what was reflected in what you found. And then of course I think: What about the efficacy?” Right. This is what we care about as practitioners, as patients. Does it work and are there any subtypes that seem to benefit the most from this combination? Dr. Breelyn Wilky: Right. So for the sarcoma patients, we treated 64 patients and 52 of those patients were evaluable for efficacy. So a decent size group of patients in sarcomas, where, you know, typically our trials are pretty small, they're very rare, but we had 52 evaluable with at least one post baseline scan. So that was our criteria. And basically we saw across all of the patients, and keep in mind, these are heavily pre-treated patients, as you mentioned, so a median of 3 prior lines of therapy, so most of these patients had had chemotherapies and then about 20% had also had prior immunotherapy as well. So PD-1 treatments or so on. The overall response rate by RECIST was 19.2% for all of the evaluable patients. And then with iRECIST, which is sort of that immune adapted response criteria that allows for early pseudo progression, we actually had another patient who did have that. And so that response rate was 21.2%. Overall, we were really excited to see this in a heavily pre-treated group of patients. But what was really exciting to me was when we looked at the subset of patients that had angiosarcoma, that blood vessel tumor I was talking about earlier with my other patient. So angios come in two flavors. One is this sort of cutaneous type, or meaning involving the skin that has a UV signature, a UV damage signature, very similar to melanoma. So these tumors tend to have a high mutation burden. And oftentimes there is a track record that we've seen responses with immunotherapy in cutaneous angiosarcomas. But the other group that we deal with is called visceral angiosarcomas. And so these are totally different biologically. These are often driven by mutations in MYC or KDR amplification, and they arise in organs, so primary breast angiosarcoma, not associated with radiation, or they can arise in the liver or the spleen or an extremity. So these are very, very different tumors, and the visceral ones almost never historically have responded to checkpoint inhibitors. So we had 18 patients with angio split - 9 with cutaneous, 9 with visceral. And we were just blown away because the response rate for that group was 27.8%. And if you looked at the responses between the hot ones and the cold ones, it was almost equal and a little bit better in the visceral. So we had a 33% response rate in visceral angiosarcoma, which is crazy, historically speaking, and about 20% again in the cutaneous angios. So for a disease where visceral angio gets treated with chemotherapy, might respond initially, but then rapidly progresses - like these people go through multiple lines of therapy - to have a third of patients responding, and then some of those responses were durable. Our median duration of response for the study was 21.7 months, which is just nuts for sarcomas where we just don't see those sorts of long term benefits with the drugs that we have. So I think those are kind of the two main things. There were other subtypes that had clinical benefit and responses as well in d-diff liposarcoma, soft tissue leiomyosarcoma, which are again thought to be fairly cold immune subtypes. So just really exciting to kind of see responses we hadn't expected in a very challenging group of tumors. Shannon Westin: We see all these patients and we have patients that respond so well to immunotherapy with other histotypes. And so it's so exciting to see an option for these really hard to treat tumors that our patients struggle with. So this is so, so very exciting. I wanted to make mention, you know, I was really impressed with the amount of translational work you were able to do in this early phase study. So do you want to review just maybe a few of the key findings that you guys discovered? Dr. Breelyn Wilky: It's always great. I'm a translational researcher at heart and we do a lot of immune correlative work. And I think the reason I got so excited about this field to begin with was trying to learn why it works for some patients and why it doesn't work for other patients. So I'm a huge believer in learning from every patient that we can. So it's such a testament to the company, Agenus, who sponsored this trial to invest their time and resources into correlative studies at this phase. It's huge. So we learned a couple of things. IL-6 or interleukin 6 is a cytokine that basically has, in other tumor types, been associated with worse outcomes. And what we were interested in this group is we saw the same thing. And again, sarcomas have very, very little correlative biology that's done. We're really in infancy and understanding the microenvironment and how that milieu balances out in our tumors. So we were really excited to see again that lower peripheral interleukin 6 associated with improved overall survival. So again, kind of sorting out a group of patients that might be immunologically favorable when it comes to this type of therapy. The other thing that's important to know about sarcoma is so the other tumor types are lucky and have PD-L1 expression and the tumor is a biomarker, but we never have PD-L1 expression. We can find it in sarcomas and it can be loosely correlated with a chance of benefit with immunotherapy. But I've had patients respond that were PD-L1 negative, and I've had patients that were loaded with PD-L1 that didn't seem to make a difference. And that's not just in this study. So we saw in this trial a trend towards improved overall survival with PD-L1 expression that wasn't significant, but there was like this trend. And it's really interesting because, again, this is largely a CTLA-4 directed therapy. And so what we wondered is if PD-L1 expression is an index of sort of this underlying potential immunogenicity. And actually PD-1 works very late in the whole immune process. That's really at the very end where you've got the T cell that's facing the tumor cell and it's just activating that T cell that's already grown up and already educated and ready to go. Whereas CTLA-4 is really educating in early immune responses and expanding the T cells that have potential to kill. So I'm interested to look into this in more depth in the future to see if this is actually the biomarker for CTLA-4 directed therapy that we've been looking for, because we really don't have a great sense about that. And then the last piece just to note is that in this trial, like most others, very, very few sarcomas had high mutational burden. Everybody was very low, which reflects the population. And it's just really more encouragement than an immune cold tumor with very crappy neoantigens can still respond to immunotherapy if we get them the right agents. Shannon Westin: Yeah, I mean, I'm taking notes because we have such a struggle with this across the gynecologic tumors. I'm like, “Okay, maybe this is finally it.” So hopefully your work will go on to really inspire us across a number of solid tumors that have been traditionally cold. So, so very exciting. And I would just say for my last question, obviously, congratulations on this successful study. What do you think are the next steps for this combination in sarcomas? Dr. Breelyn Wilky: So, again, just to your point, this trial enrolled a bunch of different subtypes, and sarcomas are not the only immune cold tumor that this combo has looked really promising for, microsatellite stable colorectal cancer, ovarian cancer that was platinum refractory, non-small cell lungs. So I think the future is really bright for immune cold tumors kind of across the board. So, yes, lots of hope for not just sarcomas but in terms of our patients, I just have to be so grateful to Agenus for their interest in a rare disease. Sometimes it's hard to get that interest for a very challenging group of patients that are all heterogeneous, they are not all the same and our big clinical trials are a few hundred patients. It's just a very different environment. But they have been so supportive and involved in making sure that sarcomas are represented in their priorities. So there are ongoing discussions about what the optimal way to explore this further in sarcomas is going to be and I cannot wait to have the official plans in place. But my hope is this will not be the last that we see of these drugs for our patients. Shannon Westin: Well, I support that and my vote is on your side. So, thank you so much again, Dr. Wilky. This time just flew by. This was such a great discussion and I mean, I think it's, again, a testament to your exciting data. And thank you to all of our listeners. This has been JCO After Hours' discussion of “Botensilimab (Fc-enhanced anti-cytotoxic lymphocyte-association protein-4 antibody) Plus Balstilimab (anti-PD-1 antibody) in Patients With Relapsed/Refractory Metastatic Sarcomas,” published in the JCO on January 27, 2025. So be sure to check out the full manuscript. And we hope that you enjoyed this podcast. And if you want to hear more about research published in the JCO, check this out on our ASCO JCO website or wherever you get your podcasts. Have an awesome day. 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. Guest statements on the 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. Dr. Wilky Disclosures Consulting or Advisory Role: SpringWorks Therapeutics, Deciphera, Epizyme, Adcendo, Polaris, Boehringer Ingelheim, AADi, InhibRx Research Funding: Exelixis Travel, Accommodations, Expenses: Agenus
On this episode of Health 411, host Dr. Jonathan Karp and student producer chat with Dr. Mona Saleh, Gynecologic Oncologist at Capital Health.
Docs Outside The Box - Ordinary Doctors Doing Extraordinary Things
SEND US A TEXT MESSAGE!!! Let Drs. Nii & Renee know what you think about the show!On this episode we introduce our podcast team and also discuss the struggles of the sandwich generation, those balancing the responsibilities of caring for aging parents while also raising children. We explore the intricacies of locum tenens positions and the potential impact of physician strikes on the healthcare system. Our conversation covers a wide range of topics so tune in so you don't miss out!Timeline0:00 Introduction & get to know our team.5:00 The Sandwich generation & taking care of your aging parents.12:16 Taking out emotions when treating your family as a doctor.20:16 Story time on a resident interfering with the wife's delivery. 28:10 The unwritten rule of not treating your family as a doctor.30:55 Q&A on Locums as a Gynecologic Oncologist.44:25 The 1% of doctors that are different.52:20 Instagram shoutout & Story time on a Locums Urologist.56:38 The just averted doctors strike in 4 New York hospitals & will you strike as a locums doctor?1:13:21 New York is different from anywhere else.1:25:42 International medical missions.1:33:35 Our upcoming locums course.1:37:01 Our themes and New Year resolutions for 2025 FREE DOWNLOAD - 7 Considerations Before Starting Locum Tenens - https://darkos.lpages.co/7-considerations-before-locumsLINKS MENTIONED Urologist who makes $400k working 7 days a month - https://youtu.be/7Id9suR3TmQNeurosurgeon who quit medicine to live off the grid - https://youtu.be/0qcbPmlOqaoQ&A and Suggestions Form - https://forms.clickup.com/9010110533/f/8cgpr25-4614/PEBFZN5LA6FKEIXTWFSIGN UP FOR OUR NEWSLETTER!WATCH THIS EPISODE ON YOUTUBE!Have a question for the podcast?Text us at 833-230-2860Twitter: @drniidarkoInstagram: @docsoutsidetheboxEmail: team@drniidarko.comMerch: https://docs-outside-the-box.creator-spring.comThis episode is sponsored by Set For Life Insurance. What the Darkos use for great disability insurance at a low cost!! Check them out at https://setforlifeinsurance.com/
Dr. Shannon Westin and her guest, Dr. Patrick Stone, discuss the article, Methylphenidate Versus Placebo for Treating Fatigue in People with Advanced Cancer, a Randomized, Double-Blind, Multicenter Placebo-Controlled Trial, recently published in JCO. TRANSCRIPT The guest on this podcast episode has no disclosures to declare. Shannon Westin: Hello, everyone, and welcome to another episode of JCO After Hours, the podcast where we go in depth on manuscripts and research published in the Journal of Clinical Oncology. I am your host, Shannon Westin, Social Media Editor for JCO and a Gynecologic Oncologist by trade. I am thrilled today to present Methylphenidate Versus Placebo for Treating Fatigue in People with Advanced Cancer, a Randomized, Double-Blind, Multicenter Placebo-Controlled Trial. This manuscript is a dual publication in the Journal of Clinical Oncology and presentation at the European Association of Palliative Care Congress here on May 17, 2024. And to review this incredible research with us will be Professor Patrick Stone, the Head of Department of Marie Curie Palliative Care Research Department, Division of Psychiatry at University College London. Welcome, Dr. Stone. Dr. Patrick Stone: Thank you very much. Thank you. Shannon Westin: Let's get right to it, we'll level set. Can you speak a bit about the definition of cancer-related fatigue and how common it is in people with advanced cancer? Dr. Patrick Stone: Sure. I think fatigue is a difficult thing to nail down really and define it clearly, and there are lots of definitions out there. In many ways, the simplest definition is the EAPC, the European Association of Palliative Care's definition of just a subjective sensation of weakness, feeling tired, and exhaustion. The reality is that that symptom is very common in the general population. And so if you really want to get a handle on it, I think a good way to do it is to think about taking an operational definition and say, “Look, if fatigue is normally distributed approximately in the general population, then we should consider severe fatigue or pathological fatigue could be defined as fatigue that is worse than 95% of the general population. And if you think that definition, then prevalence of fatigue in patients with newly diagnosed breast or prostate cancer, for instance, is around 15%, so three times as common as the most severe fatigue in the general population. If you come to patients with newly diagnosed non-small cell lung cancer, it's up to about 50%. And if you come to my area, which is palliative care and you go to a hospice and you ask people to complete a fatigue questionnaire, 78-80% of people complain of fatigue that is more severe than 95% of the general population. So that I think gives us a good handle on sort of the severity of this problem in cancer patients and how it progresses as disease progresses. Shannon Westin: I love this because I think we always struggle with exactly how to nail down the definition and exactly how to treat it. So I think that it's a really nice transition to existing treatment options for this issue and exactly how they might work. Dr. Patrick Stone: The first thing to say is in medicine if you can find a cause then you give a treatment directed at the cause and obviously that applies to fatigue as well. So the first thing is to do a thorough assessment of your patient, and if you can find an easily remediable cause such as anemia, hypocalcemia, or hypomagnesemia, or maybe other things like depression, which might manifest as fatigue, then you should try and give a treatment directed at that cause. But, for many patients, there won't be a single clearly identifiable cause you can target. And then people use more broad spectrum approaches if you like. The most well-studied I think is exercise. And exercise, there have been lots of randomized controlled trials in different types of exercise and it's a well attested treatment, which I think has good evidence of effectiveness, certainly in patients who are on treatment and in disease-free survivors. There is less evidence in advanced cancer because the trials are fewer. I would still say that there's moderate quality evidence that exercise is effective in advanced cancer. The other group of treatments, broadly speaking, would be psychological therapies, cognitive behavioral therapy and psychoeducational approaches, mindfulness based stress reduction, that sort of thing. And again, in earlier stage disease and in patients on treatment and in survivors, there's more quality evidence that that sort of approach can help, if not alleviate fatigue, allow people to cope better with fatigue. But the evidence in advanced cancer is weaker than for exercise. So I think the evidence for the effectiveness of those psychological therapies is not so strong. And then you come on to pharmacological therapies and there have been lots of trials of different agents. I won't list them all because most of them are negative and don't show any benefit. A few things which perhaps still show promise from previous trials, there have been, for instance, a few trials looking at ginseng as a herbal therapy. One very good quality trial showed benefit. Although another trial in advanced cancer didn't replicate that finding, so that ginseng is out there. Steroids, widely used in advanced cancer for general relief of many symptoms like fatigue, lack of energy, low moods, appetite. But although widely used, surprisingly little hard evidence or effectiveness, specifically for fatigue, but one relatively recent, well conducted randomized control trial, provides us with some firm evidence, also, that dexamethasone can help in the short term in advanced cancer patients. It obviously wouldn't be a recommended treatment longer term because of its side effects. And then we really come on to the crux of this study which is probably the most widely studied single agent beyond that, is methylphenidate, which is a psychostimulant agent, raises central dopamine catecholamine levels in the brain. And there's probably a thousand or so randomized control trials sort of being conducted looking at that prior to prize of this study that we're talking about. Shannon Westin: I would love to hear a summary of the data that were pre-existing in this study. So how well does methylphenidate seem to work, or what were the conflicting results that were seen prior? Dr. Patrick Stone: I think the rationale for this study was that it was the perfect background to justify another randomized controlled trial, which there have been– Well, I can't remember exactly how many there were in existence before my trial started, but when I last looked, there were 10 studies, 10 randomized controlled trials in cancer patients. Most of those trials have been neutral. They've shown no benefit over placebo, so most of the individual trials are negative. But meta-analyses always tend to show a positive result. So when you count the trials together, it gets you over the finishing line and you can see a positive benefit. But individually, the trials were quite heterogeneous, they're quite different. There were only four trials prior to the publication of this one that were done specifically in advanced cancer patients. One of them was published only a couple of years ago while my study was going on. And of those four trials, three of those have also been neutral, not showing a benefit over placebo. One study involving 28 patients and using a PRN as required dosing schedule showed some benefit. But the other studies with a total of about 330 odd patients have been neutral. Shannon Westin: I think that brings us to a great transition, just to talk a little bit about the design and objectives of your current study. Dr. Patrick Stone: Well, what we wanted to do was take the best bits, if you like, of the previous studies, and try to give ourselves the best chance of finding a clinically meaningful improvement in fatigue in patients with advanced cancer. And I was focusing on advanced cancer, principally because I'm a specialist in palliative medicine. That's the group of patients I'm most working with, whereas a lot of the studies have involved mixed groups of cancer patients or patient's disease-free or on treatment. But we looked at patients who were under the care of palliative care services, with incurable cancer, with a prognosis estimated to be less than a year or around a year. We wanted to try to get the dose of the medication up to a good level because some of the other studies which have shown benefit have got up to quite high levels of methylphenidate, approximating to about 40 to 60 milligrams of methylphenidate a day or equivalent. And we wanted to give the drug in an individually titrated dose because that would reflect the way it is used in clinical practice. You would adjust the dose like you might with morphine for pain relief. You would expect to adjust the dose of this medication up to get a therapeutic benefit. So we had this titration period where we adjusted the dose of the drug every week. We reviewed whether patients were feeling better, worse, or the same. We asked about side effects. And on the basis of the response to those questions, we either went up with the drug or kept the dose the same, or, if necessary, would come down. The primary endpoint was designed to be fatigue after six weeks of dose titration, plus or minus a window of two weeks, accepting the fact that we might miss a few patients at the six-week mark, for whatever reason. So we had a little window around that. That's what we were looking to do. Shannon Westin: And why did you choose the six-week time point? Dr. Patrick Stone: Well, there was no obvious time point to choose. One of the biggest positive studies previously was by Lower and colleagues back in 2009, and they had found their maximum benefit at around four weeks, or it took rather four weeks to reach the maximum benefit. So we wanted to give the patients in our trial every chance of demonstrating the benefit, and they'd also escalated the doses in their study up to above 40 milligrams or equivalent. And so we wanted to go up as high as we could, and we didn't feel that if we were adjusting the dose every week, that we could get up to a sufficiently high dose in any shorter time span. So six weeks sort of fitted, allowing us to titrate the dose up to a maximum of 60 milligrams a day, which is where we wanted to get up to. Shannon Westin: And what about a little bit more detail on the population you included, and maybe give us a sense of how well you think that represents your general population affected by fatigue in the setting of advanced cancer? Dr. Patrick Stone: We recruited patients from hospices, so that's inpatient palliative care units in the UK, but also from hospital palliative care services, from oncology outpatient services as well, oncology patients who are under the care of palliative care services, and we also recruited from some community palliative care services. So we had quite a good spread of settings, and all of our patients had advanced incurable cancer under the care of palliative care services. But I would say, I think by the nature of doing this randomized controlled trial, inevitably we ended up with quite a selected population, just because of the inclusion and the exclusion criteria that we had to apply. And the regulators were quite clear about who we shouldn't be putting on the drugs. And I think by the time you've excluded all the potential adverse consequences of using methylphenidate, we probably have ended up with a group of patients who were relatively fit compared to the general run-of-the-mill palliative care population, I would say. So I think that that is a limitation with regards to the generalizability of our result. Shannon Westin: How did you measure fatigue in this study? What was the mechanism for that objective? Dr. Patrick Stone: It's a subjective rating scale. We use a very well-established and well-validated measurement instrument. It's the Functional Assessment of Chronic Illness Therapy FACIT-F which is the fatigue subscale of their anemia subscale, which is a 13-item questionnaire, very well validated and widely used in lots of previous studies. Higher scores represent better quality of life and, therefore, lower levels of fatigue. So that's the scale that we used. Shannon Westin: Got it. So let's get to it. How well did methylphenidate work to impact fatigue compared to placebo? And were there any groups that seemed to have a bigger impact? Dr. Patrick Stone: Well, the bottom line, of course, is that at six weeks, plus or minus two weeks, there was no statistically significant benefit for methylphenidate over placebo. There was a two-point improvement in fatigue scores, but it wasn't statistically significant. And two points on the FACIT-F did not reach our predetermined five-point difference that we regarded as representing a minimally clinically important difference. We looked at lots of secondary fatigue endpoints. We measured fatigue every week over the whole course of the study. And actually, at weeks 2, 3, 4, 5, and 6, there was indeed a statistically, nominally statistically significant difference in fatigue scores. But I really would not want anybody to read anything over much into that finding because it was not a pre-stated hypothesis of our study. It wasn't a pre-stated endpoint, it was a secondary outcome. And moreover, even if this was regarded as a statistically significant finding, and as I say, it was only nominally statistically significant finding, the magnitude of the change was still not sufficiently large that I think it would want to influence your clinical decision making. With other groups just to say, we did look specifically at whether patients with the most severe fatigue would experience benefit over and above other patients, because in a previous study, that looked at modafinil, an agent that promotes vigilance, although the overall finding was neutral in a subgroup of patients with the most severe fatigue, modafinil seemed to work. So we thought we better check in this study whether patients with the most severe fatigue had a differential benefit. But we found no such effect. We found no difference in patients who were on or off treatment or indeed among the patients who scored highest with the depression subscale on the hospital anxiety and depression scale. None of these subgroups showed any benefit over placebo. Shannon Westin: How did patients tolerate methylphenidate? Was it tolerable? Dr. Patrick Stone: That was the thing I think that I was most relieved about. I am a cautious and anxious investigator, and the last thing I wanted to do was to put palliative care patients at risk by giving them a drug which might cause some harm. So I was very relieved when we analyzed the results to confirm that methylphenidate was very well tolerated. There was no real pattern of evidence for any increase in adverse effects over placebo. In fact, when we looked at just people who self-reported severe adverse effects, we found a higher rate in the placebo group than in the methylphenidate group in fact. And in terms of serious adverse events, there were 25 serious adverse events in both groups, so there was, again, no pattern that suggested methylphenidate was causing harm. So, yes, it was well tolerated, but did not result in a clinically important improvement in fatigue. Shannon Westin: Were you surprised by the results? Dr. Patrick Stone: I honestly went into this with an open mind. I didn't come in with a real fixed agenda that I want to prove that this thing works. In fact, although methylphenidate was being used by some of my colleagues around the country and I know it's used by some colleagues internationally, personally I was not using it because I didn't feel the evidence was strong enough to justify using it. So I was waiting for the results of my own trial before making my decision. And I don't plan now to be using it on the basis of the results of the study. Shannon Westin: Sounds pretty definitive. It's always frustrating, and I know our patients, when we tell them to exercise when they're exhausted, they're like, “Are you kidding me?” Right? So it would be wonderful if there is like the perfect pill that we can give them. It's certainly disappointing. What do you think we should be exploring next for the resolution of fatigue in this patient population? Dr. Patrick Stone: Well, I think one thing. Going back to your very first question to me about defining fatigue, I think one problem is we don't really have a mechanistic understanding of what we're talking about here necessarily with cancer related fatigue. And it's a bit of an umbrella term, I suspect, for a lot of different things, and may have a common endpoint in terms of the symptom. But maybe if we could better define, if you like, for want of a better word, the phenotype of fatigue, it may be that we could actually target a treatment in certain subgroups of patients that may be of more benefit. So maybe some greater basic science pinpointing what is causing fatigue, so that we can design the treatments, rather than just try repurposing existing drugs on the off chance that they work. And the other thing is okay, maybe we can't pinpoint a particular cause, we think it's multi factorial. If we think it's multifactorial, then perhaps we ought to be using a multimodal treatment approach and maybe it's actually exercise, psychological therapies, and diet, plus or minus a drug, and that's the approach if we can't pinpoint a specific cause. Shannon Westin: I love the idea of incorporating the translational work to really try to understand the etiology better and then use something more targeted. It's that version of precision medicine but for palliative care as well. I really like that. Well, this has been awesome. Thank you so much, Dr. Stone. I think that your insight is so much appreciated, and thank you for putting together this definitive work to help us treat our patients better every day. I really appreciate the time you took. Dr. Patrick Stone: Thank you very much. Shannon Westin: You're so welcome. And thank you to our listeners. This has been methylphenidate versus placebo for treating fatigue in people with advanced cancer, randomized, double-blind, multicenter, placebo-controlled clinical trial. And again, this is a dual publication in the JCO as well as a presentation at the European Association of Palliative Care Congress on 5/17/24. And we are so thrilled that you could join JCO After Hours and we hope you will check out our other offerings wherever you get your podcasts. Have an awesome day. 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. Guest statements on the 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.
In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Dr. Ana Luzarraga to discuss molecular profiles as predictors of endometrial recurrence. Dr. Luzarraga is a Gynecologic Oncologist currently working in the Vall d'Hebron University Hospital in Barcelona, Spain. She has completed her two years ESGO fellowship in 2023 and is currently finishing her PhD programme about molecular profile in endometrial cancer. Highlights: Molecular subgroups of endometrial cancer present distinctive recurrence patterns: p53-abn tumors relapse mostly with peritoneal and distant disease and NSMP tumors at distance. Molecular profile is a stronger independent predictor for vaginal, peritoneal, and distant recurrence than classic histologic factors. P53-abn is the sole independent predictor of peritoneal relapse. P53-abn and NSMP are independent predictors of distant recurrence.
In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Drs. Christina Fotopoulou, Ane Gerda Z. Eriksson, Glauco Baiocchi, and Oliver Zivanovic to discuss the 2024 Special Issue of IJGC, “Novel Surgical Approaches in Gynecological Oncology”. Dr. Fotopoulou is the Chair of Gynaecological Cancer Surgery at the Department of Surgery and Cancer at Imperial College London, UK. She has served as an elected ESGO council member and Chair of the ESGO and BGCS guidelines committee. Dr. Eriksson is the chair of the endometrial cancer and gyn sarcoma group at the Department of Gynecologic Oncology at the Norwegian Radium Hospital. She is currently an elected ESGO Council member and chair of the ESGO accreditation committee. Dr. Eriksson also serves on the NSGO-CTU Foundation Board. Dr. Glauco Baiocchi is the head of the Department of Gynecologic Oncology at the AC Camargo Cancer Center. He is also the president of the Brazilian Gynecologic Oncology Group – EVA Group. Oliver Zivanovic MD is a Gynecologic Oncologist and Chairman of the Department of Obstetrics and Gynecology at the Women's Heidelberg University Hospital, Germany. Highlights: Surgery is the cornerstone of treatment in gynecologic oncology. Surgery is being incorporated and adapted to the evolving treatment landscape in gynecologic oncology. This special issue highlights the opportunities of tailoring surgical approaches to individual patients both in regard to radically and novel surgical techniques. It brings together out of the box topics such as surgery for lymphedema, uterine transposition, imaging, quality of life, and medico-legal aspects. All articles were written by respected and well-known experts on each topic. Our hope and intention is that this Special Issue will become a significant resource in surgery for gyn oncology and may support and inspire surgeons to deliver better treatment.
In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Drs. Giuseppe Cucinella, Andrea Mariani, and Gretchen E. Glaser to discuss ITCs in low-risk endometrial cancer. Giuseppe Cucinella, MD, is a gynecologist working at Istituto Nazionale Tumori IRCSS Fondazione G.Pascale in Naples, Italy (Department of Gynecologic Oncology). During his residency, he worked as a research fellow at Mayo Clinic in Rochester, Minnesota, where he focused on the study of endometrial cancer. He is currently in the second year of the PhD program in "Experimental Oncology and Surgery - Gynecologic Oncology" at the University of Palermo, Palermo (Italy). Dr. Cucinella's clinical research focuses on the diagnosis and treatment of endometrial cancer and minimally invasive surgery in gynecologic oncology. Dr. Andrea Mariani is a Full Professor in the Department of Obstetrics and Gynecology, Division of Gynecologic Surgery, at Mayo Clinic in Rochester, Minnesota. Dr. Mariani is the Gynecologic Oncology Division Chair in the Department of Obstetrics and Gynecology. Dr. Mariani's research interest is endometrial cancer with a special interest in robotic surgery. He is internationally recognized for his contributions in the advancement of surgical and postoperative treatment of endometrial cancer. Gretchen E. Glaser, MD is a Gynecologic Oncologist at Mayo Clinic specializing in complex surgery for malignant and benign conditions, including minimally invasive and open approaches. In addition to her clinical work, Dr. Glaser focuses her clinical research in endometrial cancer diagnosis, treatment, and outcomes as well as quality improvement of surgical care using enhanced recovery after surgery techniques. She also serves as the Vice Chair and Practice Chair for Obstetrics and Gynecology and has a special interested in patient and physician wellness. Highlights: • The aim of our study was to evaluate the prognostic value of SLNs-isolated tumor cells in patients with low-risk endometrial cancer who underwent SLN biopsy and did not receive adjuvant therapy. Outcomes were compared with node negative patients. • Our study shows that recurrence free survival among patients with low-risk endometrial cancer and no adjuvant treatment was significantly worse in patients with SLNs–isolated tumor cells compared with negative nodes. However, we did not observe any significant difference in overall survival. • The presence of SLNs-isolated tumor cells, lymphovascular space invasion, and International Federation of Obstetrics and Gynecology (FIGO) grade 2 were significant risk factors for recurrence (any recurrence and non-vaginal recurrence). • Our group has designed a prospective multicenter cohort study called ENDO-ITC with the aim of definitively establishing the prognostic role of ITC in an otherwise low-risk population who undergo SLN biopsy. In addition, we will evaluate a standardized follow-up plan for these patients.
Dr. Shannon Westin and her guests, Dr. Judy Garber and Dr. Geoffrey Oxnard, discuss the paper "Germline EGFR Mutations and Familial Lung Cancer" recently published in the JCO. TRANCRIPT The guest on this podcast episode has no disclosures to declare. Shannon Westin: Hello, and welcome to JCO After Hours, the podcast where we get in-depth on articles that are published in the Journal of Clinical Oncology. I am your host, Shannon Westin, Social Media Editor for the JCO and Gynecologic Oncologist by trade. And it is my great pleasure to speak today with you about an amazing manuscript entitled, “Germline EGFR Mutations and Familial Lung Cancer.” It was published in the JCO on August 14, 2023. The authors have no conflicts of interest, and they are Dr. Geoffrey Oxnard, he's a Thoracic Oncologist and Associate Professor, Hematology and Medical Oncology at Boston Medical Center. Welcome, Geoff. Dr. Geoffrey Oxnard: Hi, Shannon. Thanks. Shannon Westin: And Dr. Judy Garber, the chief of the Division of Cancer Genetics and prevention at the Dana-Farber Cancer institute in Boston. Welcome, Judy. Dr. Judy Garber: Thank you. Hi, Shannon. Hi, Geoff. Shannon Westin: So excited you both could be here. Let's get started. So first I just want to levelset for our audience. Can you speak just a little briefly about the incidence and mortality of lung cancer and how that's been changing over time? Dr. Geoffrey Oxnard: Sure. Lung cancer is common and it's deadly, more than 200,000 cases a year in the United States, more than 100,000 deaths a year in the United States. But I think importantly, it's evolving. Its biology is evolving as smoking incidence goes down. We've identified these genomic subtypes of lung cancer that are sort of increasingly apparent and important as we think about its treatment. Outcomes are changing with emerging therapies, presentation is changing with lung cancer screening and with a growing ability to now find cancers early and prevent them. And so it's in that setting of a very dynamic disease that we chose to study a really unique little slice of it, which is germline risk. Shannon Westin: So let's take that one step further because I think that's really interesting. You mentioned the genomic aberrations and kind of how you're using that to target. Can you expand upon that a little bit more for me? Dr. Geoffrey Oxnard: Lung cancer that I've long studied is different than breast cancer when Judy has long studied because we think about its somatic alterations, we've always thought about KRAS mutations, EGFR mutations, and smaller and smaller splice limit. ALK, RAS, RET HER2, etc. And so tumor testing in lung cancer has one of the first to be standard across on solid tumor oncology. And the germline genetics was kind of an afterthought and is the flip, I think, of how genetic testing evolved in the breast cancer space for example. Dr. Judy Garber: I might argue a little bit if breast cancer was earlier and it was subtyped some molecularly it doesn't have as many molecular subtypes yet perhaps as lung cancer. But we've all been studying the somatic space to look for targets for therapy. And the germline space, certainly in breast cancer, came much earlier. And everybody knows about BRCA1 and 2. Now, we hope everybody knows about Lynch Syndrome, but certainly not everybody's thinking about inherited lung cancer risk. Dr. Geoffrey Oxnard: Yeah, these have converged. I think 10 years ago when this kicked off, I felt like a super outlier for thinking about, wait a second, what about the genetics behind all this that is leading to this strange variable presentation of lung cancer? For example, we know that in Asian populations, one type of lung cancer, EGFR mutant lung cancer, is more common. There must be some geneticness that leads to that. What explains the sort of pattern of presentation of these genetic subtypes in the populations we see in the US, that's pretty unclear? Dr. Judy Garber: So, I think, Shannon one of the clues about all this came from the fact that the EGFR mutations were being identified in the tumors. And then I really should let Geoff tell this story, but as the amateur thoracic person in the room here, to me, it was so interesting that there were the EGFR mutations, then there was treatment exploiting EGFR mutations, and the most common resistance mutation was this T790M variant. But when labs started testing EGFR, there was a small group of people who had that resistance variant without ever having been treated at all. So that was the obvious question, what was it doing there? And that's where Geoffrey came in. Dr. Geoffrey Oxnard: Yeah, this is a patient I met more than a decade ago at my fellowship in MSKCC. She'd been living with a T790M mutation in her tumor for years and years and years. I was like, “Well, I don't understand. Why is this sitting there?” And she had this sort of slightly mysterious history of lung cancer in her family. And we realized, wait a second, this T790M was behind her cancer from the beginning, and in fact, might have been the basis of why she developed lung cancer. And so that actually motivated a career development award I submitted to the Conquer Cancer Foundation of ASCO, a grant I received, and that then led to a program that I led at Dana-Farber under Judy's mentorship, where over the past decade, we sort of focused in and studied this strange, rare syndrome, really to dig into inheritedness as a kind of different flavor of lung cancer genetics. Dr. Judy Garber: Well, and now it's really a good time to think about this because we're recognizing there are younger cancers, colon cancer, like an epidemic, and lung cancers, and we're not sure how many of them are genetic or come from other exposures. Geoff talked about the differences in Asia, some of which are certainly genetic, some which may be environmental, especially in the lung, where that's such an issue. But trying to sort these things out, you have to be willing to think a little bit differently. And that was fun when Geoff came from the lung program, interested in the germline, we said, “Oh, we have to do this.” Shannon Westin: Well, let's talk about what you did. I would love to hear and I know the audience would as well about the design of this study, so called INHERIT study. Very good name. I love a good name. This is a good one. Dr. Geoffrey Oxnard: Yeah. So that stands for Investigating Hereditary Risk of T790M, INHERIT. I forget where we coined that. Let me give you a case example. A patient presents in his 40s. I remember this man. He has an EGFR mutation in his tumor. He has a T790M in his tumor as well. He had routine tumor testing that lung cancer patients were getting. And he says, “Oh, also, my brother had lung cancer in his 40s just a couple of years ago. He was a smoker, though. He never had genetic testing.” And so this patient we test on the study, we hypothesized that when patients present with T790M at diagnosis, that it would be a representation of an underlying germline EGFR mutation. Our hypothesis was that about 50% of the time T790M at diagnosis would be explained by a germline behind the doll. And that that could then empower families like this one to understand the kinds of lung cancer they're getting in their family, the kinds of treatment they should be getting, and the kinds of testing they should be getting to look for lung cancer at risk early on. It really saddens me that in a family that doesn't know about this condition, the brother would never get testing and would never think that I might be getting or might never get testing, might not be disposed to getting testing, and might not realize there's a therapy available to target that EGFR mutation if he died young without even much treatment. But this individual, we tested his lung cancer, we found him a therapy, we put him on a pill therapy that could last a very long time. And so we set up a program with a consortium alchemy, the Addario Lung Cancer Medical Institute, where we enrolled at three sites, both at Dana-Farber in Boston, Vanderbilt, and Ohio State, with some motivated investigators there that we appreciate their collaboration. But also, again, this is now more than 10 years ago, set up shop where people could enroll remotely, that if you found a T790M in your tumor, for whatever reason, you could reach out to the team at Dana-Farber centrally and get consented online and even get counseling. And this is one of the early ways of getting this remote participation. And you can imagine, over the course of the study, we quickly ran out of individuals at any given site, but that remote enrollment accelerated and really allowed us to get to the large population of remote study. Dr. Judy Garber: We were lucky that things were happening. The things you don't expect. So EGFR testing was not routine at that time. And the EGFR testing that had developed in Dana-Farber and NGH became standard of care at Dana-Farber so we were finding those patients, and then grew outside as well, at institutions and testing labs. And these people would somehow emerge so we were very lucky that we were able to set up remote testing. We could send and get a saliva sample and be able to test. Or these were people who got tested through their own doctors, found out they had this mutation and then went online and said, “Who knows anything about this?” I would say that we and our amazing genetic counselors who spoke to all these patients, took their detailed family histories, got their other information, and were able then to really build out these cohorts so we can understand them. And to look at, for example, Geoff's question, it was really his question, “Why did we have such clusters in certain parts of the country? Could it be that there were the so-called founder mutations that somebody had this mutation and they spread their genes around so that they're around the country and that turned out to be true. Shannon Westin: It's so fascinating, and I love how you kind of almost crowdsourced getting these patients to you because I was mystified because it's such a rare aberration and you had so many patients. Let's talk a little bit maybe about your patient population and who volunteered, and is it reflective of kind of you do think, the general population? Dr. Geoffrey Oxnard: I want to give a shout out to the GO2 Lung Cancer Foundation. That really was a lot of the ‘rah rah', getting people to know about this, having some word of mouth and spreading the word. And so certainly there are physicians around the country that have been like found patients that I've got to know because they sent us patients to study over the years. We ended up getting germline testing on 141 individuals who presented eligible for testing because of either a relative or a mutation that was suspicious for inherited. Most of those were enrolled remotely, in the end, as you might expect. We found what you might expect, that this was Mendelian in its inheritance, that if you had a first degree relatives, they had 50% chance of having this. And so we sort of slowly built these pedigrees of individuals who once they were positive, would refer in their relatives and say, “Please go get testing. Let's describe our family and help understand our risk.” It ended up boiling down to six individuals with a germline EGFR mutation from 39 different families. I remember one family where two different cousins presented separately to the program, not knowing each other was participating. And so, of course, there's not that many of these families around the United states, but we're really very lucky to have touched so many different individuals. What did we find? That if you had a germline EGFR mutation, your tumor almost always had an EGFR mutation. That really is the dominant biology of lung cancer that presents in these affected individuals, that it presents young, that the likelihood of developing lung cancer is around 55% by age 40 to 50. So it really is– I'm trying to make sure I'm quoting that right, actually, Shannon, I'm looking at the numbers here, but it was a really broad range of diagnosis. We had a 28-year-old who was affected and an 83-year-old who was affected. I saw a family where the grandson had lung cancer, but his father and grandfather who had germline EGFR mutations, did not. So variable penetrance. Judy, of course, told me, “Geoff, this is the way families present. Come on, Geoff.” But other families, incredible penetrance– not everyone having lung cancer, many of them smoking, some of them not smoking. But for these families, what a sense of empowerment to say, “Oh, this helps explain what's going on in our family, why this is happening at a younger age.” And helps explain the therapies that we had some concern about giving these potent EGFR inhibitors originally, understanding every cell in their body has this EGFR mutation. Are we going to somehow cause toxicity? No. These potent therapies can be effective, can be tolerated, and can work for many years. So we really feel hopeful that we've described a syndrome that's out there that people see and that has a distinct presentation, a distinct treatment pattern, and a clear association with lung cancer risk. Dr. Judy Garber: And I think that now the opportunity is to say, can you find these people before they get their lung cancers? Some of them have abnormalities on scans. Think of it's like the APC, the polyposis coli of lung cancer. You can see these adenomas forming, but we can't really predict exactly who's going to develop tumor when. And that, I think, is a challenge that families have to help us with because we need to continue to identify some of these people who have not had cancer. They have children. They want to know what to tell them besides not smoking adamantly and maybe with some hopes that we're going to do some screening. I am afraid there probably is not good data that EGFR inhibitors could be used for prevention, but it's tempting to think that way. So there's plenty of work to do still to sort out the questions. This is the nature of genetics. We often find inherited susceptibility and people want to know, “Well, why would I want to know? What am I going to do about it?” And here I would say, “We're going to figure out what's your risk more specifically, and how can we help reduce that risk, in addition to telling you not to smoke.” Dr. Geoffrey Oxnard: I do want to allude to Judy's comment about founder effect. I didn't tell you exactly about the presentation, but these families, first off, we only found germline EGFR mutations in Caucasian individuals and in black individuals, and it was mostly in the United States and in fact, enriched in the southeast United States. And don't get me wrong, we had enthusiastic participation from Vanderbilt. But still it seemed like there was more southeast United States prevalence. And even families I met in the Boston area would say, ‘Oh yeah, I have relatives going back to Arkansas.” And so we ended up with a bit of a suspicion for this geographic enrichment, studying the genomes of these affected individuals, and in fact did find a very large region of chromosome 7 that was shared in more than 90% of the folks we tested, suggesting a founder effect in the southeast United States, probably white and black. And that goes back hundreds of years, maybe 200, 300, 400 years, as far as we can estimate, making me think that this is a fairly unique syndrome that we're seeing in North America, but actually may not be prevalent in other parts of the globe. Though we did identify a single individual in Australia, it might be a unique phenomenon in North America. Dr. Judy Garber: At least more common. But these days, people travel, so hard to know. Shannon Westin: I don't know if you've gotten a chance to do this - any other cancer type seeming to be associated with this mutation? Dr. Judy Garber: No, fortunately not. Shannon Westin: Okay, very interesting. And what about outcome? What was the association, or was there any association of these mutations with cancer related outcomes? Dr. Geoffrey Oxnard: I would say the survival of these cancers isn't that different than EGFR mutant lung cancers. If they get to effective therapy, they can live for years on therapy. If they don't, they can do quite poorly. One interesting finding is that they can present in a multinodular fashion that might be multiple primaries. And so you can kind of use an approach of eliminating individual clones. Sometimes it's been described these different tumors have different mutations, and so you might treat them like a stage IV lung cancer, but actually they lived for a long time because actually they had multiple stage I lung cancers, so it can present a little bit differently. And then we tried to collect CT scans on affected carriers who did not yet have lung cancer to see if they might develop lung cancer. It was not required on study, and it's sort of an area of future investigation. But as you can imagine, lots of lung nodules and certainly anecdotes of individuals where we found early precancers through the screening effort, motivating the investigation that Judy was alluding to. Dr. Judy Garber: I think this is what you expect in inherited predisposition that you have an earlier chance. So some of them are younger, not the 84-year-old, but that they could be younger, that they could have multifocal disease, that their biology could be different, but could be the same, maybe accelerated, maybe not. Some of these are slower. And I think that's why we're excited to be able to continue this work with the group at Dana-Farber. Now, Jaclyn LoPiccolo is going to lead the INHERIT study, but much of the team is the same. And now the focus will be even more on trying to really quantify the risk and help think about prevention strategies and screening for these patients. It's a little tricky to want to do too much chest CT screening. On the other hand, there are lower dose CTs now, and we hope the guidelines will clarify the role of inherited risk. At ASCO this year there were a lot of talks about inherited lung cancer risk, but nothing is quite as well characterized as, I think, the T790M population. Shannon Westin: Well, thank you all so much. This was fascinating. I learned a ton and I know our listeners did as well. And thank you to our listeners. This was “Germline EGFR Mutations and Familial Lung Cancer.” Again, published in the JCO August 14, 2023. So go check it out and check out our other podcasts on the website or wherever you get your podcasts. Have an awesome day. 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. Guest statements on the 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.
In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Drs. Rene Pareja, David Viveros-Carreño, and Beatriz Navarro Santana to discuss HIPEC complications. Dr. Viveros-Carreño is a Gynecologic Oncologist at Instituto Nacional de Cancerología, Centro de Tratamiento e Investigación sobre Cáncer Luis Carlos Sarmiento Angulo (CTIC), and Clínica Universitaria Colombia in Bogotá, Colombia. Dr. Pareja is a gynecologist-oncologist at Astorga Oncology Clinic in Medellín and the National Cancer Institute in Bogotá, Colombia. Dr. Pareja is a reviewer for more than 20 specialty journals, and one of the Associate Editors for IJGC. He is the author of ten book chapters and more than 90 publications in peer-reviewed journals, and at IGCS 2021 he received an award for Community Advancement in Resource-Limited Settings. Dr. Navarro is a gynecologist-oncologist at Insular University hospital in Las Palmas, Spain. She also completed the ESGO fellowship at Institut Bergonie in France Highlights: The study aimed to assess the complications associated with HIPEC in cytoreductive surgery for epithelial ovarian cancer, examining two distinct time periods (2004–2013 and 2014–2022). This systematic review analyzed 69 studies and including 4928 patients with advanced primary or recurrent epithelial ovarian cancer. No significant differences were observed in complication rates between the two time periods. Overall, complications, including blood transfusions, gastrointestinal, infectious, respiratory, urinary complications, and thromboembolic events, showed no significant change. Rates of ICU admissions, reoperations, and deaths also remained consistent over time. The study concluded that the overall complications associated with HIPEC in ovarian cancer surgery did not decrease, and there was no reduction in the rates of ICU admissions, reoperations, or deaths.
In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Dr. Nicolò Bizzarri to discuss the SCCAN study. Dr. Bizzarri is a former IJGC Editorial Fellow under the mentorship of Prof. Pedro Ramirez. He is a Gynecologic Oncologist at Policlinico Agostino Gemelli in Rome, president of the European Network of Young Gynecologic Oncologists (ENYGO), and he happily serves on the IJGC Editorial Board. Highlights: International guidelines recommend tailoring the radicality of hysterectomy according to the known pre-operative tumor characteristics in patients with early-stage cervical cancer. However, the survival benefit associated with the extent of radical hysterectomy is still a matter of debate. Non-nerve-sparing radical hysterectomy was associated with improved 5-year disease-free survival compared to nerve sparing radical hysterectomy and represented an independent protective factor for risk of recurrence. Non-nerve sparing radical hysterectomy was associated with better 5-year disease-free survival in patients with tumors between 21-40 mm. In patients with early-stage cervical cancer, the extent of radical hysterectomy was associated with disease-free survival improvement in patients with tumors between 21-40 mm but not in patients with tumors ≤20 mm.
In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Dr. Brian Slomovitz to discuss hormonal therapy in advanced or recurrent endometrial cancer. Dr. Slomovitz is a Gynecologic Oncologist at Mount Sinai Medical Center in Miami Beach, Florida, and Professor of Obstetrics and Gynecology at the Wertheim College of Medicine at Florida International University. He is an internationally recognized leader in gynecologic oncology clinical trials, specifically in immunotherapy and novel biomarker therapeutics. He also is a leader in sentinel lymph node detection for gynecologic malignancies. Highlights: While current recommendations include chemotherapy as first-line treatment for metastatic or recurrent endometrial cancer, emerging evidence suggests that hormonal therapy, particularly in combination with other treatment regimens guided by biomarkers, could be efficacious in selected subtypes (low-grade endometrioid carcinoma of the endometrium). Hormonal therapy offers many benefits, including oral dosing and fewer side effects. If there is progression after hormonal therapy, patients would still be eligible for other trials, and use of hormonal therapy does not preclude the use or limit the benefits of future chemotherapy.
In this "Podcast Takeover," Dr. Lidia Schapira guest hosts to discuss with Dr. Shannon Westin her own JCO paper, which reports on the DUO-E Trial. Dr. Ramez Eskander also joins in this lively discussion. TRANSCRIPT The guest on this podcast episode has no disclosures to declare. Dr. Shannon Westin: Hello, everyone, and welcome to another episode of JCO After Hours, the podcast where we get in depth on manuscripts published in the Journal of Clinical Oncology. I am your host, Shannon Westin, Social Media Editor of the JCO and Gynecologic Oncologist by trade. And actually, I'm super excited today because we are going to have a podcast takeover because we are discussing my own work, which was simultaneously presented at the European Society of Medical Oncology 2023 Congress and published in the Journal of Clinical Oncology on October 21st, 2023. And this was the DUO-E trial, “Durvalumab Plus Carboplatin/Paclitaxel Followed by Maintenance Durvalumab With or Without Olaparib as First-Line Treatment for Advanced Endometrial Cancer.” Because we're discussing this work and we wanted you to have an unbiased podcast discussion, Dr. Lidia Schapira, who is a Professor of Medical Oncology at Stanford University and an Associate Editor of JCO and the Art of Oncology podcast host, is going to take over this podcast and really just pepper me with questions about this exciting work. Welcome, Dr. Schapira. Dr. Lidia Schapira: Thank you so much. It's such a pleasure to be with you. Dr. Shannon Westin: And before I turn over the reins, I also want to introduce one of my colleagues, who's going to be providing quite a bit of insight on this topic, Dr. Ramez Eskander, who is Professor of Obstetrics, Gynecology, and Reproductive Sciences at the University of California, San Diego. And you will know he's the principal investigator of the GY-018 study, which established pembrolizumab and chemotherapy as the new standard of care in endometrial cancer. Welcome, Ramez. Dr. Ramez Eskander: Thank you. Thank you, Dr. Westin. It's a pleasure to be here. And congratulations again to you and your study team for this exceptional work. Dr. Shannon Westin: Thank you. And congratulations to you. Dr. Schapira, thank you for being here and please do take it away. Dr. Lidia Schapira: So let's start by having you tell us a little bit about the standard of care for women with endometrial cancer and advanced endometrial cancer prior to this study. Ramez, I'm going to direct this question to you first. Dr. Ramez Eskander: For many years, actually since about 2012, carboplatin and paclitaxel, which ironically is a chemotherapy backbone really across all of our gynecologic tumors, emerged as the preferred doublet chemotherapy regimen for the management of advanced-stage metastatic or recurrent endometrial cancer. It evolved through a series of different clinical trials, in fact taking us from whole abdominal radiation, systemic chemotherapy, comparing single agents to doublets and then triplet regimen of TAP to carboplatin and paclitaxel, which ultimately, then, following the presentation of GOG Protocol 209 and its publication, as the chemotherapy backbone, being carboplatin and paclitaxel. And it's been that way for many, many years. Dr. Lidia Schapira: And how effective is the regimen? Dr. Ramez Eskander: The response rates to carboplatin and paclitaxel are actually quite reasonable in the patients who have advanced-stage disease, particularly if they haven't had prior systemic chemotherapy. Response rates in the 50% to 60% range. The issue is that the responses tend to be limited and disease recurrence is an expectation in these patients who have advanced-stage disease. And so that really highlighted the importance of trying to continue to advance therapeutic opportunities in these patients to improve long-term outcomes. Dr. Lidia Schapira: As we think about improved long-term outcomes, we're thinking about a better treatment and also a kinder treatment, perhaps one that is also less toxic. Can you talk a little bit about the population of women with endometrial cancer? Are these older women? Do they have comorbidities? Dr. Ramez Eskander: What we're seeing is, interestingly, there has been an evolution a bit in this space. Historically, we used to think about endometrial cancer as—the phrases we used to use are type I and type II. These type I tumors, we would say, are estrogen-driven malignancies; they tend to be seen in overweight or obese patients. And we would identify them in a theoretically younger patient population. And then we had these type II, or what we termed estrogen-independent malignancies, that we would see in an older patient population. Of course, with obesity came metabolic syndrome and other cardiovascular comorbidities, etc. But really, that narrative has evolved dramatically, and that's really something that will be highlighted in, I think, our discussion of these studies today, where the nomenclature that we used to historically use has evolved because of our understanding of the molecular characterization of this disease. So we've really gone away from that, and now we understand that we're seeing all of these different heterogeneous endometrial cancer types amongst patients of different ages, different comorbidities, different races and ethnicities. And so it's created a more complex picture for us. But certainly, there are comorbidities that these patients face, and that's important as we look to identify treatments strategies that are both effective and tolerable. Dr. Lidia Schapira: My final question before we jump into this very exciting study is about the Cancer Genome Atlas work. Can you tell us how that's changed the thinking and the design of the studies? Dr. Ramez Eskander: It was a seminal publication, really, back in 2012/2013 looking at an assessment of endometrial cancers to try and determine whether or not all of these "endometrial cancers" that we used to enroll on a single study are similar or divergent. And it's important because the study I referenced that really established the standard of care, GOG Protocol 209, as carboplatin and paclitaxel, there was no real consideration of molecular characterization at all. We enrolled all patients onto this study without thinking about these variables, of course, because it was designed, conducted, and completed before the TCGA data emerged. But what we learned from the TCGA is there appeared to be four distinct molecular subgroups. There were the POLE-mutated patient population. There was the mismatch repair deficient or MSI-high endometrial cancer population. There was the copy number-high or what we say are the p53-mutated. And then the last cohort was called the NSMP (no specific molecular profile). But now, that's even evolved; some people term it TP53 wild type. That's a bit of even a heterogeneous cohort amongst itself. So we're going to take these subsets, independent of POLE and an MSI-high, and we're going to look at TP53 or copy number-high, and that will probably be divvied out further, and the NSMP, and that will probably be subdivided. But really, it gave us these four components, which has then evolved. Many of you may have heard of the ProMisE algorithm or ProMisE Plus, which looked to take the data from TCGA so that we can start to really look at it in clinical practice. So it's really revolutionized how we think about these patients, how we think about the disease, and how we design trials. Dr. Shannon Westin: And I just want to add to that because I think that it's so important, what Ramez said about the way we were developing trials, the way we were designing trials. We knew that these classifiers—we were learning these classifiers are prognostic. Now what we're really trying to hone in on is how predictive they are. And certainly, one of the major classifiers that we're going to talking about today is mismatch repair status, and that is most definitely predictive of response to therapies. But we're still learning about the other classifiers and how we might adjust the way we treat people, even deescalating care for certain patients. That is still being proven in clinical trials, although we suspect that it's going to be borne out as other clinical trials report. Dr. Lidia Schapira: It's a perfect segue to this current trial. Tell us a little bit about the objectives and the design of DUO-E. Dr. Shannon Westin: As Ramez said, the standard of care was chemotherapy. And so we wanted to see if there was a way to improve outcomes for these women with advanced and recurrent endometrial cancer in a really clinically relevant, meaningful fashion for patients. And so we knew that this TCGA classifier, the mismatch repair, was so important, and we thought that the addition of immunotherapy to chemotherapy would most certainly work in that population but could even work in the entire population because, generally, endometrial cancer seems to be a little bit more responsive to immunotherapy and to activation of the immune system than, say, some of our other gynecologic malignancies. And so we set out to see what the addition of durvalumab, which is a PDL-1 inhibitor, would add to chemotherapy. And this was two chemo as well as followed by durvalumab maintenance. But even further, we had some really kind of exciting science data from our lab that said that if we combined a PARP inhibitor with immunotherapy that we could accentuate on the response to therapy and we could get more benefit. And there's kind of a lot behind that, but essentially, what we thought was that the damage that's caused by the PARP inhibitors would create an activation of different immuno-pathways, like STING pathway and activating cytokine release, and that we would get this synergistic activity. So one of the other objectives was to see if the addition of the olaparib, the PARP inhibitor, to durvalumab in that maintenance setting could even further improve benefit. So we had a dual primary endpoint looking at progression-free survival, so the amount of time people live without their cancer coming back. And that endpoint was first, the durvalumab-alone arm to control, and then the second portion of that was the durvalumab/olaparib arm back to control. Dr. Lidia Schapira: So before you tell us about the results, tell us a little bit about the study itself. I mean, I was very impressed that you did it in so many different locations. Tell us about that effort. Dr. Shannon Westin: This was a huge collaborative effort both with the GOG Foundation, the Gynecologic Oncology Group Foundation, as well as ENGOT, which is our European colleagues that do amazing clinical trials. But in addition to that, we really worked very closely with our industry partner to really make sure we spanned the globe. And so we had groups from all over the world that participated and really were exceptional. The care that was taken and the hard work that went into this type of study across the world really can't be overstated. We were very lucky to have a wonderful infrastructure group. We met weekly for a long time, just keeping an eye on the data and making sure that everything was as positive as possible and, of course, that we were watching the outcomes of the patients very closely and making sure that there was no evidence of harm or issue. And so it really did take a village, truly, to run this study and to ensure that at the end of it, we got really great data that we can trust. Dr. Lidia Schapira: So tell us the results. Dr. Shannon Westin: So DUO-E was positive for both of its primary endpoints, which was very thrilling. So for the first analysis, which is the durva-alone arm to control, we saw a reduction in the risk of progression of 29%, so a hazard ratio of 0.71. And then the addition of olaparib seemed to further enhance this benefit, so a 45% reduction in the risk of progression for a hazard ratio of 0.55. But what's really exciting is our follow-up time was pretty long; it was about 17 months, so we were able to look at a couple of different analyses, including an 18-month landmark analysis where we saw approximately 50% of the patients were still alive progression free at 18 months, as compared to only 21% of patients being alive progression free in the control arm. So there was a doubling in that progression-free survival time point at 18 months, which is thrilling. Dr. Lidia Schapira: So Ramez, as an expert in the field, what was your reaction when you read or heard these results? Dr. Ramez Eskander: It's exciting, honestly. So we have gone a long time without seeing really significant successes in the endometrial cancer space, a testament to the fact that we hadn't yet developed our understanding of how we could move this needle forward. But Dr. Westin and the DUO-E team conducted an exceptional clinical trial, as you mentioned, international study, rational and important hypothesis to adjudicate. And what we saw here was both now we had other studies—the RUBY trial, the GY018 trial, the AtTEnd—and now here DUO-E, which added this hypothesis of PARP maintenance in addition to checkpoint to try to augment response and consistent, really provocative data, exciting, in line with what we've seen and hopefully will continue to drive the science in this space, most importantly. Dr. Lidia Schapira: So let me ask you a follow-up question to that. What kind of scientific questions are in the air now as a result of this trial and what the trial found? Dr. Ramez Eskander: Oh, goodness. Shannon and I could both take this, I'm sure. But I think in the dMMR population, we recognize that there's a ton of data that is supportive of the fact that these tumors are immune responsive, particularly in dMMR endometrial cancer, whether it's an epigenetic promoter hypermethylation, or a mismatch repair gene mutation. I think the data has emerged that immunotherapy is here to stay for these patients in the newly diagnosed advanced stage, even chemo naïve, who need adjuvant therapy. The pMMR population, this is where we're seeing more and more questions emerge because we realize that that may be a cohort of different cancers. And I'll let Shannon speak to this briefly, but even the incorporation of the PARP inhibitor, in addition to the checkpoint, there's a biologic rationale for combining those two together to augment response. And to see the benefit in that trial—arm three and arm two, we can look at descriptively and look at the differences, but who are those patients? Where is the PARP and the checkpoint most effective? How do we expand that to a larger population of patients potentially? These are questions that emerged because, as Dr. Weston will allude to, I know we also talk about HRR mutations, which are captured, but we even have a lot to understand about that in endometrial cancer, where we've had more research in the ovarian cancer space. Dr. Shannon Westin: Being mindful of time, because I have, like, 1,000 hypotheses that have been generated by this study, which, I think, shows it's a great study, right? Because you get some answers, and as our colleague Brad Monk says, “The only definitive study is the negative studies.” This most certainly was not that. But just kind of expanding on what Ramez said, the interesting thing about DUO-E is that really the biggest benefit for the combination of the durvalumab and olaparib was in that mismatch repair proficient group. And I personally thought that we were going to see accentuation of the impact in the mismatch repair deficient group based on the science, but that just wasn't borne out by the data. It doesn't seem that the combination has that much to add in that mismatch repair deficient group. And when we tease out the mismatch repair proficient group, I think that's where a lot of interesting information is going to come because, to Ramez's point, we're going to tease out: Is it driven by the P53-mutant population? Is it driven by the population that has homologous recombination deficiency? How do we even measure homologous recombination deficiency in endometrial cancer? So I'm super excited about what we found and how that may help us to make those decisions for the patient in front of us. The other thing I think needs to be made mention of—and this was something we saw in DUO-E as well as AtTEnd—we had a large population of patients that were recruited in Asia, 30%. Interestingly, when we look at the forest plot, that group doesn't seem to benefit as much from the addition of the olaparib. So we really need to tease out what's different about that population because what Nicoletta Colombo presented around AtTEnd, it looked like they didn't benefit from the atezolizumab either in that study. So there's clearly something different about that population, and we have a really big opportunity to look at that since we had such a large proportion of patients that were enrolled there. So that's another, I think, really intriguing question. Dr. Lidia Schapira: So how does this fit in the context of endometrial cancer treatment, and what are we going to do with patients in the clinic? I'd love to hear both of your perspectives, starting with you, Ramez. Dr. Ramez Eskander: It's an evolving answer, to say the least. What we can say definitively is that we have a United States FDA approval for the regimen of dostarlimab plus carboplatin and paclitaxel in the mismatch repair deficient, advanced-stage/recurrent or metastatic patient cohort. And again, that's because the magnitude of benefit that we saw in the RUBY trial, which looked at that, was actually analogous to what we saw in 018, AtTEnd, and DUO-E, again, consistently highlighting the benefit of the IO and the dMMR. We have yet to see how this is going to evolve the landscape in the larger patient population, which is the pMMR patient population. And it may be that based on the data that we have, we will see immunotherapy plus carboplatin and paclitaxel as the new standard of care in the pMMR cohort, or it may not. That's yet to be defined. And I think Dr. Westin will add to this, but I think that's also going to depend on the perception of how we view the cohort. Is it one group of patients? Are we going to have to think about subsets within the pMMR population? That is an active conversation. Dr. Shannon Westin: I would just add, having treated patients on this combo regimen with the durvalumab and olaparib, I have multiple patients that still remain on study, and this—we're looking at three and four years out. I just never saw anything like that before with standard chemotherapy, so there's definitely something here. So I want to know who those patients are, who benefits really the best from the combination, and who could we just give the immunotherapy to and get that same benefit. So we obviously always want people to live as long as possible. That's the bottom line. But we don't want to overtreat. And so I think balancing that is really important. Dr. Ramez Eskander: The point that was made earlier: We have yet, aside from MMR response to checkpoint, within the pMMR population, we understand that there may be subsets, but we have yet to prospectively validate that these molecular cohorts within the pMMR population are truly defining response to a particular therapeutic strategy. So we have to be cautious not to limit the treatment opportunities for these patients without having the data that we need to do so because, as Dr. Westin mentioned, for us—whether it was the Gy018 trial, the RUBY, the DUO-E trial—what we saw is there are pMMR patients who have a dramatic response even though they are “biomarker negative.” They're pMMR, they're TMB low, they're not POLE mutated, but yet they still derive a dramatic benefit. And so that goes back to the hypothesis about why we're even combining checkpoint with chemotherapy in which, for example, in lung cancer, there's been established success and approval. So I think we're all eager to see these strategies emerge as treatment opportunities for the pMMR patients as we work to still develop additional effective opportunities. Dr. Lidia Schapira: So, based on all of this and sort of the new twists on the scientific hypotheses that are now generated, what are the next steps? Dr. Shannon Westin: Well, I think we have to see if these drugs are available for patients. So looking at things like compendium listing and regulatory approvals obviously is going to be very important. But from the things that I can control, we are looking at the different molecular subtypes and understanding the different mutation status and trying to tease out who may be driving the biggest benefits so that we can help advise and make sure that we're doing the right thing for the patients. Dr. Lidia Schapira: And wearing my supportive care hat, I have to ask you, Shannon, about the tolerability. We often find that the quality of life and studies come out after, sometimes months or years after, the original trials are published. So let me take this opportunity to ask you now: How did women tolerate these drugs? Dr. Shannon Westin: The bottom line, Lidia, is, as expected, when you add additional drugs, you see additional side-effects. I think the good thing is that we're very comfortable with immunotherapy and we're very comfortable with PARP inhibition in gynecology because we have had access to these agents and so we know how to manage the toxicities. And so, from a standpoint of incidence, there was a higher incidence of grade three and higher adverse events in the group that had durvalumab/olaparib. But this was primarily driven by anemia, which is as expected and is usually pretty time-limited at the start of olaparib. From a long-term standpoint, there was a slightly higher proportion of patients that discontinued therapy, but it actually wasn't as much as I was worried about. So we saw a 19% discontinuation rate in the group that was just the control arm, and that went up to 24% in the dual arm, so definitely higher, but not that much higher. And when we moved to maintenance, which is really where—that's where the arm becomes unique, it was much lower at about 12%. And so that's exciting to me, that patients were able to stay on a drug and were able to tolerate it. And then, to your other point, we do have a very nice patient-reported outcomes plan, and that is actually being analyzed as we speak with the hope of presenting it at the next major meeting, our Society of GYN Oncology meeting in March. So not right away, but I think in a pretty timely fashion, we'll have those data. Dr. Lidia Schapira: Congratulations, Shannon, on leading and presenting this wonderful study. So it's been a real pleasure to chat with the two of you. Dr. Ramez Eskander: Thank you. Dr. Shannon Westin: Thanks so much, Lidia. I really appreciate it. Thanks, Ramez, for being here. And I will just say thank you to all of our listeners. We really hope you enjoyed this episode of JCO After Hours, where we discussed the DUO-E trial, which is a phase III trial evaluating durvalumab plus carboplatin/paclitaxel followed by maintenance durvalumab with or without olaparib as first-line treatment for advanced endometrial cancer. And again, please do enjoy this publication that was online at the Journal of Clinical Oncology on October 21st, 2023. And do check out our other podcast offerings wherever you get your podcasts. Have a wonderful day. 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. Guest statements on the 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.
Shannon Westin speaks with Holly Prigerson and Alfred Neugut about their thought-provoking editorial, "You Get (Offered) What You (Can) Pay For: Explaining Disparities in End-of-Life Cancer Care." TRANSCRIPT The guest on this podcast episode has no disclosures to declare. Dr. Shannon Westin: Hello, everyone, and welcome to another episode of the JCO After Hours podcast. And this is where we get in-depth on manuscripts and editorials that have been published in the Journal of Clinical Oncology. As always, I am your host, Shannon Westin, Gynecologic Oncologist and Social Media Editor for the Journal of Clinical Oncology, and I'm so excited to be here today. We are going to be talking about a very compelling editorial that is called “You Get (offered) What You (can) Pay for: Explaining Disparities in End-of-Life Cancer Care." And this was published on June 20th, 2023, in the Journal of Clinical Oncology as an editorial on an article entitled the "End-of-Life Systemic Oncologic Treatment in the Immunotherapy Era: The Role of Race, Insurance, and Practice Setting." So a very timely topic and very exciting for us to discuss today. I'm joined by two of the authors of the editorial, Dr. Holly Prigerson, Professor of Sociology and Medicine, the Irving Sherwood Wright Professor in Geriatrics Medicine at the Weill Cornell Medical College and the Director of Cornell Center for Research on End-of-Life Care. Welcome, Dr. Prigerson. Dr. Holly Prigerson: Great to be here. Dr. Shannon Westin: And also accompanied by Dr. Alfred Neugut, the Myron M. Studner Professor of Cancer Research and Professor of Medicine and Epidemiology at Columbia University and the former Associate Director for Population Science and Racial Disparities Program for the Herbert Irving Comprehensive Cancer Center at Columbia. Welcome, Dr. Neugut. Dr. Alfred Neugut: Thank you very much. Dr. Shannon Westin: Very excited to talk about this topic today, and I like to always start with a little bit of level setting. So I'd love for one of you to discuss: How common is the use of systemic anticancer treatment at the end of life? Dr. Holly Prigerson: So, based on the article, it looks like the rates within the last 30 days of death, it was 34% on average overall. So that was sort of the—you say level setting—the base statistic. Within 14 days of death, it dropped to 13% overall. So all the associations that are described are really disparities from that level. Dr. Neugut: Speaking as an oncologist, I don't think any of my clinical colleagues will be surprised that it's that high. There is an effort made really to, in desperation, try to help. Patients want it. Families want it. So there really is efforts made to try to do that to prolong life or palliate or whatever. Dr. Holly Prigerson: The design also, which is probably going to be a question that's coming up, does raise a question for me that I'm wondering if Al could enlighten at least me on. They did select patients who were getting treatment for metastatic or advanced cancer starting in 2011 and then who died four years later. Does the selection for the fact that they were getting treatment initially—because everyone, that's how they sampled the study—does that increase the likelihood that they'll get treatment later on so that the rates are somewhat inflated is my question. Dr. Alfred Neugut: Yeah, no, for sure. People who start chemo tend to continue partially because there is a certain amount of those who do well do well. If you respond to chemo initially, you tend to respond to the second-line therapy, you tend to respond to third-line therapy. If you didn't do well on first-line chemo, you're not likely to respond to a second line or a third line, so you don't have the enthusiasm to continue with it, and the patient certainly tends to lose interest in it. So you're right; there is a certain, call it, momentum or inertia in going forward with chemo once you've started. Dr. Shannon Westin: I mean, I think this just always highlights some of the issues we have, right, with any kind of retrospective data is how well can we design a population without—because we can't always do randomized control trials, and certainly not in this kind of setting. That would not be acceptable, I think, to providers nor patients. And I do agree that it can be tricky. Any other kind of, maybe just to help the listeners if they haven't gotten a chance to read this Canavan study, about the design, exactly what they were looking at in this population? Dr. Holly Prigerson: Basically, they took these patients who were getting systemic therapy and had advanced metastatic cancer prior, and then who died. So there's always a question about the sampling on death issue, that they had to have died to be in the sample. So those are methodological issues, but there's really very little way around that. If you want to know what treatments people received in the last month of life, they have to die for there to be a last month of life. So then the treatments were divided into chemotherapy alone, chemotherapy with immunotherapy, and then immunotherapy with and without targeted therapy. So there were three types of treatment, which is sort of an important update because Al and I had published something in 2015 on chemotherapy and the outcome of what was called palliative chemotherapy at that time. And this was sort of a very refreshing–well, not—I shouldn't say refreshing, but important update to our study, which had said that there are questionable outcomes of palliating someone with palliative chemotherapy so far along in the disease. And then the question became, well, is it different? Is it different with immunotherapies? Is it different with targeted therapies? And that's why I was delighted to see this paper, because it answered… Dr. Alfred Neugut: I'd have to say there are probably differing views on this, but Holly and I are probably relatively nihilistic in terms of thinking that chemotherapy in late stages or near terminal patients is probably not all that helpful. Third-line, fourth-line therapy probably not going to get you very far. And maybe it's best to be thinking more about hospice care and supportive care. And now we have terrific palliative care programs at most or all cancer centers, and we really should be taking advantage of this. I think a real benchmark study was the Temel study from 2010 or 2011, which really—for those of your listeners who haven't read it or seen it, they should really take a look at it. It really changes the playing field and makes you realize that treatment is not really always the best thing for patients, and there are other options. And we go to hospice care or palliative care really, I think, too late in the game a lot of the time, and we really should be thinking otherwise. Dr. Holly Prigerson: That is one of the outcomes that we had looked at before. So we had looked at palliative chemo, and not only does it not palliate, and we didn't show that it significantly enhanced survival; we also showed that it resulted in a lower likelihood of earlier enrollment in hospice, a higher likelihood of not dying where your family members thought you would have wanted to die, a higher likelihood of dying in the ICU or getting some kind of aggressive care. So it's not only what the chemo does or doesn't do in terms of treatment or survival or quality of life; it also seems to exacerbate and put someone at risk for very burdensome interventions that having avoided it might have enabled patients to avoid getting very burdensome care that's largely futile. But as Al said, we are probably more the nihilistic type. Dr. Shannon Westin: Well, I think you bring up a couple of good points because you've got objective data, and these studies that you're mentioning are just some of them that show that early hospice care and early enrollment and even just a palliative care program or a supportive care program or whatever terminology we want to use, people do better, right? They live longer actually from that piece rather than necessarily the more “aggressive measures” of chemotherapy and things. Dr. Holly Prigerson: When there was an extra analysis of the Temel data, I believe they had shown that some of the survival advantage was explained by avoiding toxic chemo. So that's directly relevant. Dr. Alfred Neugut: There is an on the other hand, as always, which is that patients and families often don't want to do that. I mean, they realize that doing that is giving up, so they're reluctant to take hospice care or palliative care as an alternative to another cycle of chemo or another type of chemo. And as you say, you never know; maybe the next one is going to be the winner and there'll be a miracle or there'll be at least some substantial benefit. And then there's always experimental therapy, and now immunotherapy, which is the topic of this article, is the new winner on the block. And it has bright lights around it, and everybody has great hope for it. And it's the new kid on the block, and everyone hopes that that's going to be the big savior. Dr. Shannon Westin: Right, and I think everyone knows of a story of somebody that was “on death's door” and got immunotherapy or the newest targeted therapy or the newest ADC, so that definitely colors it. And that also colors, I think, the physicians that are offering it, right? Because, yes, I've definitely heard this, and I'm sure you guys have too: nobody should die with such and such cancer without receiving immunotherapy once or without receiving such and such targeted therapy. I hear people say this all the time, and I don't necessarily disagree. It's more that when are we giving it, right? So we should be thoughtful about when we're placing those things. But you're right; there's so many factors that go into these decisions, and it's not cut and dry around what the patients and the family members and the physicians are going to decide. Dr. Holly Prigerson: And I think that Al hits on a really key issue when he used the word “hope” because that seems like what the negotiation appears to be all about. You don't want to disparage someone or not offer them hope if there might… No one wants to say that there isn't hope. No one wants to be the bearer of that kind of bad news. And I guess it leads to—I think that that's part of the driver that ends up providing the gas that drives people to getting more aggressive therapies is because no one wants to be the person to be the wet blanket and disparage hope. And so it might affect how treatments are sold to patients or at least communicated to patients. There was this one finding in this report that was curious, and it was that patients with undocumented performance status were the ECOG group most likely to get treatment. And so, in terms of what could be done going forward to make people more realistic and not offer hope where it's really, really unlikely, maybe employing more decision rules about requiring the documentation of performance status and ensuring that it's what the ASCO guidelines permit for administering another line of treatment. Because that might be a way to sort of use data to help correct what in psychology we call cognitive distortion, so correct the distortion of this hyper-optimism. It might help correct some of that. We don't want to overcorrect and make people hopeless or depressed, but we want to offer realistic options. I think that's part of why this paper is so important, and it sort of informs future research to try to unpack some of the findings that they didn't have data on physician characteristics or communication discussions between patients and their oncologists. And maybe that's where the money is. Maybe that's where offering hope in a realistic way or different forms of hope, what to hope for, might be better communicated through more effective communication strategies and ways to enhance patients' abilities to understand what they're agreeing to or not agreeing to. Dr. Alfred Neugut: And I would add that it's easy for us to sit here and be dispassionate or scientific interlocutors and saying, you know, “It doesn't work, and therefore we're not going to offer it or you shouldn't get it or go on to hospice.” But it's different when you're on the other side of the table. And even us doctors or healthcare professionals or scientists, when you're sitting on the other side of the table and you're the one who's got the cancer or your mother or child, you're not going to be so easily dismissive of getting third-line chemotherapy and having your 5% chance that the tumor will respond to some cocktail of who knows what and you never know. I don't want to say anybody's wrong or that it's stupid. Everybody has to do what they have to do, and we at least have to think about it and know what we're doing and have realistic—at least some idea of the realism of what we're putting people through and the costs and the toxicities and what to expect. Dr. Shannon Westin: I think you guys brought up some really great points, and I do think that there is a huge impact around the communication piece. And we actually just did a podcast on discussion of goals of care at the end of life for adolescents and young adults and how those conversations can be different. I think the other thing that really caught my eye and, of course, caught your eye when you did the editorial around the Canavan study was this idea that the patients with insurance—with all other things being equal, that the patients with insurance were more likely to receive end-of-life systemic treatment. And it's interesting because typically I feel like we think having insurance and having that support is always a positive thing and has a positive impact on our health, and it most certainly does. So that's not up for grabs. But then this particular study showed that it could potentially have been negative because of all the things that you all just said about the negative impact of care in this 30 days or even 14 days near the end of life. What are the opportunities for intervention at the insurance level? You talked a little bit about provider level and communication. Are there opportunities at the insurance level that we could address? Dr. Holly Prigerson: It does seem like having insurance companies determine what is reasonable and not reasonable to reimburse for. So including things, I would think, like having performance status factored in. What are the criteria for determining whether it's high value care or not? And I'm not an oncologist, so I really am going out on a limb, and I really want Al to respond to that question. But from my perspective, it seems like the ASCO guidelines determine when it's—“low-value care” is how they put. It's wasteful and futile and burdensome. And they have guidelines of performance status, having not responded to multiple lines of chemotherapy, so that there could be guidelines for when there is value and when there isn't and that it could be more values driven in terms of guidelines of what they would reimburse. Because, as our title implicated, it seems like you get offered what insurance companies are willing to pay for, and that leads to potential disparities in equity if you have different insurance than other people and fairness and justice. Those seem like valid questions to raise. Dr. Alfred Neugut: I mean, I think if we're following randomized trials and evidence-based medicine, then I think we're in a reasonable area of what should be done and could be done and needs to be done. And almost always, insurance will follow those. You don't usually end up then having to argue with a peer-to-peer call to the insurance company under those circumstances. Where things get sticky is when you want to treat someone off-label or go off the reservation. I don't know if that's to some degree what this paper talked about. And there you probably don't get much benefit from treatment if it's not a data-driven use of the drug. So that's really, I think, where the line needs to be drawn. I don't think there you'll have an insurance problem if you've stated those sorts of guidelines. If you want to use NCCN or the ASCO guidelines, all good and reasonable. The problem is when someone's desperate and you're trying to make them happy, so you give them something even though there's no reason on God's earth why it should work, but just so they feel like you're getting something and you're not being abandoned, which sometimes you do feel pressured to do that, and very commonly you do. And maybe that's where racial disparities save the uninsured from being tortured for something that's not likely to really be very helpful. Dr. Holly Prigerson: But as someone who's a disparities researcher as well, it raises the question were Black patients—which these data couldn't answer: were they offered different treatments than the White patients? And I think we all agree that low-value treatments shouldn't be offered or received, but the fact that Black patients receive less of the expensive stuff, the newer cutting edge, is problematic. And I think there does need to be more research into equity in terms of the options presented to patients with similar diagnoses. That was the troubling aspect of it, not that they weren't getting, in essence, better end-of-life cancer care, but that's beside the point. In terms of ethics, it would be nice to have known whether they were offered the same things and declined it. I think all of us are a little suspicious that maybe they weren't. Dr. Shannon Westin: Yeah, that definitely—I like how you said it. It struck a nerve. Like, when I was reading through both the article and your editorial, that was something that caught my eye is this evidence of how implicit bias is impacting what people are offered. And yes, it ended up being an overall benefit to underrepresented minority patients. However, that wasn't necessarily the intention or why that happened. So I would be interested to hear what you all think about what we know about how implicit bias impacts the care of patients with cancer, just for our listeners, and specifically what particular treatments are offered, not necessarily just at the end of life, but just across the cancer continuum. Dr. Alfred Neugut: There are estimates—if you read the medical literature on health policy and things like that, there are estimates that we overdo a lot of things in medicine and give—I don't know. I've read that like 70% of what we do in medicine is unnecessary. I'm not saying in oncology necessarily, but screening and wellness care, etc. And so oncology probably is equally guilty of such things. And there are biases in that as well, so, you know, that's what happens. Dr. Holly Prigerson: And in the article, they had cited, I think it's Penner. There was a study that showed that ratings of an oncologist's implicit bias were negatively associated with Black patients' willingness to undergo their treatment recommendations. So the dynamic between what's offered, what's heard, what's trusted. There's obvious history of Tuskegee and concerns about being denied treatment. So this article kind of feeds into why was the latest and greatest types of treatment not as common? That said, the actual differences, if you look in the tables, the actual differences weren't that disparate. They were statistically significant, but we're talking like 37% to 34%. So the disparity isn't as wide as to cause serious alarm bells to go off that people are being treated so differently. But it does raise a lot of underlying concerns that you would want to make sure that everyone's being offered the same things. So it does imply—that Penner article implied—it's basically medical mistrust may be interfering with a Black patient's willingness to undergo or accept some treatment offered. So if you follow the logic on that through, then the intervention would be: What are ways to enhance medical mistrust of their oncologist? What are the reasons for it? And how can patients feel that they are being treated by someone who treats them fairly and no differently than White patients? And so efforts in those directions seem like they might pay off in terms of enhancing and addressing implicit bias. Dr. Shannon Westin: Well, this has been a really great discussion. I'd love to hear just kind of your last thoughts from each of you around some of the unmet needs. We've heard themes throughout the discussion, but maybe just sum it up for the podcast listeners, bring them back and where we need to go next here. Dr. Holly Prigerson: Al and I have been working on a few different projects to address medical mistrust and leveraging things like healthcare chaplains, who might be liaisons within an outpatient oncology setting. We also have interventions that try to enhance clinical communication, like what we call a GIST, so that patients easily get the gist, the essential meaning of things like scan results to sort of level the playing field so that patients have adequate information to know what the harms and benefits of the treatments that they're being offered might be and have a better background to be engaged in those decisions in the first place. Dr. Alfred Neugut: My own thing is that you should be telling patients right from the get-go that they have incurable diseases and not letting them meander along thinking that we can actually help cure them in some meaningful way. We know who's incurable, and even if they have two or three years of survival coming to them, colorectal cancer or breast and prostate, etc., it's still fair to tell them that we can't cure them. And then when the time does come two, three, four years later, they're not going to be shocked, and they'll deal with it, I think, in a better way because they've known all along that this day is going to come, and then they don't react badly in the last two weeks, three weeks, four weeks, because they've been prepared for all those years before. I think the real problem is no one ever tells them directly, or many doctors don't tell them directly upfront. And so, when it comes near the end, they don't tell them until they're almost semiconscious. Then it's a shock out of the blue. And then of course they want to be treated more aggressively at the end. And I think that's where some of the issues may come. Dr. Holly Prigerson: And with the immunotherapies, that probably raises a lot more questions, even from the oncologist's perspective, about what they can call incurable because maybe there is hope, maybe there are these outliers. That's where it seems like it's wonderful that there are advances, but if the rates are so low and people have a misunderstanding of their chances, I think we're on the side of understanding what the best data suggests are the likely outcomes. And I think all the new advances sort of undermine disparaging hope because that's what they're there to do. They're there to offer hope. Dr. Shannon Westin: And everybody wants to be the tail of the curve, right? They all want to be that person. So that's exactly—you're totally right. When we're trying to communicate, “Okay, this is the most common outcome. Yes, there are people that are way over here but…” Dr. Holly Prigerson: That's going to be me. Dr. Shannon Westin: Yes. They always say, “That's going to be my miracle.” Well, great. Well, thank you both so much. This was such a lively discussion, and I know the listeners learned a ton. I know I did. Again, thank you all for listening to JCO After Hours. We were discussing "You Get (offered) What You (can) Pay For: Explaining Disparities in End-of-Life Cancer Care," published in the JCO 6/20/23. We're so excited that you took the time to listen. If you're looking for more podcasts, check out our website, or you can find us wherever you get your podcasts. Have a wonderful day. 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. Guest statements on the 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.
Dr. Mahdi Sheikh and Dr. David Zaridze join Dr. Shannon Westin to discuss how quitting smoking after diagnosis may impact survival in kidney cancer. TRANSCRIPT The guest on this podcast episode has no disclosures to declare. Dr. Shannon Westin: Hello everyone, and welcome to another episode of JCO After Hours. This is the podcast where we get in-depth on manuscripts that have been published in the Journal of Clinical Oncology. As always, I'm your host, Shannon Westin, Gynecologic Oncologist and Social Media Editor for the JCO. And I am so excited to be here today. We are going to be discussing the paper, “Smoking Cessation After Diagnosis of Kidney Cancer Is Associated With Reduced Risk of Mortality and Cancer Progression: A Prospective Cohort Study,” which was published in the JCO on March 29, 2023. And this very intriguing paper, I have two of the major authors from this paper. First is Mahdi Sheikh, who is a scientist and epidemiologist at the International Agency for Research on Cancer, the World Health Organization in Lyon, France. Welcome, Dr. Sheikh. Dr. Mahdi Sheikh: Thank you very much, Dr. Westin, and thanks for having us. Dr. Shannon Westin: And then with Dr. Sheikh is Dr. David Zaridze. He is the Director of the Department of Clinical Epidemiology at the N.N. Blokhin Russian Cancer Research Center in Moscow and also the President of the Russian Cancer Society. We are with greatness today. Dr. David Zaridze: Thank you. Thank you very much. Nice to be with you. Dr. Shannon Westin: Very nice to be with the two of you. So, let's get started. I first wanted to just level set. Could one of you review just the overall incidence of kidney cancer and what proportion of patients with kidney cancer are known to be smokers at diagnosis? Dr. David Zaridze: The figures I'm going to present are rates. They are adjusted to standard world population. Why am I saying that? Because in America you sometimes use adjustment to the US population. These figures will be different from what you are accustomed to see. Okay, incidence of kidney cancer in Russia, in men, 14.1 per 100,000. I compare this with the United States of America, men, 16.5. Very small difference. Women in Russia, 8 per 100,000. In the United States of America, 8.8 per 100,000 of population. Exactly the same. Very close. These rates are sort of high-ish, but there are very high rates, for example, in the Czech Republic, where rates are more than 20 and other Central European countries. In Russia, kidney cancer mortality in men is 6 per 100,000. In USA, 3 per 100,000. In women in Russia, 1.9. In the United States, 1.3. I would say that there is a difference in mortality in men, not much in women. The incidence of kidney cancer is increasing in Russia sharply, sharply. Since 1990 it has increased - it's tripled. It increased from 5 per 100,000 in 1990 to 14 per 100,000 in 2019. Mortality is stable or declining. This is suggesting that kidney cancer is overdiagnosed in Russia and probably elsewhere. But this is not a problem of our discussion now. The frequency of the prevalence of smoking in kidney cancer patients. It is estimated that 15% to 20% of patients with kidney cancer smoke. In Russia, we have results only from our study. 18% of patients smoked at admission to our cancer center. Dr. Shannon Westin: Got it. Okay, good. Well, that's really helpful, especially to those of us that don't take care of patients with kidney cancer every day. It helps us just understand. And I guess the next question is what do we know about the impact of tobacco cessation on the risk of kidney cancer? So you were talking about that increasing incidence. How does tobacco cessation impact that? Dr. Mahdi Sheikh: Tobacco smoking is a known risk factor for kidney cancer and an estimated 17% of the kidney cancer burden worldwide can be attributed to tobacco smoking. There is a recent meta-analysis of 56 studies that was published a few years ago that clearly showed a dose-response relationship between smoking and kidney cancer, meaning that the more cigarettes a day you smoke, the risk of kidney cancer will go up. For example, the risk that was shown for five cigarettes per day was 20%. It goes up until 70% for 30 cigarettes per day. And also with a duration, the more years you smoke, the risk for kidney cancer will go higher. However, the good news is that when you quit smoking, there is strong evidence that the risk for developing kidney cancer will be lower compared to if you continue smoking. And there is some evidence that shows again dose-response relationship, meaning that the more years you spend in quitting smoking, the lower your risk would be for developing kidney cancer compared to if you continue smoking. So this is not only about renal cancer or kidney cancer but also true about many other cancer sites as well. Dr. Shannon Westin: Okay, that's super helpful. And then I guess prior to your study that we're about to talk about, did we have any information on what happens when patients quit smoking after their diagnosis? Any limitations to those data that were available? Dr. David Zaridze: You mean the data which was prior our study? You know, the negative effect of smoking after diagnosis has been shown nearly three decades ago. The information exists already for thirty years, but it was largely ignored not only in clinical practice but also in clinical trials. And I have to stress that in clinical trials this information is still ignored. I came across these studies and decided to review them some time ago. All they were case-control studies and to my knowledge, none of them assessed the effect of quitting smoking. I decided to review these studies and included this review in my book, Smoking: A Major Cause of Cancer, which was published in 2012 and was dedicated to Professor Richard Doll's anniversary. In fact, this was a stimulus for the study we are discussing. And in fact, the component of this study we are discussing today was built in and baked into the existing cohort study to which we added the active follow-up component for assessing the changes in smoking habit and disease status. Dr. Mahdi Sheikh: If you review the evidence, before publishing this study just like a few years ago, we find that there are many studies published talking about the effects of smoking cessation on cancer survival. However, as David mentioned when you go deep into these studies, you'll find a lot of limitations. First of all, most of these studies are retrospective studies, which means that either case-control or retrospective course that patients developed the outcome, and then some investigators came to see their records to assess or ask family members before they developed the outcomes. There are a lot of biases with these types of studies. And with the epidemiologic study, perspective study that we did, has less limitations compared to retrospective ones. Another one is that when we go into the study you see, they only assess a small number of patients, small sample size. Some studies just assess 10 smokers, some assess like 30. By this study we try to assess a large number of smokers who quit smoking after diagnosis. Another limitation is that– First, let's see what exposure and what setting we are talking about. We're talking about smoking which is a very dynamic behavior. People quit smoking and they relapse smoking and they quit smoking and so on. So if you access this exposure for only a limited time, for example, for one year, then you may miss what happens after that which results in misclassification of some of the participants. So repeated assessment was not done in other studies that we did here in this study. Another one, you are talking about special setting patients who are diagnosed with cancer. These patients have special circumstances, they have treatments, they have family support, they might go under the stress of cancer, and all these different stages at diagnosis. And most studies that are available, they didn't account for this. They didn't adjust or they didn't try to understand the role of these compounding factors, as we call it in epidemiology, on that, the thing that we're trying to address. And a prospective study, as I said, long follow-up time. Even the very few prospective studies that were available for other cancer sites that have only one year or maximum two years of follow-up with this type of exposure, so it is important to follow them for a long time. Another thing I would say was exposure assessment. Not only did we repeatedly try to assess exposure among participants, but try to call the people– David and his team who did the study in the field, called the participants and tried to ask the family members and sometimes their physicians about their smoking behaviors. When you go to current evidence you see, mostly smoking behavior was assessed using the record that is available like treatment records or patient records, which again has some limitations if you do not assess exposure among qualified participants. Finally, we're talking about a dynamic behavior in the follow-ups. Some people might change smoking. But there is a very important thing, in this study, we also collect at the time of quitting smoking. There's a very important thing in statistics we call Survivorship Bias, meaning that, if you were assessing an exposure doing the follow-up and if you do not pay attention to this, you will assess an exposure that is a proxy of people who lived longer. Meaning that people have enough time, they have a long time, and those who have longer time, will have more time to quit smoking. And then you will be assessing this, actually, not the exposure, but you're only assessing people who quit smoking, and then whatever you assess, you would end up with a beneficial effect. But if you have the time of quitting smoking and follow up and all these statistical things and lower sample size, you are able to account for this very very important bias in epidemiology. Dr. Shannon Westin: Before we go further, I'd love for just a bit of a description of exactly how you laid out your study to really add to where this data are so limited around survival and tobacco cessation. So maybe review the primary/secondary objectives, basic design, just to make sure our listeners are all on the same page. Dr. David Zaridze: The study has classical prospective cohort design that the study, which was basically a basic study, in which the new component was built in. This study used a user's questionnaire-based exposure assessment and molecular epidemiologic approach. I mean that, in addition to the questionnaire approach, we collected blood and tumor tissues for molecular studies. All patients with kidney cancer admitted to the cancer center were interviewed at admission before receiving any treatment. A structured lifestyle questionnaire was used. Participants were asked about their lifetime smoking history which included questions about the duration and frequency of smoking cigarettes, the average number of cigarettes smoked every day. They were also asked about their lifetime history of alcohol drinking. The questions included questions about exposures to carcinogens other than smoking, and health conditions, including chronic kidney diseases, hypertension, diabetes and so on. Height and weight were measured. Today, this study generated and continues to generate plenty of results and papers published in most prestigious journals such as Nature Genetics, for example. So, as you know, we started from 2012, we started the follow up of the cohort members, we were focusing on Moscow residents and the follow-up includes regular annual contacts with the patients personally or via telephone or with patients' household members, etc. Again, we collected information about changes in smoking behavior and disease status. We also used information from the regional cancer registry to confirm the information obtained from patients. The average period of follow up was eight years. And this is quite a long follow-up. Repeated assessment of smoking status reduces the likelihood that exposure to smoking was misclassified. However, regrettably, the self-reported information on smoking was not supported by biochemical tests, for example, by blood cotinine testing. To my knowledge, this is the only prospective cohort study in patients with cancer, not only with kidney cancer that have collected data on participants' smoking status prospectively for quite a long time. The average follow-up time was eight years. Dr. Shannon Westin: That was incredible. That definitely caught my eye. And I was looking, I was like, “Oh, how many did they lose?” And you guys kept 80-100% of the patients. I just was so impressed by that. And now hearing the mechanisms in which you did that, it makes sense. You were very diligent, multiple ways to contact patients and confirm the data. So you really are to be congratulated for the work that you're able to achieve. Dr. Sheikh, I'd love to hear, you talked a little bit about how some of the studies didn't really think about confounding variables. Can you kind of highlight some of the confounding variables that you all controlled for in order to really assess the impact of the cessation on survival? Dr. Mahdi Sheikh: Thanks to the high-quality data and also the large sample size and the way the study was designed, we were able to adjust for a lot of confounding. So we tried to adjust for all these things. So we used three approaches. The first approach was adjustment. When you ran this in the analysis, we tried a statistical model, we tried to adjust for these confounders like age, sex, treatment, socioeconomic status, smoking intensity, alcohol, and other factors. This is one effect, one approach. The second approach was stratification, meaning that we come and see the effect within people who have been diagnosed with only earlier stage tumors to see if the effect among people with earlier stage tumors differs with the effect that we see among people with higher stage tumors. But again, if you read the paper, you see that we saw the protective effects of smoking cessation on both groups of people, those who were diagnosed at earlier stages and those who were diagnosed at later stages. And also heavy smokers or mild to moderate smokers, again, we tried stratified analysis excluding those heavy smokers and saw the effect, again, among those who were light smokers or moderate smokers and also with the heavy smokers. I want to say that we tried all these types of analytical approaches and we really saw the protective effects across all patient subgroups. Finally, I talked again about the survivorship bias. So we used really strict statistical approaches to address this confounding, and because we had the time of quitting, we had the follow up time and all these things. And, again, whatever we did in the study we still could see the effects of smoking and all this is due to the good design, the large sample size, and the good questionnaire data that we have. Dr. Shannon Westin: That's awesome. I think, of course, now let's get to the bottom line. 40% reported that they quit smoking after diagnosis with none relapsing during the time period. And what did you see was the impact on overall survival as well as cancer-specific survival? Dr. Mahdi Sheikh: So we tried several outcomes - overall survival, cancer-specific survival, but also progression-free survival. And then because we had the large sample size we could assess all this. Interestingly, we saw the effect on all the three outcomes that we assessed. So the overall survival was better among those during the quitting time and also the cancer-specific survival was also better and also progression-free survival was better among all these participants. Dr. Shannon Westin: I think most people that have read this paper - and if you haven't read this paper you should run to read it right now - I really was impressed with that kind of clear benefit across cancer-specific mentality across all subgroups regardless of how much they smoked. So I don't know why you get a sense of like, “Oh, if you smoke a little bit you wouldn't see as big of an impact,” but a very clear impact. And I would love to hear why you think smoking negatively impacts these outcomes. How does the cessation help? This is a perfect time for that. Dr. Mahdi Sheikh: When we review the evidence about how smoking cessation may be beneficial for patients, for the survivorship of patients with cancer, we come to five mechanisms that are suggested in the literature. So the first one can be, is suggested, that is altered cancer biology. Smoke and tobacco smoke contain numerous carcinogens and mutagens. So it has been shown that cancer cells that are exposed to tobacco smoke, they may become more aggressive and the risk of metastasis might go higher and also, angiogenesis and all other effects on the biology of cancer cells. So it may affect the cancer cell biology. Another suggested mechanism might be altered immune response. So tobacco smoking affects the immune system and then the immune response among those who are exposed to tobacco might be affected by tobacco smoking. So their response to the cancer cells but also other bacteria, viruses, and other things might be affected as well. The third possible mechanism suggested altered drug metabolism. It has been shown that tobacco smoke and smoking can affect some of the enzymes that have metabolic responsibilities and metabolism of the drugs. So that can affect the washout period for the drug. It might not stay enough in the blood or vice versa as well. It might affect the toxicity. There is some evidence about this. The fourth mechanism suggested is about increasing treating-related complications or treatment-related complications. People who smoke have delayed wound healing, they have more complications, the surgery, the time they spend at the hospital might be longer. And this is also part of which smoking may affect the outcomes that we saw here. And finally, that is we are talking about tobacco smoking and patients with cancer are human beings with all these systems. So we know that smoking causes damage to the cardiovascular system, to the pulmonary system and also to the lungs and other things. So this is why we see different outcomes are affected by cancer. Dr. David Zaridze: I was impressed by the data that exposure to tobacco smoke condensate induces changes in tumor microenvironment. For example, it inhibits formation of interferons, interferon alpha and gamma, inhibits the migration to tumor microenvironment of the immune cells. The number of CD8+ T lymphocytes, T killers, are significantly lower in the tumor microenvironment of current smokers compared to former smokers and never smokers. And even more interestingly, the number of PD-L1+ cells are also lower in the tumor microenvironment of current smokers than former or never smokers. This is probably very important in terms of effectiveness of impairment by smoking of the immunotherapeutic approaches in cancer treatment. Dr. Shannon Westin: That's very important and we know the microenvironment has a huge impact on just the way the cells respond to treatment and develop resistance and so that makes a lot of sense. Okay, well, this has been amazing and I think one thing that you just said just struck me, Dr. Sheikh, that you've obviously shown this in lung cancer and you're looking at this in other cancers. I guess the question is: What should we be doing? How should we be implementing tobacco cessation efforts across all cancer diagnoses to help all patients that have really any diagnosis of cancer? Dr. David Zaridze: Let me first underline the clinical importance of these results. The benefits from quitting smoking are comparable or even superior to those recorded in the clinical trials of modern kidney cancer treatments such as immune checkpoint inhibitors. I refer to the results of pivotal trials in advanced renal cell cancer in the frontline setting and these results were reported at ASCO Meeting 2023 recently in May. If you compare the results of our study with results of these pivotal trials, it is very impressive. It is clear that our findings strengthen the case for making tobacco cessation treatment a standard part of the routine health care for all people with cancer, however, smoking is still quite high in cancer patients. And I would like to quote Peter Shields who is saying that, in the United States,10% to 50% of cancer patients smoke. As far as Russia is concerned, in our study, 80% of kidney cancer patients smoke, and in our lung cancer study, 58% of cancer patients smoke. The barrier is that the oncologists do not believe or are accepting with a great deal of skepticism the results of our study. They don't believe the idea that anything else besides surgical, radiological, or medical treatment could improve the outlook of cancer patients. It's difficult for them to apprehend. Many of them think that smoking cessation after diagnosis is simply a waste of time. Many patients simply don't know that smoking cessation after diagnosis may be beneficial for them. In addition, they are pessimistic and they feel discouraged to quit smoking, as they might think it is too late. I would like to quote my favorite quote: “Smoking cessation treatment has to become the fourth pillar of cancer treatment, one that could affect cancer treatment outcomes as powerfully as surgery, chemotherapy, or radiation therapy.” This is Dr. Fiore, 2019. Dr. Shannon Westin: Thank you so much. And Dr. Sheikh, anything to add there around cessation efforts? Dr. Mahdi Sheikh: As we saw the results of these studies that smoking cessation is feasible and it is accessible at a minimum cost for many patients, it should really be integrated in the management of patients with cancer. It is feasible, it is cheap, it is accessible. But unfortunately, when we review the evidence we see that only less than half of the physicians, like around 40% of physicians, send the patients to tobacco smoking cessation services. And even some do not discuss this issue. And as David mentioned, they do not know the effect of smoking cessation. So when you go through these studies to find the major barriers, in addition to what David had mentioned, we find two important points. First one is lack of education or experience in providing tobacco cessation interventions among those who deal with patients with cancer. So they do not have the education. And second is lack of available resources for referrals. Now we're not only talking about the United States but also many other countries even high-income countries, we do not see the resources for referrals on smoking cessation services in cancer care settings. The take home message probably from this study and also from these barriers, would be for three groups. First, for the policymakers, we would recommend sustainable funding should be dedicated to tobacco cessation services. As we saw, the effect is huge and seems to be a very big effect and it is cheap so why not implement this smoking cessation service within cancer care settings. And the second one, tobacco treatment training programs for healthcare providers. This is also very, very important that we try to implement this training program in the curriculum of healthcare providers, especially those who deal with cancers and tobacco-related outcomes. And also for physicians, we recommend that physicians should assess and address tobacco use in all patients with cancer. They should talk about this topic and also show the benefits of quitting smoking. And patients with cancer who smoke should be supported to stop smoking at any time and each visit after diagnosis is not like some time pass, as we saw, all patient subgroups could benefit from smoking cessation. This is important. But something also very, very important that we shouldn't forget that cancer itself causes a lot of fear and anxiety and stress. And smoking cessation sometimes may be associated with stress and more anxiety. So it is very, very important to think about this point and provide the psychosocial support to patients who quit smoking. Sometimes they may relapse just because of the fear and anxiety they have. So it's not only showing the evidence, but also supporting these patients, telling them how to do that and also supporting them emotionally and also psychosocially. And finally for the patients, I would like to give this message that we see and we know that it is never too late to quit smoking. As David said, patients may feel like, “It is too late now I've developed cancers,” but no, it's really not too late. And if you quit smoking at any time after diagnosis, you would benefit a lot from smoking cessation. Dr. David Zaridze: In the United States there are guidelines, several guidelines for smoking cessation, specifically for cancer patients because smoking cessation in cancer patients is very different from smoking cessation in general population. In the general population, we more or less succeeded, I would say, and we have to look now at this direction to the smoking cessation in cancer patients. And this is a message to WHO, that countries, members of WHO, based on the recommendation guidelines of WHO, develop their own specific guidelines for smoking cessation in cancer patients. And that should be used in all cancer clinics and that should be a must, absolutely important part of anti-cancer treatment. And as I already told, it should be the fourth pillar in cancer treatment, as treatment, as surgery, chemotherapy and radiation. Dr. Shannon Westin: Thank you both. That was such a great discussion, and I hope that we've convinced everyone that this is a critical effort that they need to be addressing every day. I just want to thank everyone who listened. This has been "Smoking Cessation after Diagnosis of Kidney Cancers Associated with Reduced Risk of Mortality and Cancer Progression: A Prospective Cohort Study", again published in the JCO on March 29, 2023. Thank you guys again for listening to JCO After Hours. Please check out our other podcast offerings. You can check them out on the website or wherever you get your podcasts and let us know what you think about the podcast on Twitter. Dr. David Zaridze: Thank you. Dr. Mahdi Sheikh: Thank you very much. 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. Guest statements on the 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.
Moderator: Róisín O'Cearbhaill, MD, Gynecologic Medical Oncologist, Memorial Sloan Kettering Cancer Center, New York Featuring: BJ Rimel, MD, Gynecologic Oncologist, Cedars-Sinai Medical Center Erin Crane, MD, MPH, Gynecologic Oncologist, Levine Cancer Institute Vicky Makker, MD, Medical Oncologist, Memorial Sloan Kettering Cancer Center Jennifer MacDonald, PharmD, Oncology Clinical Pharmacy Specialist, Medical University of South Carolina
TKI Toxicities: A Society of Gynecologic Oncology Podcast Moderator:Róisín O'Cearbhaill, MD, Gynecologic Medical Oncologist, Memorial Sloan Kettering Cancer Center, New York Speakers: BJ Rimel, MD, Gynecologic Oncologist, Cedars-Sinai Medical CenterErin Crane, MD, MPH, Gynecologic Oncologist, Levine Cancer InstituteVicky Makker, MD, Medical Oncologist, Memorial Sloan Kettering Cancer Center Jennifer MacDonald, PharmD, Oncology Clinical Pharmacy Specialist, Medical University of South Carolina Róisín O'Cearbhaill, MD, is joined by BJ Rimel, MD, Erin Crane, MD, MPH, Vicky Makker, MD, and Jennifer McDonald, PharmD, to review the clinical management of tyrosine kinase inhibitors (TKIs) in gynecologic cancers with consideration for dose adjustments and modifications. The speakers discuss the optimal management of commonly encountered toxicities, such as hypertension and hypothyroidism, that are associated with several of the TKIs. They also highlight management strategies, patient reference materials and anticipatory prescriptions for antihypertensives, antidiarrheals, and antiemetics. The podcast includes two patient cases that delve into information about the differences in toxicities between lenvatinib and pazopanib, hypertension and which drugs to use in which order (both starting dose and dose adjustments), and medical access and lab intervals. These practical clinical pearls in managing toxicities aim to guide practitioners on how best to use these drugs to treat gynecologic cancers. This podcast was developed by the Society of Gynecologic Oncology for Gynecologic Oncology. Additional Resources: Tyrosine kinase inhibitor toxicities: A Society of Gynecologic Oncology review and recommendations Download audio Browse all Gynecologic Oncology audio
Host: Dr. Sarah Sterling, associate professor of Emergency Medicine at the University of Mississippi Medical CenterGuest: Dr. Christy Haygood, Gynecologic Oncologist at the University of Mississippi Medical CenterTopic: Gynecological CancerEmail the show: remedy@mpbonline.org. Hosted on Acast. See acast.com/privacy for more information.
May is Asian American and Pacific Islander Heritage Month! In this episode, Cervivor Podcast Host, Joslyn Paguio discusses health disparities within the Asian, Asian American, and Pacific Islander communities and the possible reasons why with Dr. Mihae Song, a Gynecologic Oncologist at City of Hope, and Arlene Simpson, a cervical cancer survivor. Through this conversation, you'll hear the personal stories of each guest and where they are at today. Communication is key to understanding one's health and building a long-lasting relationship with their primary care physician. So, what happens when you aren't taught the proper terminology? What if you were never taught how to talk about things…particularly below the belt? We realize that knowledge is power. Some experience no abnormal symptoms and are diagnosed with cervical cancer. Then there are some, like Arlene, a Cervivor community member, who realized that "abnormal was her normal." Arlene accepted that as a way of life because of associated diagnoses which later led to her cervical cancer. More about the guests: Arlene Simpson is a loving mom, a devoted wife, a Financial Services professional focusing on the importance of Financial Literacy in America, and a one-year cervical cancer survivor and patient advocate. MIHAE SONG, M.D., has provided free health care for pregnant women in Pakistan, cared for blind and autistic children in South Korea, mentored grade school kids and trained future medical school students in surgical techniques. She's earned a long list of awards and honors for her skills in the operating room and the classroom. Dr. Song is passionate about women's health and an expert in minimally invasive surgeries, as well as more complex abdominal procedures. A graduate of New York's Columbia University, Dr. Song studied medicine at SUNY Downstate College of Medicine in Brooklyn, New York, and continued her training with fellowships in health equity leadership and gynecologic oncology at University of Minnesota in Minneapolis. Dr. Song is excited about new cancer therapies and is eager to help bring them about through clinical trials. It's one big reason she's joined City of Hope which, she says, “has the best ingredients to bring research from the laboratories to clinical trials to the clinic.” Did you connect with this episode? Share your thoughts with us on social media using #CervivorPodcast or by emailing us. For more Cervivor-related content, check out: Cervivor.org. Follow Cervivor on all social media platforms. If you would like to be interviewed as a potential guest for an upcoming episode or would like to request a speaker or topic for a future podcast episode, email us at info@cervivor.org. --- Support this podcast: https://podcasters.spotify.com/pod/show/cervivor/support
This is the first of the three-part podcast series, Keeping up with the Chemos on Mirvetuximab soravtansine. After going over some general information on Mirvetuximab soravtansine including mechanism of action and indication. The multidisciplinary panel will discuss the aspects of getting a team of APP, Optometrist, and Gynecologic Oncologist educated and prepared for giving Mirvetuximab soravtansine. The session wraps up with some key take home points on Mirvetuximab soravtansine. 2022-2023 SGO Chemotherapy and Targeted Therapies Subcommittee Members and Moderators:Tracilyn Hall, MDJudith A. Smith, B.S., Pharm.D, BCOP, CPHQSpeakers:Julia Canestraro, OD, FAAO Karen Lyle, PA-CKathleen Moore, MDSound engineered and produced by Betheon Whyte on behalf of the Society of Gynecologic Oncology.
I sit down with Dr Dana Chase to discuss the role of the Gynecologic Oncologist. Gyn Oncs as they're called frequently, is a labor of love as there's tremendous amount of time and effort put into initially attaining this unique role in the care of women, including those with Lynch Syndrome. We talk ovarian cancer, endometrial cancer, fallopian tubes and more.
In this episode of the IJGC podcast, Editor-in-Chief, Dr. Pedro Ramirez, is joined by Dr. Nicolò Bizzarri to discuss the SCCAN study. Dr. Bizzarri is a former IJGC Editorial Fellow under the mentorship of Prof. Pedro Ramirez. He is a Gynecologic Oncologist at Policlinico Agostino Gemelli in Rome, president of the European Network of Young Gynecologic Oncologists (ENYGO), and he happily serves on the IJGC Early Career Editorial Board. Highlights: - Women with early-stage cervical cancer treated with primary radical hysterectomy had improved disease free survival if treated in hospitals with a higher number of radical hysterectomies per year. - Surgical volume of centers represented an independent prognostic factor affecting disease-free survival. - Increasing number of radical hysterectomies performed in each center every year was associated with improved disease-free survival.
In this episode of the IJGC podcast, Editor-in-Chief, Dr. Pedro Ramirez, is joined by Drs. Ainhoa Madariaga and Robert Coleman, two of the Guest Editors for this month's special issue entitled “Novel Therapies Leading to a New Landscape in Gynecologic Tumors”. Dr. Madariaga is a Medical Oncologist in the Gynecologic Cancer Unit at 12 de Octubre University Hospital in Madrid, Spain. She is the chair of the Young and Early Career Investigator - EORTC Gynecological Cancer Group. Her research interests include patient reported outcomes and drug development. Dr. Coleman is a Gynecologic Oncologist and Chief Medical Officer at Sarah Cannon Research Institute (SCRI) in Nashville, TN. His research interests include drug development, clinical trial design and global medical education in gynecologic oncology. Highlights: - The alignment of cancer biology and novel treatment approaches are significantly extending the lives of patients with gynecologic malignancies, particularly with agents such as antibody drug conjugates, immunotherapy, and targeted agents. - The evolving therapeutic landscape is escalating the need for a clearer understanding of how precision medicine can most efficiently be implemented. - Emergence of drug resistance provides new challenges and opportunities through creative and strategic investigation of novel treatment and combinations. - Advances in testing platforms in bringing genomic testing to the global audience. - Clinical trial interpretation requires critical evaluation of analytical primary and hypothesis-generating secondary endpoints – strategies to make appropriate inference is key to clinical trial design.
In this episode of the IJGC podcast, Editor-in-Chief, Dr. Pedro Ramirez, is joined by Dr. Robert Coleman. Dr. Coleman is a Gynecologic Oncologist and Chief Medical Officer at Sarah Cannon Research Institute (SCRI) in Nashville, TN. His research interests include drug development, clinical trial design and global medical education in gynecologic oncology. Highlights: - Strong mentorship is vital to personal and academic development. However, it is a two-way street. True synergy will come from bilateral engagement. - Remember your clinic is your “laboratory” – keep a keen eye for clinical relationships, build hypotheses, and practice the exercise of how to best test it. Even in resource-constrained situations, the process of discovery and hypothesis testing will arm one to be a better investigator and to most appropriately interrogate the literature. - A strong balance between personal and professional responsibilities will provide the environment for sustainability – this is the long game!
Moderator: Kari Hacker, MD, PhD, Gynecologic Oncologist, New York University Langone Health Speakers: Christine Walsh, MD, MS, Gynecologic Oncologist, University of Colorado Carolyn McCourt, MD, Gynecologic Oncologist, Washington University School of Medicine Kari Hacker, MD, PhD, is joined by Christine Walsh, MD, MS, and Carolyn McCourt, MD, to review basic molecular classification as well as more complex biomarkers in endometrial cancer. They discuss how testing can be utilized to inform patient prognosis and to guide second line systemic treatment decisions. They also highlight several ongoing trials investigating treatment strategies based on molecular features, the results of which will help clinicians make better therapeutic decisions, resulting in better outcomes for patients with endometrial cancer. This podcast was developed by the Society of Gynecologic Oncology for Gynecologic Oncology. Additional Resources: Molecular testing for endometrial cancer: An SGO clinical practice statement
बात जब खुद का ख़याल रखने की आती है हम महिलाएं इसमें सबसे पीछे हैं। ऐसा मैं नहीं कहती , रिसर्च कहती हैं ! Dear women , Your Attention Please क्यूंकि आज FYI में सिर्फ आपकी बात होगी। नहीं आज कोई women's day नहीं है , लेकिन इस बात को करने के लिए किसी ख़ास occassion का wait कर भी नहीं सकते। इंडिया में सबसे ज़्यादा सर्वाइकल कैंसर के case पाए गए हैं। क्यों , कैसे , क्या है ये , बचें कैसे , वो क्या गलतियां हैं जो आप रोज़ाना कर रही हैं लाइफ में , बात करेंगे। मैं मानसी हूँ आपके साथ , और मेरे साथ डॉ कनिका बत्रा मोदी, Gynecologic Oncologist , Max healthcare super speciality hospital, saket, Delhi लैंसेट (Lancet study) की एक चौकने वाली रिपोर्ट आई है जिसमें कि दुनियाभर में सर्वाइकल कैंसर की स्थिति का खुलासा किया गया है। भारत में महिलाओं में होने वाली 23 प्रतिशत मौत का कारण सर्वाइकल कैंसर (cervical cancer in hindi) है। इस रिपोर्ट की मानें तो, एशिया में सर्वाइकल कैंसर के सबसे अधिक मामले भारत में हैं। More than 58% of all cases of cervical cancer globally were estimated in Asia, with India accounting for the highest number of cases 21% भारत में , इसके बाद चीन में 18%. Lancet स्टडी कहती है की सर्वाइकल कैंसर से होने वाली 40 परसेंट डेथ mein 23% भारत में होती हैं और ये सबसे ज़्यादा है ! but इंडिया में क्यों ? कैसे होता है सर्वाइकल कैंसर ? क्या ये जेनेटिक है ? symptoms ? क्या कोई आगे है जिसमें ये सबसे ज़्यादा होता है ? diagnosis ?treatment ? HPV क्या है ? हम सब कहाँ गलती कर रहे हैं अपना ख्याल रखने में ? जानिए ABP LIVE PODCASTS पर मानसी के साथ FYI में
In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Drs. David Viveros-Carreño and Rene Pareja to discuss Sedlis criteria. Dr. Viveros-Carreño is a Gynecologic Oncologist at Instituto Nacional de Cancerología, Clínica Universitaria Colombia and Clínica Los Nogales in Bogotá, Colombia. Dr. Pareja is a gynecologist oncologist at Astorga Oncology Clinic in Medellín and the National Cancer Institute in Bogotá, Colombia. Dr. Pareja is a reviewer for more than 20 specialty journals, an Associate Editor for IJGC, and a member of the board of directors of the International Gynecological Cancer Society (IGCS). He is the author of nine book chapters and more than 70 publications in peer-reviewed journals, and at IGCS 2021 he received an award for Community Advancement in Resource-Limited Settings. Highlights: -There is currently a debate regarding the role of adjuvant therapy for intermediate-risk cervical cancer. -Adjuvant pelvic radiotherapy showed lower risk of recurrence for intermediate-risk cervical cancer in a randomized controlled trial more than 20 years ago. -Preoperative imaging, surgery, pathology, and radiotherapy techniques have changed since the evidence for intermediate risk adjuvant treatments was described. -The risk of recurrence for intermediate risk cervical cancer is probably lower now, and observation could be an option. -New evidence from two randomized controlled trials (GOG 263 and CERVANTES trials) is expected to change definitions of intermediate risk and adjuvant algorithms.
Gynecological Oncology...Oh My! While medical terms and titles are a mouthful, they are vital in providing life saving care. In this episode we deep dive into the world of women's cancer with Gynecologic Oncologist, Dr. Mike Finan and defining what Gynecological Oncology really means.
Hosted by: David E. Cohn, MD, MBA, FACHE, Editor-in-Chief of Gynecologic Oncology Featuring: Joshua G. Cohen, MD, Gynecologic Oncologist, City of Hope Orange County Fumiko Chino, MD, Affordability Working Group, Radiation Oncologist, Memorial Sloan Kettering Cancer Center Editor's Choice Paper: Insurance-based disparities and risk of financial toxicity among patients undergoing gynecologic cancer operations Editorial: Financial toxicity of surgical treatment for gynecological cancer: A growing malignancy
Moderator: Leslie Clark, MD, Gynecologic Oncologist, University of North Carolina in Chapel Hill Speakers: Róisín O'Cearbhaill, MD, Medical Oncologist, Memorial Sloan Kettering Cancer Center Ramez Eskander, MD, Gynecologic Oncologist, University of California San Diego Additional Resources: Immunotherapy toxicities: An SGO clinical practice statement
When it comes to success, most people desire perfection without the process of overcoming their failures. This episode shines light on what it means to attain success in every area of your life while overcoming societal pressures and distractions. Dr. Tyler Woodard, a Gynecologic Oncologist proves that as a black male doctor, he is in fact changing the game to what it means to be a black man in a white coat. Follow and Subscribe to Pin N Paper Podcast Spotify https://open.spotify.com/show/1UOkeQFpxRqk7fCf8ZXw6t Instagram https://www.instagram.com/pinnpaperpodcast/ Apple https://podcasts.apple.com/us/podcast/pin-n-paper-podcast/id1583104487 Anchor https://anchor.fm/kammi-wilson Youtube https://www.youtube.com/channel/UCvfxWk8XjS6nbWKBT4UxkEA --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/kammi-wilson/support
In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Dr. David Viveros-Carreño. Dr. Viveros-Carreño is a Gynecologic Oncologist at Instituto Nacional de Cancerología, Clínica Universitaria Colombia and Clínica Los Nogales in Bogotá, Colombia. Highlights: - Fertility-sparing surgery after neoadjuvant chemotherapy in cervical cancer >4 cm is feasible, but the evidence is limited and should be considered as an experimental intervention. - A complete pathological response occurred in 56% of patients. - At least one pregnancy was achieved in 67% of cases and 60% were pre-term deliveries.
Episode 7: Not throwing away my shot. What if you could get one vaccine to help prevent SIX different types of cancer? What if you knew that vaccine was nearly 100% effective against a hard-to-identify cancer? And what if you could protect your kids starting as young as age 9? You can. Learn more about HPV vaccines, their effectiveness, and how to protect yourself and your children from this common virus from Gynecologic Oncologist, Dr. Mike Finan.
Dr. Rick Boulay is a Gynecologic Oncologist and Director of Survivorship with St. Luke's University Health Network. He studied at the University of Pittsburgh School of Medicine and has worked in Gynecologic Oncology for over 25 years. Subjects discussed include cancer treatment, the primary causes of cancer today, the increasing success in treating cancer, what is survivorship and why do some people hate that term?, Singing, alternative medicine, and more!https://www.slhn.org/
Moderator: Floor Backes, Gynecologic Oncologist, The Ohio State University Comprehensive Cancer Center
Moderator: Floor Backes, MD, Gynecologic Oncologist, The Ohio State University Comprehensive Cancer Center Speakers: Vicky Makker, MD, Medical Oncologist, Memorial Sloan Kettering Cancer Center Matthew Powell, MD, Gynecologic Oncologist and Chief, Division of Gynecologic Oncology, Washington University School of Medicine Siteman Cancer Center Amanda Nickles Fader, MD, Gynecologic Oncologist and Professor, Johns Hopkins School of Medicine Description: Dr. Floor Backes is joined by Drs. Vicky Makker, Matthew Powell, and Amanda Nickles Fader to discuss best practices in utilizing molecular and pathologic tests to inform treatment of patients with recurrent metastatic endometrial cancer. The conversation begins with a patient case for the panelists' discussion, followed by a series of scenarios to provide context for different considerations in the therapeutic regimen based on the patient's molecular and sequencing results, histology, and response to treatment. This podcast was developed by the Society of Gynecologic Oncology for Gynecologic Oncology.Additional Resources: SGO ConnectEd: Chemotherapy & Targeted Therapy Flash Cards
Welcome to episode 8 of IMPACT Medicom's podcast series on Precision Medicine in Oncology, the first in a series of episodes focusing on ovarian cancer. In this episode, we discuss the importance of BRCA testing for patients with advanced epithelial ovarian cancer and how national initiatives have helped to improve BRCA testing standards across the country. Our Guests:Dr. Janice Kwon, Gynecologic Oncologist at Vancouver Coastal Health and Vice Head and Professor in the Department of Obstetrics and Gynecology at the University of British Columbia. Dr. Kwon serves as Chair of both the Priority and Evaluations Committee at BC Cancer and the National BRCA Collaborative. Her expertise is in hereditary cancer syndromes and conducting cost-effectiveness analyses of testing criteria and risk-reducinginterventions.Dr. Alon Altman, Gynecologic Oncologist and Professor at the University of Manitoba, and the Winnipeg Health Sciences Centre/Cancercare Manitoba. Dr. Altman is the president elect for the Society of Gynecologic Oncology of Canada (the GOC). He is actively involved in multiple other university, national and international committees including serving as program director for the department of Obstetrics and Gynecology, chair of the University Medical Group (UMG), vice chair for the Medical Management Safety Committee (MMSC) at CancerCare Manitoba, and Gynecologic oncology track lead for the FIGO 2021 Scientific planning committee.This podcast episode was sponsored by AstraZeneca Canada and Merck Canada.If you enjoy our podcast, please review and subscribe. For more podcasts and other medical education content, visit our website at: https://www.impactmedicom.com
In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez, is joined by Drs. Ate van der Zee and Brian Slomovitz to discuss the GROINSS-V-II/GOG 270 Trial. Dr. Brian Slomovitz is a Gynecologic Oncologist at Broward Health and Professor of Obstetrics and Gynecology at the Wertheim College of Medicine at Florida International University. He is an internationally recognized leader in gynecologic oncology clinical trials, specifically in immunotherapy and novel biomarker therapeutics. He also is a leader in sentinel lymph node detection for gynecologic malignancies. Dr. Ate Van der Zee is Chairman of the Board of Directors at the University Medical Center Groningen and professor of Gynaecological Oncology. His current research focuses on translational and clinical research in vulvar cancer. Together with Dr. Oonk he leads a world-wide consortium (GROINSS-V), which performs landmark clinical studies in vulvar cancer. Dr. van der Zee combines his current position chairman position with clinical work and academic research. Highlights •Radiotherapy instead of inguinofemoral lymphadenectomy is a safe treatment option for vulvar cancer patients with a metastasis < 2 mm in the sentinel node •Radiotherapy instead of inguinofemoral lymphadenectomy is associated with less treatment-related morbidity in vulvar cancer patients with a metastasis < 2 mm in the sentinel node •Prospective phase II treatment trials with stopping rules are excellent tools to explore new diagnostic and therapeutic options and to provide evidence-based medicine in rare tumors such as vulvar cancer. •Leading a world-wide consortium (GROINSS-V) is very rewarding and great fun! Ate van der Zee and Brian Slomovitz (@AteZee / @gyncancermd / @umcg / @browardhealth, @FIU)
September is Ovarian Cancer Awareness Month, and The Source is going teal! Because of its vague, “silent” symptoms, ovarian cancer is often not diagnosed until its later stages. Dr. Mildred Ridgway is a Gynecologic Oncologist at University of Mississippi Medical Center and has dedicated her life to treating women with ovarian cancer and other gynecologic cancers. Inside Source talked with Dr. Ridgway about her career in medicine and why she chose GYN oncology as her specialty.
In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez, is joined by Drs. Oliver Zivanovic and Roisin O'Cearbhaill. Dr. Roisin O'Cearbhaill, MD, is a medical oncologist and the Research Director of the Gynecologic Medical Oncology Service and the Clinical Director of the Solid Tumor Program, Cellular Therapy Service at Memorial Sloan Kettering Cancer Center, with a joint faculty appointment at Weill Cornell Medical College. Nationally, she serves as the Chair, Developmental Therapeutics, NRG Oncology. Dr. Oliver Zivanovic MD is a Gynecologic Oncologist at the Department of Surgery at Memorial Sloan Ketteting Cancer Center with a joint faculty appointment at Weill Cornell Medical College. He serves as the Institutional Principle Investigator for NRG Oncology. @ROCearbhaill / @zivanovicmd / @TeamOvary_MSK / @sloan_kettering Highlights: -HIPEC with carboplatin at secondary cytoreductive surgery for first platinum-sensitive recurrent ovarian cancer was not superior to secondary cytoreduction without HIPEC. -HIPEC for recurrent ovarian cancer should be conducted in the setting of a clinical trial
On this episode of WE Have Cancer, womens' cancer surgeon Dr. Valena Wright, MD chats with Lee about her decades of experience treating gynecologic cancers, and the many preventative measures women may not know about. From symptoms of ovarian cancer to the power of positivity to the benefits of music therapy, Dr. Wright shares her professional advice to empower women to be prepared and informed when it comes to their health and well-being. Guest Biography: Dr. Valena Wright is a board-certified gynecologic oncologist and surgeon with more than 25 years of clinical practice experience in the realm of women's health. When Valena lost her older sister to Stage IC Ovarian Cancer, she knew she wanted to start advocating even more about women's cancer prevention. Her new book, It's Time You Knew: The Power of Your Choices to Prevent Women's Cancer is available now. Table of Contents:It's All in the Family Valena's Grandmother was one of the first public health nurses on Prince Edward Island, at a time when not many women had access to such an education. Her trailblazing success greatly inspired Valena to enter the medical field as well. "Not Your Mother's Hysterectomy" Valena says she thinks her grandmother would be astonished by today's technology, and by how surgery is performed today; but Valena can also imagine her shaking her finger at today's medical practitioners, because public health isn't what it should be. The Most Common Women's Cancer The most common cancer Dr. Wright treats as a gynecologic oncologist is uterine cancer, which arises in the lining of the uterus and usually occurs after menopause, but not always. Sometimes pre-menopausal women dismiss the symptoms of abnormal bleeding that can point to uterine cancer. What are the Symptoms of Ovarian Cancer? Ovarian Cancer symptoms can be subtle, but might include bloating, feeling full even if you haven't eaten, fatigue, increased urinary frequency. A pelvic mass can grow quite large over time, even if you haven't noticed any subtle symptoms. Should You Rely on Family History? About 20% of ovarian cancers can be hereditary, but family history is not always reliable without genetic testing. After her sister's ovarian cancer diagnosis, Valena had genetic testing done, and elected to have risk-reducing surgery. Diet, Exercise, and What Else? Diseases can affect women in different ways than men; heart disease is the perfect example. Valena strongly believes it's important to be able to speak up and ask for what you need, and to understand the gynecologic anatomy. And, since many women are frequently multitasking, prioritizing a full night's sleep is extremely important for well-being, mental health, and stress. Integrated Medicine for Women's Wellbeing Integrated medicine can help with the mind-to-body relationship in patients. It's important to remain positive because the brain looks for what we focus on the most, which is critically important for cancer patients. Valena reminds listeners, "there is always hope." The Rejuvenating Power of Music Music lights up our brains and neural pathways in unique ways. Music therapy can be very powerful. Athletes use music to train and visualize, surgeons use music to focus, and patients can use music too. How Can Women take the Best Precautions for their Wellbeing? Women should be aware of the screenings available to them, the importance of nutrition, family history, knowing their risk and getting genetic testing. Recognize their choices and putting them into the context of their daily lives. Valena wants women to have their best health, so that they can truly enjoy their lives. Links mentioned in the show: Dr. Wright's Book: https://www.amazon.com/Its-Time-You-Knew-Choices/dp/1736008609 (It's Time You Knew) Dr. Wright's Website: https://valenawrightmd.com/ (Valena Wright MD) Support the Child of the Month; Benny - https://wehavecancershow.com/benny...
Dr. Field is a nationally recognized gynecologic oncologist. He brings more than 15 years of oncology experience to Mid-Michigan. Dr. Field specializes in minimally invasive surgery, open debulking of ovarian cancer, chemotherapy, and hormone therapy treatments for women with gynecologic cancers, including ovarian and endometrial cancer. Since 2012, he has served as principal investigator for Gynecologic Oncology Group, NRG Oncology Clinical Trials, which is responsible for improving and expanding cancer diagnosis and treatment. He is assistant professor and director of the Division of Gynecologic Oncology in the Department of Obstetrics, Gynecology, and Reproductive Biology in the College of Human Medicine at Michigan State University. “Gynecologic oncology has a bit of a name problem,” says Field. “We're basically specialists in women's cancer. We treat women with cancers of the reproductive tract and sometimes benign problems as well, so problems with the uterus, the cervix, the ovaries, and the tubes. We do both surgery and chemotherapy and coordinate radiation oncology care for women with gynecologic cancer. We're a bit like the primary care doctor for women with those types of cancers.”What attracted Dr. Field to MSU?“The biggest thing that a gynecologic oncologist likes to do is be busy taking care of patients, and this area has been without a gynecologic oncologist. Everyone was really enthusiastic about being able to offer those services in this area. My main goal is to take excellent care of patients and do excellent surgery and care for patients through the life cycle after their diagnosis with a cancer.”Dr. Field says there have been “amazing breakthroughs” in the last three years.“We'd gone through sort of a 10-year dry period with not a lot of new treatments, and in the last three years, we've got a whole new class of treatments for patients with ovarian cancer that overlaps with breast cancer patients. The PARP inhibitors are really effective in patients with genetic predisposition to breast and ovarian cancer. But we're finding that 50 percent of patients, whether they've inherited those mutations or not, can benefit from those drugs, which is really exciting. We're realizing how much earlier to offer those treatments to patients. The next step is combinations of new therapies to treat patients once they've developed resistance to drugs.”Field talks about the role telemedicine has played during the pandemic, and he thinks it will remain in some form even after the pandemic.“This was a breakthrough. The increase was almost instantaneous last March and was automatically approved to be used as a regular visit. A lot of my patients are elderly and are brought to me by their kids or their relatives and have transportation issues and functional limitations. To be able to not have to get out, get in the car, get in a parking spot and make their way into a clinic and instead be able to hook up to somebody's smartphone, I think is just really nice for patients. I don't know that I'm great at it yet, but I just think it's really nice for patients to have that as an option.”Do you think we'll ever cure cancer?“Cancer isn't one thing. It's one of the reasons that what I do is so interesting. Ovarian cancers, from a doctor's perspective and a scientist's perspective, are really interesting because the ovaries can make anything, a whole person. The range of cancers that come from the ovary are so different. I'm always in awe of my pathologists to be able to tell the difference in types of cancer just from the small amount of tissue that we give them. There's so much variety. I think we're getting better and better. In the last three, four, five years, things have sort of rapidly moved in a direction that nobody anticipated just from 10 years ago. So always the hope is to get rid of it, but it's not one thing. It's not that simple.”Dr. Field says the main things patients can do to prevent cancer are the things we do for ourselves every day.“Two-thirds of cancers can be prevented by things like not smoking and eating healthy and exercising. Several of the cancers I take care of are really helped by people who live a healthy lifestyle; that's probably the biggest thing you can do. The next step is to see your doctor yearly. For women, I think they should be seeing their gynecologist yearly. They're going to screen them for cancers, like cervical cancer, and ask them questions related to the other types of cancers that I treat. “If they notice differences in their body, like bleeding when they haven't had a period in a long time or problems where they're losing weight and not really trying to lose weight or having trouble eating or problems using the bathroom or new pains or discomforts that they haven't had before and those symptoms stick around for three weeks, they should get those checked out by their primary doctor and their gynecologist. Usually, the way I see patients is their excellent primary doctors have picked up that something's wrong and oftentimes sent them for tests or imaging. By the time I see them, it's very obvious what's going on, whereas it can sometimes take weeks, months, and even a year to figure out that first part, who they need to see.”MSU Today airs Sunday mornings at 9:00 on 105.1 FM, AM 870, and wkar.org. Find “MSU Today with Russ White” on Spotify, Apple Podcasts, and wherever you get your shows.
Michigan State University Health Care and Karmanos Cancer Institute at McLaren Greater Lansing have welcomed their newest physician, Jayson B. Field, MD.
In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez, is joined by Dr. Brian Slomovitz to discuss asbestos and ovarian cancer. Dr. Slomovitzs is a Gynecologic Oncologist at Broward Health and Professor of Obstetrics and Gynecology at the Wertheim College of Medicine at Florida International University. He is an internationally recognized leader in gynecologic oncology clinical trials, specifically in immunotherapy and novel biomarker therapeutics. He also is a leader in sentinel lymph node detection for gynecologic malignancies. Highlights a. Asbestos comprises a family of small silicate fibers that are found in nature. b. Asbestos is known to cause different types of cancer. c. The causal association between asbestos and ovarian cancer is weak and inconsistent d. Peritoneal mesothelioma is histologically similar to ovarian cancer and pathologic confirmation of diagnosis is required before causal assumptions are made
Hello and welcome to the latest episode of our podcast P for Parenting. Anubha and Anjali are back with a very powerful show discussing things that people tend to avoid. This week P for Parenting is talking all about women's well-being. About the guest: This week P for Parenting is in talks with Dr. Kanica Batra Modi. She is a Gynecologic Oncologist at Max Institute of Cancer Care, Max Hospital, Saket, Delhi. If you want to connect with her mail her at kanica.batra@gmail.com They talked about: -The importance of a gynecologist in the life of a woman -Types of gynecologists -How frequently women need to visit their gynecologist? -Types of cancer gynecological cancer -The menstruation cycle. Also, check out: -Let's talk Toilet Training: https://srmpodcasts.com/lets-talk-toilet-training/ -What is Positive Parenting?: https://srmpodcasts.com/what-is-positive-parenting/ -What it takes a mom to be an Entrepreneur?: https://srmpodcasts.com/what-it-takes-a-mom-to-be-an-entrepreneur/ If you have any query, mail us at contact@srmpodcasts.com
September is Gynecologic Cancer Awareness Month, so it's the perfect time to learn about cancers of the cervix, vagina, vulva, ovaries and uterus, including early detection and prevention. Dr. Oakley and Dr. Kevin Schuler, a gynecologic oncologist with TriState Gynecologic Oncology, and sees patients at the St. Elizabeth Cancer Center, discuss what diagnosis and treatment look like and ways to reduce the risk of developing these types of cancer. The Lady Bod Podcast is presented by St. Elizabeth Healthcare and Physicians
In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez, is joined by Drs. Gregg Nelson and Geetu Bhandoria to discuss the ERAS Global Survey. Their article, "Enhanced Recovery After Surgery (ERAS) in gynecologic oncology: an international survey of peri-operative practice” (https://ijgc.bmj.com/content/early/2020/08/28/ijgc-2020-001683), is the Lead Article in the October 2020 of IJGC. Dr. Gregg Nelson is Professor and Chief of Gynecologic Oncology at the Tom Baker Cancer Centre in Calgary, Alberta, Canada. His main research interest is the development and study of Enhanced Recovery After Surgery (ERAS) protocols in cancer and ObGyn surgery. Dr. Nelson is Secretary of the ERAS Society. Dr. Geetu Bhandoria is a Gynecologic Oncologist and obstetrician at Command Hospital in Pune, India. He as completed fellowship in Gynecologic Oncology. His research interests are advanced ovarian cancer, enhanced recovery protocols and the use of social media as a research tool. He is also currently serving as one of IJGC’s Editorial Fellows.
September is Gynecologic Cancer Awareness Month, so it’s the perfect time to learn about cancers of the cervix, vagina, vulva, ovaries and uterus, including early detection and prevention. Dr. Oakley and Dr. Kevin Schuler, a gynecologic oncologist with TriState Gynecologic Oncology, and sees patients at the St. Elizabeth Cancer Center, discuss what diagnosis and treatment look like and ways to reduce the risk of developing these types of cancer. The Lady Bod Podcast is presented by St. Elizabeth Healthcare and Physicians
In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez, is joined by Emeline Aviki to discuss hospital volume and outcomes in early cervical cancer. Dr. Emeline Aviki, MD, MBA is a Gynecologic Oncologist at Memorial Sloan Kettering Cancer Center and former research fellow in the health outcomes research group at MSKCC. Dr. Aviki's research focus is in health outcomes and care delivery innovation to improve the affordability of care for patients.
Cancer Care Today - Leading Cancer Doctors talk about the Latest Treatments
Get to know Lori Weinberg, MD, gynecologic oncologist and surgeon with Minnesota Oncology as well as mother to three children ages three and under. In this episode, Dr. Weinberg discusses the latest updates in gynecologic cancers such as ovarian and cervical cancer as well as what has changed in surgery and medical oncology due to COVID-19. Learn more about Minnesota Oncology team approach to cancer care and how Dr. Weinberg and her team work together for the best outcomes for patients. HOST: Dave Swerdlick This podcast is provided for general informational purposes only. In no event will the Practice be liable for any action taken upon the information or content contained in the podcast. © MMXX MnOncology.com- All Rights Reserved.
Join us as we explore the importance of pap tests, what really causes cervical cancer and how you can protect yourself. We'll be discussing the latest guidelines in Canada so you know when your pap is due, how your immune system can fight cervical cancer, what you can expect if you have an abnormal pap, and more! Featuring Dr. Schepansky a Gynecologic Oncologist in the Department of Obstetrics and Gynecology at the University of Alberta. Her practice is based at the Cross Cancer Institute and the Royal Alexandra Hospital in Edmonton. She has done work as the Chair of Colposcopy Quality Improvement Committee for the Alberta Cervical Cancer Screening Program. Resources: (1) Screening For Life (includes info on cervical cancer and a risk assessment tool): http://screeningforlife.ca/cervical-cancer-at-a-glance/ (2) Choosing Wisely: https://choosingwiselycanada.org/pap-tests/ (3) Canadian Cancer Society: https://www.cancer.ca/en/cancer-information/diagnosis-and-treatment/tests-and-procedures/pap-test/?region=on (4) My Health Alberta: https://myhealth.alberta.ca/Health/pages/conditions.aspx?hwid=tw9600 (5) Alberta Health Services - A Patient's Guide to Colposcopy: https://www.youtube.com/watch?v=57EXw9oU9TA&feature=youtu.be Summary Sheet: CervicalCancerandPapTests.html
We all know and love Cobie Smulders in her roles as Robin Scherbatsky on How I Met Your Mother and as Maria Hill on the big screen film, Avengers. What may surprise you is that she was diagnosed with ovarian cancer when she was 25 years old. Cobie knows firsthand the emotional toll the disease and the high threat of recurrence can take on women and their loved ones. She has partnered with biopharma company Tesaro and directed a PSA for Not on My Watch https://www.notonmywatch.com to empower women with recurrent ovarian cancer to take a proactive role in managing their disease. Each time Cobie's PSA is shared on social media, Tesaro will donate $5 to ovarian cancer patient organizations! So, please share! Cobie is joined by Dr. Amina Ahmed, Visit www.MD.com/doctor/amina-ahmed-1-md for information about Dr. Amina Ahmed, Gynecologic Oncologist in Illinois.
034 - Women's Cancers: The Importance of Knowing Your Body with Dr. Noah Goldman "It's about knowing yourself and knowing what's normal for you... taking the initiative to seek help if there's something that just doesn't seem right to you." --Dr. Noah Goldman Today Dr. Goldman and I talked about: The Importance of listening to your body ALWAYS have abnormal bleeding checked by a doctor. It probably isn't cancer, but it's a sign something isn't right. Why you should have your screenings, even as you get older. Why to do monthly breast self-exam. How often to have mammogram and pap screenings. Symptoms of women's cancers - (Many times there aren't any symptoms.) Cervical: Abnormal bleeding, abnormal vaginal discharge Uterine: Abnormal bleeding Ovarian: Abdominal pain and bloating, urinating more frequently, abnormal bleeding. Often there are no symptoms. See your doctor if you believe there might be a problem, that's why they're there. New cancer treatments including biologic treatments We talked about more, listen to find out the rest. Who is Dr. Noah Goldman? Dr. Goldman is a board certified and fellowship trained Gynecologic Oncologist and serves in the role of Associate Professor and Vice Chair of Clinical Affairs, Obstetrics, Gynecology and Women's Health, and the Associate Division Director of the Division of Gynecologic Oncology at Rutgers New Jersey Medical School and Rutgers Cancer Institute of New Jersey. Previously, Dr. Goldman served as the Subspecialty Director of Gynecologic Oncology at The Valley Hospital in Ridgewood, New Jersey. He previously held academic and teaching positions at the New York University School of Medicine and Albert Einstein College of Medicine/Montefiore Medical Center. Dr. Goldman treats women with preinvasive and invasive disease of the female genital tract including cervix, uterine, ovarian, vulvar, and vaginal cancers. He has a special interest in the use of minimally-invasive surgery to treat women with gynecologic malignancies as well as complex gynecologic issues, including the use of the DaVinci® Robotics System. He has taught on this subject at national and international meetings and published in peer-reviewed literature. Dr. Goldman earned a Doctor of Medicine degree from the University of Medicine and Dentistry of New Jersey - New Jersey Medical School and an undergraduate degree in Biochemistry from the University of Rochester. He also completed an internship and residency in Obstetrics and Gynecology at the Mount Sinai School of Medicine in New York, where he also served as the Administrative Chief Resident. Dr. Goldman completed his fellowship in Gynecologic Oncology at Albert Einstein College of Medicine and Montefiore Medical Center in the Bronx, New York. Dr. Goldman's advice to women: Know yourself and know what's normal for you. Take the initiative to seek help if there's something that just doesn't seem right to you. Go to the doctor and have your screenings. Dr. Goldman's superpower: The ability to help people feel calm. Patients walk into his office anxious because of the word cancer, but leave knowing they'll be taken care of. Where to find good information about women's cancer: Society of Gynecologic Oncology: sgo.org - And - To learn more or connect with the Foundation for Women's Cancer (FWC), please visit their website at foundationforwomenscancer.org or follow the FWC on: Facebook: facebook.com/foundationforwomenscancer Instagram: instagram.com/foundationforwomenscancer Twitter: twitter.com/GYNCancer Want to connect? You can find me (Jen): Instagram: https://www.instagram.com/thejenhardy/ Facebook: https://www.facebook.com/authorjenhardy Chronically Positive Moms Group on Facebook: https://www.facebook.com/groups/chronicallypositivemoms/ Thank you for joining me today! Want more? Go to HardyMom.com and you'll find ways to live well, grow, and enjoy your life again -with any health challenges. I'd love to hear what you think about this episode! Send me a message at HardyMom.com/contact Have a blessed week, Jen p.s. Why am I interviewing someone who isn't a woman or a mom with a chronic illness? Listen until the end and find out! Like the show? It would be great if you could help out by subscribing and rating it on your favorite podcast app. Our music is "A New Day," by Scott Holmes
In this episode, with the help of Dr. Jimenez, a Gynecologic Oncologist from the Juravinski Cancer Centre, 3rd year McMaster medical student Emma Herrington discusses an overview of, and approach to, endometrial cancer. After listening to this episode, learners should be able to: Have a general approach for classifying the different histopathologies of endometrial cancer Develop an overall framework of staging Relate staging to treatment options
In this episode, with the help of Dr. Jimenez, a Gynecologic Oncologist from the Juravinski Cancer Centre, 3rd year McMaster medical student Emma Herrington discusses an overview of, and approach to, endometrial cancer. After listening to this episode, learners should be able to: Recognize the common clinical presentation of endometrial cancer; Understand how to diagnose endometrial cancer;
In the world of electronic health records, and an increase in the aging population, many physicians find themselves subjected to more intense scrutiny of quality and performance, while they face an ever increasing patient load. They can experience depression and burnout the way many professional do, however, as physicians they may be tempted to care for others before they care for themselves. Here to discuss the consequences and possible solutions to worrisome physician burnout is J. Michael Straughn Jr.,MD. He is a Gynecologic Oncologist at UAB Medicine.
Borderline ovarian tumors represent a small subset of epithelial ovarian tumors. Because it's an uncommon and unfamiliar diagnosis, it's often misunderstood.Joining the show to discuss the prognosis for a low malignant potential ovarian tumor, and treatment options available, is Peter Frederick, MD. He is a Gynecologic Oncologist with Roswell Park Comprehensive Cancer Center.
Borderline ovarian tumors represent a small subset of epithelial ovarian tumors. Because it's an uncommon and unfamiliar diagnosis, it's often misunderstood.Joining the show to discuss the prognosis for a low malignant potential ovarian tumor, and treatment options available, is Peter Frederick, MD. He is a Gynecologic Oncologist with Roswell Park Comprehensive Cancer Center.
The FDA recently approved a molecular test for HPV DNA as a first-line, stand-alone screen for cervical cancer. It's controversial, especially when you compare the cost. Guest: Dr. Rick Boulay, Gynecologic Oncologist. We discuss many issues associated with cervical cancer screening, including testing guidelines, over-diagnosis, and whether boys should get the HPV vaccine. Co-Host Dr. Peter Hofland, www.oncozine.com. Joni live M-F at 2:00 p.m. ET on www.W4CS.com. www.JoniAldrich.com
WORD of HOPE Ovarian Cancer Podcast. Episode 06, Topic 8 of 10.This is the sixth episode in the series of "10 Exciting Ovarian Research Topics from 2010". This episode focuses on Neoadjuvant Chemotherapy in Late Stage Ovarian Cancer and the importance of getting to a Gynecologic Oncologist when treating Ovarian Cancer. Be sure to look for the remaining topics of this series in subsequent episodes of WORD of HOPE Ovarian Cancer Podcast. For show notes, links, info, and how to subscribe, visit: www.wordofhopepodcast.com
Moderator: Floor Backes, MD, Gynecologic Oncologist, The Ohio State University Comprehensive Cancer Center Speakers: Vicky Makker, MD, Medical Oncologist, Memorial Sloan Kettering Cancer Center Matthew Powell, MD, Gynecologic Oncologist and Chief, Division of Gynecologic Oncology, Washington University School of Medicine Siteman Cancer Center Amanda Nickles Fader, MD, Gynecologic Oncologist and Professor, Johns Hopkins School of Medicine Description: Dr. Floor Backes is joined by Drs. Vicky Makker, Matthew Powell, and Amanda Nickles Fader to discuss best practices in utilizing molecular and pathologic tests to inform treatment of patients with recurrent metastatic endometrial cancer. The conversation begins with a patient case for the panelists' discussion, followed by a series of scenarios to provide context for different considerations in the therapeutic regimen based on the patient's molecular and sequencing results, histology, and response to treatment. This podcast was developed by the Society of Gynecologic Oncology for Gynecologic Oncology.Additional Resources: SGO ConnectEd: Chemotherapy & Targeted Therapy Flash Cards
Moderator:Leslie Clark, MD, Gynecologic Oncologist, University of North Carolina in Chapel Hill Speakers: Róisín O'Cearbhaill, MD, Medical Oncologist, Memorial Sloan Kettering Cancer Center Ramez Eskander, MD, Gynecologic Oncologist, University of California San Diego Description: Dr. Leslie Clark presents a patient case to frame a discussion on the management of immunotherapy-related toxicities in gynecologic cancers. Drs. Róisín O'Cearbhaill and Ramez Eskander provide clinical management strategies for adverse events that gynecologic oncologists commonly encounter, such as diarrhea, rash, and hypothyroidism, as well as their approaches to situations that can be more difficult to discern, such as pneumonitis. This podcast was developed by the Society of Gynecologic Oncology for Gynecologic Oncology. Editor's Choice Paper: Immunotherapy toxicities: An SGO clinical practice statement