Podcasts about oncotype

In this episode Shannon and I talk about her dual diagnosis and how her career helped her navigate her diagnosis which in turn has helped so many others.Shannon talks about her diagnosis, her family history, and the importance of the Oncotype test to ehlp others with their decision after their diagnosis. She also expresses how important it is to make sure you have a great team to navigate your journey with.Shannon is a true example of someone helping me Change The World, One S.M.I.L.E. At A Time by leading by example at such a young age. Cancer does not discriminate!➡️If you or someone you know would like to be a guest on our podcast, please email SMILE@shannonburrows.com➡️If you have any real estate needs anywhere in the world, please email shannonburrowsrealtor@gmail.comFollow Shannon Haynes at:● Email:  Shannonhaynes2@yahoo.comFollow us at:● Personal Instagram: @‌shannonmburrows● Podcast Instagram Page: @‌bustinoutofbreastcancer● Personal Facebook: Shannon M Burrows● Podcast Facebook Page: Bustin' Out of Breast Cancer PodcastDon't forget to Follow, Subscribe and Share this podcast so you can help us Change The World, One S.M.I.L.E. At A Time!

Welcome to The Hormone Prescription Podcast, where we bring you inspiring stories and expert insights to help you elevate your health and wellness. Today, we're excited to have the energetic and passionate Emmy-winning TV host, Samantha Harris, join us to talk about her incredible journey to health and wellness. Her story begins with a shocking breast cancer diagnosis at the age of 40, which led her to rise above the challenge and become a breast cancer "thriver." Samantha channeled her energy into becoming a Certified Health Coach, trainer, and author of the bestselling book "YOUR HEALTHIEST HEALTHY: 8 Easy Ways to Take Control, Help Prevent and Fight Cancer, and Live a Longer, Cleaner, Happier Life."    In this episode, you'll discover: - How Samantha's life took an unexpected turn with her breast cancer diagnosis - The ways in which she fought and thrived despite the challenge presented by this life-changing event  - The inspiration behind her bestselling book, "YOUR HEALTHIEST HEALTHY: 8 Easy Ways to Take Control" - Samantha's perspective on health and wellness as a Certified Health Coach and trainer  - The importance of taking control of your health and living your healthiest, happiest life   If you're inspired by Samantha's story and want to learn more, subscribe to The Hormone Prescription Podcast for more uplifting stories and informative interviews.    Remember to stay healthy, stay inspired, and keep on listening!   Speaker 1 (00:00): Keep doing what you're doing and you will keep getting what you're getting. Samantha Harris, stay tuned for amazing story of healing from breast cancer and beyond to your healthiest healthy. Speaker 2 (00:14): So the big question is, how do women over 40 like us keep weight off, have great energy, balance our hormones and our moods, feel sexy and confident, and master midlife? If you're like most of us, you are not getting the answers you need and remain confused and pretty hopeless to ever feel like yourself Again. As an ob gyn, I had to discover for myself the truth about what creates a rock solid metabolism, lasting weight loss, and supercharged energy after 40, in order to lose a hundred pounds and fix my fatigue, now I'm on a mission. This podcast is designed to share the natural tools you need for impactful results and to give you clarity on the answers to your midlife metabolism challenges. Join me for tangible, natural strategies to crush the hormone imbalances you are facing and help you get unstuck from the sidelines of life. My name is Dr. Kyrin Dunston. Welcome to the Hormone Prescription Podcast. Speaker 1 (01:07): Hi everybody. Welcome back to another episode of The Hormone Prescription with Dr. Kyrin. Thank you so much for joining me today. You're gonna love my guest today. She has an amazing story of healing from breast cancer and beyond, to becoming her healthiest healthy, and now that's what she's gonna help you do is become your healthiest healthy. In this episode, she is passionate about health and healing, but more than that, vitality and living a full and meaningful life. So she's gonna teach you all about that. She's very inspiring and she has some amazing wisdom to share about detecting breast cancer, trusting yourself and so many other things. It's just too much for me to tell you. You're gonna love this episode and we're gonna dive into the teaser that I shared with you. Keep doing what you're doing and you'll keep getting what you're getting, which is kind of a motto that she lives by. Speaker 1 (02:04): And she's gonna talk about how being kind to herself and really slowing down has been vital to becoming her healthiest, healthy, and might be a key to yours and so much more. So let me tell you a little bit about Samantha and then we'll get started. She's an Emmy winning TV host and she may be best known for her eight seasons as the host of Dancing With the Stars and Years as host of host, such as Entertainment Tonight and Extra from hosting every major Hollywood award show red carpet to starring on Broadway in the musical Chicago. She has been a fixture in the entertainment world. She's currently the host of the World play Game show, tug of Words on Game Show Network. Please help me welcome Samantha Harris to the show. Dr. Kier, I love what you do and how you really help. You know, as a, as a breast cancer survivor who's had to deal with a lot of hormonal issues because I had a hormone positive breast cancer, I am grateful for all the information that you put out there for anyone, whether they've had a deal with a diagnosis or not. Speaker 1 (03:08): So thank you for that. Oh, it's my pleasure. It's my passion. It's what I love doing. You know, when I discovered a root cause resolution way to heal my body and lose a hundred pounds and get off all the medications, I said that I would commit my life to teaching other women about this. And so that's why we're here. And I know that you have an amazing story about having estrogen. Was it estrogen receptor positive breast cancer? Oh yeah, pro progesterone, both. And, and so breast cancer is the thing that scares women more than anything. We're all petrified about getting breast cancer, I guess, because so many of us will get it in our lifetimes. It's not common to have your life shortened by it anymore because we have such advances in treatment. But it is possible. My maternal grandmother actually passed away at a very young age due to breast cancer. Speaker 1 (04:02): So I'm wondering if you could share your journey with everyone. Absolutely. And I think that it is so important to be able to let women know that we have so much more power and control than we may think. So as I've been a national ambassador for Susan g Koman, probably because of all my time hosting, dancing with the Stars in Entertainment Tonight and all of those and having a, a great national platform for that, but since my breast cancer diagnosis. And so I learned that one in eight women will receive a breast cancer diagnosis over the course of her lifetime, which a alone was shocking, but to me the most shocking part of it was that only five to 10% of those breast cancers are actually hereditary. And when I found out, because I had a, a grandmother who had breast cancer and now she was postmenopausal, so they don't connect premenopausal like mine to hers. Speaker 1 (04:52): She lived to 95, thank goodness my dad had colon cancer died at age 50, but he also had Crohn's disease before that. And there are, there is a breast colon hereditary connection. We looked at that, no connection there. So I had no, and I've done 180 genetic tests that are currently available for breast cancer. None of them detected it. So I'm in that 80 or 95, you know, to to 90, 95% of people who don't have a genetic predisposition. Right. And I'm sure there's probably, sure you could throw up a random number like 5% that are just, gosh, who knows what the heck it is. It's some sort of fluke. But, so let's say now that we're at like a good 85 to 90% of breast cancers being not genetic, not being able to be chalked up to some crazy other thing happening in their body. Speaker 1 (05:44): And we know the power of epigenetics, right? How our habits and lifestyle choices and our environment that we are living in impact our risk of disease in this case. Mm-Hmm. breast cancer, that was one of the most empowering things that I learned in my early cancer. Versity when I was learning as much as I possibly could. And so as a journalist, I started a research journey to seek out answers. Why are so many women getting it? Why when the hereditary links are so few? And I found it really is what we are putting in and around our bodies that leads not just to breast cancer but other cancers, type two diabetes, heart disease, neurodegenerative disorders and decline. And when I learned that, it made me realize, wow, there's so much more for my health and my outcome of my future that I have con potential control of. Speaker 1 (06:36): And I kept, took my power back, I was back in the saddle, I took the reins and I started to make slow but systematic changes in my life. Yeah, I love what you said and how you outline that 90 to 95% of what goes into causing breast cancer is under your control. And, but we're really taught that we're powerless, that we're at the whim or victimization of some nebulous kind of cancer causing God. But the truth is, it's what how we're living your lives, right? Which is what you teach people about in your programs. It's what we're putting in our mouths, what we're putting in our bodies, what we're putting on our hair, what we're not getting rid of, right? What we're not pooping out, what we're not peeing out. Yes. All of these disruptors. So yeah, share a little bit about your journey. I did see, you know, on your website you have some very personal pictures of you going through some very specific cancer treatments. Speaker 1 (07:33): If you would love to talk about that. I'm sure women would love to hear about how you survived that very difficult time, what it was like for you. And then coming out of that, what was it like the, the ultimate healing that you did after they got rid of the cancer? Well, I think sharing my journey is really important to me. And, and this is why we have to be our own best health advocates. We need to know our bodies better than anyone else, including the person in the lab coat with all respect to those of you who are in the profession of medicine. And then goodness you are. But we need to know our bodies better than the doctor we're walking into the room with. And that means noticing small changes and not bearing your head in the sand when you find them. So I had a clear M mammogram. Speaker 1 (08:17): I was about to turn 40, this is in 2014 actually, 2013. And the results came back clear. It's exactly what I had anticipated because I was the healthy one among my friends and family. I worked out every day I ate my cheese list pizzas and my snack well cookies that were low fat cuz god forbid we eat any fat , you know, I had a meal of red vines because they were fat free. Oh my God. They were the, I had literally, I would go and buy like from smart and final or Costco, like the tub of red vines cuz they would advertise fra fat free food. So I thought free fine to have, forget the fact that I now have learned it's high fructose corn syrup and red dye 40 and all these very harmful and cancerous things. But I didn't know that at the time. Speaker 1 (09:00): Right? And so here I am, I'm thinking I'm so healthy and I'm eating copious amounts of animal protein. Breakfast, lunch, dinner, whether it was yogurt or eggs for breakfast and Turkey or chicken or fish or something for lunch and dinner every single day of the week. And I grew up in Minnesota eating every part of the cow. There was so a lot of, a lot of animal in my life. And then here I was, you know, blindsided by this breast cancer diagnosis, which I didn't know because I had a clear mammogram. 11 days later I found a lump changing after a workout, again, knowing your body. And you know, you know, you take off that really tight constricting sports bra and you circle 'em to the left, you circle 'em to the right, you know, you gotta get them moving again. And there I was circling and I went, oh well that's weird. Speaker 1 (09:44): What is, what's that lump? I, that's definitely not been there before. But I just had a clear mammogram 11 days before that still didn't stick my head in the sand, didn't realize I needed to be my best health advocate. But I still called the ob. G Y n had me come in the next day, felt around, said it's nothing you, you're returning 40, it's probably glandular. This is what 40 year old breast looked like. Sent me on my way. Said it was nothing a month later, still there, but of course not breast cancer. So went to see my internist, same thing, quick clinical exam, it's nothing sent me on my way. And then it was the holidays and by the time I came up for air, it was about four months after I found that lump and it was still there. And I finally listened to my, now my inner voice screaming at me saying go to someone who looks at breasts every day and that only that the only expert who does is a breast oncologist. Speaker 1 (10:36): So I found myself at a cancer center thinking this is ridiculous. I don't have cancer, why am I here? And she did two ne two ultrasounds, a needle biopsy, a subsequent M r i, after those appointments, not one test detected the cancer. And yet she said, you're not crazy though. There's something there. So I'm going to advise. We do a lumpectomy. And we took it out, woke up from that surgery still saying no cancer. Went back a week later, told my husband, you don't need to come with me. It's not cancer. Go literally. I told him, go golf, it's a gorgeous day. Don't waste it in a dark, you know, office in the bottom of basement of a hospital with me. And then I was alone as the words you have ductal carcinoma and site do. And I'm trying to unravel what the heck that means. Speaker 1 (11:16): But I just heard the word carcinoma and I knew that meant cancer and lots of diagrams and dots and things she was drawing. And I, all of a sudden the adrenaline and the anxiety and the overwhelm and the scared feelings and every emotion you can imagine hearing you have cancer. My daughters were, our daughters were three and six at the time. I lost my dad when he was 50 and here I was at 40 and I thought like hell, I'm not gonna be there for my kids. And that's when my cancer journey began. And that was, that was 40. Wow. Turning 40 is an event for all of us, but certainly sounds like it was an extreme sport almost for you or an extreme life event. And so then what type of treatment did you undergo for that? So the, this is when you know a lot of personal choice comes into effect as well as many opinions. Speaker 1 (12:03): So again, taking your health into your hands and be your own best healthcare advocate. Don't take doctor number one's information as the only, you know the word of God. So literally within the span of a week I saw two more surgical oncologists. So three opinions. I took the lab results to a separate pathologist at a different university hospital just to make sure because we were all basing, you know, it on one lab reading. So we made sure that they agreed that it was actually this particular cancer. Mm-Hmm . It turned out that not only was it ductal carcinoma in situ, which is contained within the duct and really the kind of breast cancer you want because they take it out, it's gone. You're all good. Mm-Hmm . But finding great experts is really important because she listened, the surgeon listened to her gut and in the surgery she said, you know, there was an area on the border, it looked like healthy tissue. Speaker 1 (12:53): But for some reason my, my inner voice was saying I needed to take a sample that turned out to be invasive breast cancer. Oh my gosh. So in that moment, my breast cancer journey went from breast cancer light to breast cancer. Serious. And now it was not, you're done now cuz you had the lumpectomy, but it's okay, what's next? So my options were another lumpectomy to make sure we had clear margins and then six weeks of radiation every day or mm-hmm. A single or double mastectomy with or without reconstruction. I opted for the double with reconstruction. I saw multiple, I saw two different radiation oncologists to get their opinions. I saw, I have a second medical oncologist. So I had two opinions about chemo and treatment going forward in the end. And you guys, anyone who is out there listening and maybe newly diagnosed or one what to do, please feel free to always DM me and ask me questions. Speaker 1 (13:44): I respond to every single woman who is worried about a cancer diagnosis or is diagnosed and it is Samantha Harris tv, like television on Instagram and, and Facebook, Samantha Harris tv. But then I can explain why I chose not to do the chemo and not to do the radiation. Mm-Hmm . And it's a very personal decision of it on the chemo. Cause a lot of people will probably wanna know is I had a very low Oncotype score, which really show, and I had a very small tumor. So it, to me that was the decision. And now, now, you know, 2014 to now all these years later, I am very grateful that I didn't undergo chemo because of everything else I now know. However, had it been in a much more aggressive tumor, I don't think I would've made that choice. Right. And that's a very personal decision, like you said. Speaker 1 (14:29): So if there is anybody listening and you've got every sin cancer diagnosis, I love what you said about getting second opinions, even third opinions, really you do have to be the ceo, get all the information and then make a wise choice for yourself. So I do wanna have that disclaimer that what you necessarily did might not be right for someone listening. So get your healthcare providers and consult and yes, definitely reach out on social media if you do have questions, because I think the more people you can talk to about what's going on with you personally, the better you are. But no one person is the guru for you. You are the expert on your body and your health. I love how you really demonstrated that Samantha, by, even though you had a negative mammogram, 11 days later you felt a lump and you didn't just discount what you felt about your body. Speaker 1 (15:26): And I want every woman listening to really hear that because part of what I want you to learn is that you really are the expert. Nobody else can tell you when your body is working on all cylinders at a hundred percent you'll know that inside yourself, in your skin when you feel at home and you have great energy and your weight is where you want it to be and your sleep and your hair and your libido and yes, all the things. So after you got out of the acute phase, your oncologist doctors, they're like, okay Samantha, you're good. We're gonna follow you pretty closely I would imagine. But yes. What did you then do for yourself that you now teach other women? Well, this was the biggest thing, again, the eyeopening that we can be in better control of our health and our health future than we realized. Speaker 1 (16:18): So I put that journalist hat on tightly and I dug into research and I spoke to every expert I could and I sought out opinions and answers and asked some really deep questions. And here I was, you know, living my life thinking I was healthy, living my career in a makeup chair every single day. Being as any, whether you're working on TV like very few of us, or doing the nine to five or the mom 6:00 AM to 11:00 PM we all put on makeup or potions and lotions and hair stuff and whatever the shellacking that was done of chemical bombs of potential harmful carcinogens and endocrine disruptors with mess, mess with our hormones, allergens, neurotoxins that are in our products that our own f d A here in the US approves no big deal. No oversight from these companies. No responsibility from these big brands. They just market to us. Speaker 1 (17:13): It's October Pink ribbons, slap it on, but hey, we're also giving you breast cancer at the same time. So yes, it sounds very cynical, but I've learned so much and yeah, I'm saying overnight you need to throw out everything in your house and start over. But making small methodical changes that end up changing how you are living your day-to-day life is, is really important. And so I realized the makeup and the haircare I was using the personal care products at home, the cleaning supplies all were filled with toxic junk. The foods I was eating and how I was eating and when I was eating all were really not coming into play to make me live my healthiest healthy life. See, I thought I was healthy and I realized I needed to be my healthiest healthy. And that's, that's why, you know, my whole thing has now the your healthiest healthy from the your healthiest healthy book that really launched a whole program, a membership community with my life coaching and workouts and experts to my live, my courses that are offered and my retreats and really just answering anyone I possibly can through social media and putting as much information out there so that we have the, the tools at our disposal. Speaker 1 (18:23): So what were some of the most, you mentioned general categories, makeup, cleaning products, the things you were eating, what were some of the, the specific things that really shocked you when you're like, oh, and I mean maybe you don't wanna mention name brand names of products. I just realized that honestly any major big brand is pretty much like anything. You go to the department store pretty much you can is has a lot of toxic chemicals in it anytime you go down to the drugstore aisle, most of it also pretty toxic, thank goodness. And I will tell you the difference between now and back in 2014, thankfully we have so many the demand as consumers, right? They're finally hearing us, right? Even the big, big brands are starting to have little offshoot brands or an offshoot line of, I mean whether it's, you know, big brand x deodorant that is filled with aluminum and other toxic stuff. Speaker 1 (19:16): Now they have their aluminum free version because they realize they were losing some of the market share. And more and more, more kind of mom and pop shopper boutique like makeup brands and skincare brands are now becoming more str mainstream. You go into a place like a Sephora, they finally, and even Target, they finally have their clean brands. I have to look into what their requirements are. I don't know if they're like Samantha's level of clean, but you know what, it's a much baby steps. Might as well start there and you can always level up from there after that. Yes. And I'd say for anyone curious, if you want to look@ewg.org environmental working group.org, they list a lot of the mainstream brands and they, they give the products ratings. They tell you the ingredients that are toxic. But, and yes, a lot of these big brands are offering so-called quote unquote non-toxic products. Speaker 1 (20:10): I say that with little quotes, my fingers in the air because they're aware that consumers know certain ingredients are toxic, but they're also aware that consumers are not so educated that they will miss certain other names. So they will actually create different ingredients that have different names that you won't recognize that are probably toxic too. So I find, and what I've done and what I teach my people to do is find the small brands that really are 100% non-toxic and all natural and they just don't have any chemicals. And you're not not gonna find 'em in a big box store. You might find a lot of them online and ask for referrals from friends. There are a lot of blog posts now where you can kind of Google top 15 all natural makeup brands and then research it yourself. Don't take their word for it and discover what's best for you. Speaker 1 (21:05): What guidelines do you offer for that? Well, first of all, I you, you already brought up the Environmental Working Group, which is a fantastic resource. They're a nonprofit. I love their one through 10 ratings. One being the cleanest for an overall product or one also being ingredient to ingredient, how toxic that ingredient is. 10 being like runaway fragrance. By the way, red alert is a nine and that's because fragrance is proprietary. So if you have fragrance as an ingredient and that company isn't being transparent and this clo what that fragrance is made of within the product, stay away from it. Because it oftentimes has a lot of one four dioxane, which is a, an endocrine disruptor. It has phthalates, which are endocrine disruptors. And another great point Dr. Karen that you made, which is that a brand might say here's our clean version, but, and it doesn't have to be quote unquote all natural because that also there are synthetic chemicals that are not harmful that the, the good brands will make sure that they are transparent and disclose that are in the ingredients labels. Speaker 1 (22:07): So, cause I think people get scared away with all, all natural, that's not gonna work for me. It's not gonna have the staying power if you guys want. So I just finished shooting 65 episodes of a TV show and I had my hair makeup team who I've worked with for many years who are more than happy, they jumped at this and I was so happy we became teammates in this. I said, look, I'm going back on tv, I don't want toxic stuff in the dressing room every day on my face and our hair, us breathing it in. So before we shot, I tasked them with a challenge which was only bring in clean. And if you have a question about it, send the brand my way. I will vet it and let you know if I, if I'm like, it's approved or it's not. And Uhhuh tried a lot of different brands because there are a lot of clean brands. Speaker 1 (22:51): But then do they work? Is they, are they effective? Do they give you the appearance that you want on your face or with your hair? Do they have the lasting power? And I was shooting 12 hours a day, six episodes a day. So it was a very intense schedule. So if you want my list as you're listening of Clean Beauty that's been vetted, skincare, makeup, haircare, send me a DM on, mostly on Instagram, but you can try me on Facebook, Samantha Harris tv, like television, I will send you my list. I don't have skin in the game with most of the brands or anything like that. There are one or two that I've partnered with, but you don't have to use them. I'm gonna give you all the info and be straight up with you. Awesome. That's so generous. I hope you will take her up on that offer. Speaker 1 (23:30): And I know that in your healthiest healthy eight easy ways to take control is one of those switching out your your beauty products. It is, it is. It's a huge step. And again, it doesn't have to be overnight baby steps. So let's say you're like, okay, I'm ready to switch out my makeup. I know how much money we spend on makeup and all of these things. Mm-Hmm. , right? So I'm not saying go dump out your drawer tomorrow, but maybe start with, in terms of skincare and makeup, start with your lotion, right? Your face cream. Cuz you're covering the biggest amount of skin and surface area, which of course is our biggest organ. It's absorbing all of it into our bloodstream and then your foundation and then level up from there. Maybe it's lipstick because you're eating a lot of it, you know, then maybe move to blush and eyeshadows and so on and just start to level up. Speaker 1 (24:18): And the other thing for feminine care, and I know, you know, some of you may already be menopausal and you're not having to deal with menstrual cycles, but for those of you who are still, or you're at that later stage and you're having urine leakage and you have to have those types of pads, make sure that they're 100% organic cotton. Because if I show you what is in, we're talking about the bleach, the cotton that's been grown and and sprayed with Monsanto, glyphosate, and all these other horrible toxic chemicals, and you're putting it next to your most thin permeable skin. No, no, no. Or inside. No, no, no, no, no. , you do not wanna do this. So that's, that's my other little public service announcement. Preach Samantha, preach please. I love it. Right. So, you know, they, people hear people like me out here saying this stuff all the time, but it's about time. Speaker 1 (25:10): I love that you come from kind of a more traditional journalist background and that you discovered all this for yourself. I hate how you had to discover it. And I love that you're sharing this information and you're empowering women with this vital information, right? When people see you on TV and they think, oh, she's the pinnacle of beauty. And then you hear what she's sharing y'all about her hair and makeup and she told her people, I'm not sitting in this toxic soup for 12 hours a day every day for how many days. So what other kinds of ways to take control do you think are important for women to know about, to take control of their health? Well, a huge one. And I think possibly one of the biggest things people say, well, you know, I, especially I I even have my my 15 year old who wants, you know, it's all about how do I look, how do I look compared to everybody else? Speaker 1 (26:03): I think most of your listeners like, I, I mean we all wanna look good, but I'm kind of past that. I wanna just feel great. I wanna live a long, healthy life in this one vessel that I have. So what can I do? How can I treat my body so that it doesn't just look good, but that it feels amazing and gives me the ability to do the things I need to accomplish. Not just the day to day, but the big picture of things that I yearn to do. Right? I wanna go hike mountains in Italy and I have like all, you know, I wanna get down to the ground with my eventual grandchildren and play and be able to get back up. So you, first of all, you can't out exercise a bad diet. However, right? Daily movement is essential, very, very essential. But food is possibly one of the biggest changes you can make. Speaker 1 (26:49): I'm not telling you you have to give up your favorite corner bakery or you have to not have that steak when you go to the restaurant that you just love at that steakhouse. But when we're looking at food in general, we really wanna focus on a plant forward or plant-based diet. So the biggest thing is that women only get about 12 grams of fiber per day on average. And what we need to thrive and live optimally is closer to 30 to 35 grams of fiber per day. And even our own U S D A only says 25 grams, which actually you can talk to any expert worth their salt, they will tell you it's over 30 grams a day we need. And so the way to get that is increase your vegetable intake, you know, really non-starchy veggies. So if you're having a bunch of baked potatoes every day, that's not really qualifying non-starchy. Speaker 1 (27:37): We're talking about your cruciferous veggies, which are great cancer fighters. That's gonna be your Brussels sprouts and your broccoli and your cauliflower broccoli sprouts are amazing. You know, all of those cr kale and then leafy greens are at the top of that nutrient density pyramid. If you could only have one thing and you gotta choose what's the best nutrient density for my caloric buck, it would be leafy green, dark leafy greens, but adding in berries, great cancer fighters, tons of fiber getting in those, the chia seeds, the flax seeded flax seeds, also a great cancer fighter, matcha green tea powder changing up kind and the color of veggies that you're having and really making sure that your microbiome right, that's the, the diversity within your gut is as diverse as possible. So you wanna aim for about 30 different plant-based foods per week. And that means not just fruits and veggies, but also nuts and seeds and legumes whole grains. Speaker 1 (28:32): So quinoa, taf, amaranth Pharaoh, things like that. All count, which is great. And actually spices and herbs also count, and if you don't, doesn't even take a lot of those to count of as one of those 30. So that was the biggest food change I did was I flipped my plate as the meat eating Minnesotan with a slab front and center. I flip my plate to fill at least half my plate full of veggies at every meal. So my day starts with a smoothie and that's, I began to intermittent fast during covid. So now that's part of my life that's really can be very beneficial as well. And you guys can reach out to me on, on more about intermittent fasting, but so whenever I'm breaking my fast, it's with some cashews or cashews and almonds and then my smoothie because you can pack so many of the nutrients that are great for you and beneficial. Speaker 1 (29:22): I think I have something like 18 of my 30, all of fruit and vegetables all in my smoothie in one, one fell swoop. So it's, it's great, you know, you can throw all the goodness in there and then really just getting that variety in. Yes. So what you're eating super important. You've gotta work on that plant forward, plant-based plant predominant for sure. Intermittent fasting is a great tool. We've had a lot of the experts on that on the show. Talking about intermittent fasting, it's a tool that I use as well, but I love to say it's a tool, not necessarily a religion. Yeah. So treat it like, like a tool. All right. So we've talked about getting rid of the toxins. We've talked about your diet. What are some of the other easy ways to take control? And I know you have a lot more in your book, you have a lot more in your programs to go in depth, but I want people to kind of get a, an idea. Speaker 1 (30:11): Well, you know, the other thing is that leads to disease is stress. And we all live in such a stressful world because our phones are always dinging us. We're trying to fit 28 hours into 24 or maybe 30. In my mind, in my mind, I feel like I'm always trying to fit too much in and in this go, go, go world, we forget, we, we are praised for lack of sleep and overwork and grinding it out. When really that's to our detriment. First of all, it's not good for our hormones, it's not good, right? Our levels of cortisol, the stress hormone goes through the roof mm-hmm. . And when we live in a state of chronic stress that leads to chronic inflammation, which is the underlying cause of many diseases. So really taking that time every day for self-care and working in, whether it's breath work, meditation, a yoga, a hike, or walk in nature, time with friends, socializing, laughing, these are all stress relievers that are really important to add into your every day life to help beat depression, beat obesity, and beat inflammation. Speaker 1 (31:16): Yeah, you're super busy , you're a wife, you're a mom, you're a TV personality, you've got your own programs, your own platform. You're, you're DMing people on Instagram. You know, we tell women this all the time and do we do it a lot of times? No , we don't know how to say no, we don't know how to slow down. We don't know how to sit and just be. How have you reduced the stress in your life to help your co cortisol? I'm, I'm sure everybody would love to know. Breathwork I think has been one of the most powerful tools. I thought for the longest time only meditation and getting to sit for 30 minutes without moving was going to be what I needed to do. I'm still struggling to try to get in a, you know, a 15 or 20 minute meditation on a daily basis. Speaker 1 (32:01): But what I did realize that I could do was breathe and breathe, whether it's for 30 seconds or for five minutes or for 15, if I can, where I'm taking good deep belly breaths. There's a whole variety. You guys can google it, you can reach out to Dr. Kirin or to me. There's so many different ways to integrate breath work into your life. But even taking that, you know, two seconds of deep and exhales before you go into a meeting, when you park the car and turn off the ignition before you get out, finding those little cracks in the day where you can add in a couple of deep breaths, it immediately ignites your parasympathetic your rest and digest nervous system. And that can't be active if your sympathetic is in fight or flight. So it automatically deactivates the fight or flight and activates this resting, calming wonderful part of your nervous system. Speaker 1 (32:57): And that makes a big difference as well, I find. Mm-Hmm. . The other part is mindfulness. So if you're out maybe walking the dogs or you know, walking from the parking lot to the in, you know, the entrance to a building. If you can do it in a way that's mindful instead of the 4,000 thoughts that are in your head, take a moment while you're to breathe and focus on do you hear the birds chirping? You feel the warmth of the sun on your face, the breeze in your hair. If you're washing the dishes, maybe turn out off the noise around you. Do you feel the warmth of the water and the feel of the suds? Just things like that that are little actually add up to make big impact. Yes. Little things, mindfulness, breathing. Not everybody can meditate and sit still and empty their mind. Speaker 1 (33:45): And what about the role of self love? We hear a lot about that. I don't, to me that's not a mani-pedi you share this quote with me before we started that I love be kind, especially to yourself. So can you talk about that and, and how self-love has played a role? I'm sure it has in you healing and doing all of the things that you do and supporting all the people that you support. How does that show up? How are you kind to yourself? Well, in two different ways with self-care, for sure. And my mornings when I'm not traveling or shooting my mornings have become self-care mornings, and sometimes I get guilty about it because I realize all the other things on my to-do list are not getting done like I want them to get done, but I'm giving myself time for that workout to make the smoothie. Speaker 1 (34:35): And I have an infrared sauna that I sit at in. And I will say I started out meditating in there and now I, I will say I, I, I'll be honest, I do answer a lot of my dms while I'm in there, but no infrared sweat. I try to put it down for at least 10 minutes and put on a, a guided meditation. So I do breathe and I, I lay down, I put my legs up the wall in the sauna and it's a little portable popup. You guys can reach out to me. I love it because it's much more affordable than those big, you know, structured ones that you see at like infrared Sauna place or in like, some big Hollywood celebrities house that nobody can afford. I'm all about affordable ways to have healthcare hacks. But the other thing is how we talk to ourself in terms of being kind to ourself. Speaker 1 (35:16): We oftentimes are worse to ourselves and talk to ourselves whether we're in thought or out loud, worse than we would ever speak to somebody else. So when you pass that mirror next time, and the first thought is, oh gosh, I'm so wrinkled, gosh, I look so fat, whatever it is, first just acknowledge, just acknowledge that you had that thought as your first thought. It's a process. Then the next challenge is flip the script on yourself and find something positive that you like. I love the twinkle in my eye. I love how strong my arms are because I can carry my kids or I can hug my family or whatever that is. So that eventually the more positive self-talk we have and the more we push out the negative self-talk, it's something that our brain, even if we're not saying it out loud, if we're thinking it, our whole body hears it. Speaker 1 (36:03): And so it affects our wellbeing and our sense of satisfaction for life and happiness with ourselves. So being kind to yourself and then also it's, you know, the saying of it's a lot easier what to treat someone with syrup than with salt or I with vinegar. I don't know. There's some sort of saying like, but it it, the, the gentle smile to a stranger, someone who's off because you, you know, you cut in front of them and you didn't mean to a warm wave and smile of apology. It will actually go a long way versus giving them the finger back . Yes, so true. And I do think it's so important that we be kind to ourselves and just noticing my own self-talk and hearing other women how they talk about themselves and just this lack of self-love. I was doing an interview earlier and she was the, she was saying that I literally realized that I hated myself and I treated myself that way. Speaker 1 (36:58): And then now she's really cultivating this self-love. I totally wish we had time to go through all eight aspects of what you teach women, but we don't have enough time. So I'm gonna direct everyone before we sign off, we'll have you share your program. We'll have the links in the show notes, we'll have you share again, all the places they can find you. But I wanna ask you a question. I don't know if anyone's ever asked you this and you share this quote with me before we started that I love keep doing what you're doing and you will keep getting what you're getting. Where do you think you would be and what do you think would have happened if after your cancer diagnosis and your immediate treatment, you hadn't done the research, you didn't look into this, you just accepted what most women accept. Speaker 1 (37:49): Oh, cancer just happens out of the blue. I always say, not out of the blue, but out of the oblivious, where do you think you would be now? Which is what, 10 years later? I first of all would fear the recurrence, but a hundred percent because my chance of recurrence would've been a a lot greater if I hadn't started to make the changes that I am making or the, or the diagnosis, maybe not at this point, but maybe in another 10 or 20 years of another chronic disease that, you know, again, we can't take, I wish we could take 100% control by making these changes. We can't. And if you're stressing too much that, oh gosh, I'm supposed to be intermittent fasting and I broke it at 8:00 AM or I shouldn't be drinking too much wine because it could increase breast cancer risk and I had two glasses last night with friends, that stress is actually going to be more harmful. Speaker 1 (38:36): So we have to take everything in stride and find that, that the, the 90 10 rule or even the 80 20 rule, where the majority of the time you're making these helpful decisions. If I hadn't made these choices, first of all, I wouldn't have connected with the incredible women who I have been able to connect with and help and support and guide. And to me that has been the biggest gift of cancer and helping others live their healthiest healthy lives. That's amazing. Yes. Connection. And then with your voice and your platform, what you're able to offer every one in terms of information, I always say knowledge, tools, and support. That's what every woman needs. And so you're able to offer that. Thank you so much for coming on the hormone prescription and sharing your journey and your wisdom and your knowledge, tools and support. Speaker 1 (39:23): We'll have all the links in the show notes, but please do talk a little bit about your healthiest healthy community that you've created and the other places that people can find you online. Well, I love that. You know, first of all, I love live television. So the fact that I do live coaching, live workouts and bring in a live guest expert interview every week is just very much in line with what I love to do because I love to talk, but sharing and giving good takeaway. So the, your Healthiest healthy community is a membership based subscription platform, and you get access to me and immediate, you know, or pretty immediate responses in helping you live your healthiest healthy life for those who aren't interested in being part of a, a full group like that. Then I just recently launched Your Healthiest Healthy Courses, and these are basically both coaching sessions and expert guests who are giving topic-based information through the courses. Speaker 1 (40:14): So I have a two-part thriving after breast cancer course, a course on intermittent fasting, on gut health, on weight loss. We have them coming up on sleep and hormone balance and so many other topics. So that way you can go, okay, I'm just really right now focused on this. So that's what I want from Samantha. And then the other big thing that I just love and I live for every year are my, your healthiest healthy retreats. I have one in Santa Monica, California Beachside every year does a two day workshop. And then in Utah usually in October or November this year, it's October of 2023, but your Healthiest Healthy retreat. So four days and three nights hiking for all levels, by the way, and meditation and workshops with me and a lot of one-on-one coaching and advice and so much more. And I just, I, I, I just, it's my favorite thing in the whole year. Speaker 1 (41:03): I love that. Thank you so much for those amazing resources, Anne, for sharing your brilliance and wisdom with us today on the show. Thank you. Thank you. And again, you guys reach out to me, DM me and I will get back to you. Awesome. Thank you for watch for joining us for another episode of The Hormone Prescription with Dr. Kyrin. I know that you learned something inspiring, uplifting, informative today, and I'm gonna challenge you to take action, take one step. What's one thing you could do differently today? Maybe take a couple deep breaths as we're closing out this episode. Thanks so much for joining me, and I look forward to seeing you again next week for another episode of The Hormone Prescription. Until then, peace, love, and hormones, y'all. Speaker 2 (41:45): Thank you so much for listening. I know that incredible vitality occurs for women over 40 when we learn to speak hormone and balance these vital regulators to create the health and the life that we deserve. If you're enjoying this podcast, I'd love it if you'd give me a review and subscribe. It really does help this podcast out so much. You can visit the hormone prescription.com where we have some free gifts for you, and you can sign up to have a hormone evaluation with me on the podcast to gain clarity into your personal situation. Until next time, remember, take small steps each day to balance your hormones and watch the wonderful changes in your health that begin to unfold for you. Talk to you soon.   ► Become your healthiest healthy! Get Samantha Harris's complimentary course - CLICK HERE.   ► Feeling tired? Can't seem to lose weight, no matter how hard you try? It might be time to check your hormones. Most people don't even know that their hormones could be the culprit behind their problems. But at Her Hormone Club, we specialize in hormone testing and treatment. We can help you figure out what's going on with your hormones and get you back on track. We offer advanced hormone testing and treatment from Board Certified Practitioners, so you can feel confident that you're getting the best possible care. Plus, our convenient online consultation process makes it easy to get started. Try Her Hormone Club for 30 days and see how it can help you feel better than before. CLICK HERE.   If you enjoyed this episode, don't forget to subscribe, rate, and review The Hormone Prescription Podcast on your preferred podcast platform. Your support helps us reach even more listeners, allowing them to benefit from our expert advice and knowledge. ✨    

Today, Tasha Keeney sits down with Simon Barnett to talk about ARK's valuation of Exact Sciences and to share our outlook about the company's trajectory in the next five years. Exact Sciences is the cancer testing company that has brought to market both Cologuard and Oncotype. This conversation covers the prominence and acceptance of these two testing franchises, Exact Sciences' product leadership, Exact's recent performance in the market, the models that ARK has developed for gauging the company's outlook, and the areas of risk that investors should be aware of. One of the main focuses of today's chat is what Exact Sciences' progress symbolizes in terms of the future of the cancer treatment field, with Simon making an argument for why he sees them holding onto their market-leading position for the foreseeable future. We also spend some time at the end of the episode considering what this means for healthcare and individual wellbeing in general, so make sure to catch it all in this episode of For Your Innovation! Please refer to the Exact Sciences valuation article for a more comprehensive explanation of ARK's model, including its risks and limitations. “Cancer care is something that is totally divorced from interest rate changes or consumer sentiment. It's something that's very predictable, and it's something that's very important.” — @sbarnettARK Key Points From This Episode: Introducing Exact Sciences and its two biggest testing franchises: Cologuard and Oncotype. Valuation of Exact Sciences and how ARK has approached creating these models. Calculations for the price target of the company. Sales and marketing at Exact Sciences and the positive brand recognition they have built. Benchmarks for analyzing companies like Exact Sciences. Comparing ARK's process and view on Exact Sciences to other opinions in the market. How the lowered price of genome sequencing has affected the outlook for the market. The route to the aggregate gross margin structure for Exact Sciences. Qualitative elements that matter most to ARK; how Exact Science fits into our rubric. Alignment between the expectations of Exact Science's management and our estimations. A look at the three main areas of risk: competition, time, and financing. Simon explains how thesis risk applies to the healthcare space. Thoughts on the company's net income and cash flow in the near future. Reasons to be excited about the next few years in the healthcare space.

El Gran Musical - Adriana Sánchez, Prueba Genómica Oncotype

Dr. Allison Zibelli, of the Sidney Kimmel Cancer Center – Jefferson Health, highlights key advances from the EMBER study and promising data on QOL for HR+/HER2- patients taking checkpoint inhibitors featured at the 2022 ASCO Annual Meeting.   Transcript:  ASCO Daily News: Hello and welcome to the ASCO Daily News Podcast. I'm Geraldine Carroll, a reporter for the ASCO Daily News. My guest today is Dr. Allison Zibelli, a breast medical oncologist and assistant professor of medicine at the Sidney Kimmel Cancer Center Jefferson Health.  Dr. Zibelli will highlight key posters on breast cancer that will be featured at the 2022 ASCO Annual Meeting. Dr. Zibelli's full disclosures are available in our show notes, and disclosures of all guests on the podcast can be found on our transcripts at asco.org/podcasts.  Dr. Zibelli, it's great to have you on the podcast today.  Dr. Allison Zibelli: Thank you. It's nice to be here.  ASCO Daily News: Let's begin with Abstract 1021 and the “Phase 1 EMBER Study.” Can you tell us why this study should be on our radar?  Dr. Allison Zibelli: This study was very interesting because it's testing a novel therapy, which is imlunestrant, an orally bioavailable SERD, or a selective estrogen receptor degrader. This drug is for patients with ER-positive, HER2-negative advanced breast cancer. And they're presenting updated data from the dose-escalation phase and the dose-expansion phase of the EMBER trial.  This trial enrolled 138 patients at a median age of 62 years. The median number of prior therapies for these women was 2. The adverse events were low. They could have prior platinum therapy but no prior fulvestrant or aromatase inhibitor. The premenopausal women in the study received concomitant GnRH antagonist. They had substantial clinical benefit with this therapy with no dose-limiting toxicities.  It had a favorable side effect profile with no cardiac or ophthalmic safety signals, and it had excellent efficacy in patients with heavily pretreated ER-positive advanced breast cancer. This is the first study showing efficacy and safety with an oral SERD. And we're all looking for new oral, well-tolerated therapies for our patients with metastatic estrogen receptor-positive breast cancer.  These patients were heavily pretreated, and they had a median of 2 prior therapies. Most of the patients with advanced breast cancer had prior endocrine therapy, 92% had a prior CDK 4/6 inhibitor, 50% had fulvestrant, and 26% had chemotherapy.  Despite this, they had an overall response rate of 5% with a clinical benefit rate of 47%. So, it'll be very interesting for us to see what happens with this new class of SERDs in the future.  ASCO Daily News: Excellent! So, moving on to Abstract 514. This study addressed patients with high-risk early breast cancer who received pembrolizumab within the new adjuvant biomarker rich I-SPY 2 trial. Can you tell us more about this study?  Dr. Allison Zibelli: This is a very interesting study, which is a platform study comparing various investigational treatments to a standard therapy which was ACT, with or without herceptin, depending on the HER2 status of the patient versus an experimental agent.  One arm of the I-SPY study was neoadjuvant pembrolizumab. This paper is very interesting to me because it's hard to know in advance who will respond to immune checkpoint inhibitors. And that's what this study was designed to answer.  So, they took 69 patients who were on the I-SPY study, they all had high-risk MammaPrint scores, and all of them were HER2 negative, and with these patients, they had 31 complete responses to neoadjuvant pembrolizumab and 38 patients with a residual disease after neoadjuvant pembrolizumab. Notably, of the 31 complete responses, 12 were ER-positive, and 19 were triple-negative.  In the residual disease patients, 28 were ER-positive and 10 were triple-negative. If you compare this with historical data, the response rate for pembrolizumab is about 20% for patients who are triple-negative and about 12% for patients who are ER-positive.  So, the response rates that they had were higher in general. So, what the study did was they found a signature of 53 genes which they named imprint, which was identified with a greater than 90% sensitivity and greater than 80% specificity for predicting complete response to pembrolizumab in all patients.  This worked equally well for the patients who are estrogen receptor-negative and estrogen receptor-positive. In KEYNOTE-086 cohort B, which was presented at the American Association for Cancer Research Annual Meeting (AACR), PD-L1 of greater than 1% only predicted a 23% response rate to pembrolizumab.  So, if we could use the imprint study to predict patients who would respond to pembrolizumab, it would save a lot of needless toxicity and a lot of needless expense, in treating the patients who would have benefit.  So, this is going to be a very useful method to identify patients that we want to treat with pembrolizumab, and perhaps other immune checkpoint inhibitors as well. I think this might be the next “Oncotype” as it were, in that it will be able to predict who will benefit from a specific therapy.  ASCO Daily News: Thank you! Let's move on to Abstract 519. This is a randomized pre-surgical trial of alternative dosing of exemestane in postmenopausal women with early ER-positive breast cancer. What are your key takeaways here?  Dr. Allison Zibelli: I thought this was a great design of a study. It was a window of opportunity for the test. So, what they did was, they tested 3 different dosing schedules of exemestane in patients waiting for surgery for ER-receptor-positive breast cancer.  The patients were randomly assigned to either receive exemestane 20 milligrams a day, the standard schedule, 25 milligrams 3 times a week, or 25 milligrams once a week for 4 to 6 weeks prior to surgery.  Their endpoint was percent decrease in circulating estradiol and what they found was the 3 times a week schedule was comparable to the daily schedule. The once-a-week schedule didn't seem to be adequate to decrease estradiol, but 3 times a week was equivalent to daily.  This was really interesting because we know that our patients have difficulty tolerating aromatase inhibitors. We know from formal studies that about 25% of patients discontinue aromatase inhibitors prematurely because of side effects. Small studies in actual practice settings show it's probably even higher than that—between 30 and 50% of patients discontinue aromatase inhibitors.  So, for the patient that can't tolerate daily therapy, 3 times a week therapy is an attractive option, that may be just as good as daily. I think it is very important for patients who have to take these drugs for years that they have a way to take them that is tolerable.  ASCO Daily News: Absolutely. Well, the last study I'd like to ask you about is Abstract 1015. This looks at the quality of life for patients with HR-positive, HER2 negative advanced breast cancer. So, what does this study tell us about quality of life with different CDK 4/6 inhibitors?  Dr. Allison Zibelli: So, we have a lot of studies of CDK 4/6 inhibitors. And we know that they dramatically improve the overall survival of women with ER-positive metastatic breast cancer. What we also know is that they have a lot of side effects. And for women that have to take these drugs for years, that's important.  So, this study was a matching adjusted indirect comparison study. This is a method that uses individual patient data to create balanced trial populations across separate studies, and they use patients from the MONALEESA-2 trial, which was ribociclib plus AI, compared to MONARCH 3, which used abemaciclib plus AI, the endpoint was something they called “time to sustain deterioration,” which was a decrease in 10 points in the quality of life score, they use the QLQ-C30 questionnaire. The upshot of their data was that ribociclib was more tolerable, mostly with less appetite loss, less diarrhea, and less fatigue than abemaciclib.  So, this is 1 of the first studies we've seen that directly compares, well sort of directly compares the quality of life between these 2 drugs, and this may be a data point that favors ribociclib.  ASCO Daily News: Well, thank you, Dr. Zibelli, for highlighting some really important advances in breast cancer that will be featured at the 2022 ASCO Annual Meeting. We really appreciate it.  Dr. Allison Zibelli: Thank you very much for having me.  ASCO Daily News: And thank you to our listeners for joining us today. If you're enjoying the content on the ASCO Daily News podcast. Please take a moment to rate review and subscribe wherever you get your podcasts.  Disclosures:   Dr. Allison Zibelli: None disclosed.  Disclaimer:  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.     

Harry traveled to the San Francisco Bay Area this summer, and while there he interviewed the co-founders of three local data-driven diagnostics and drug discovery startups, all of whom participated in the same graduate program: the Biomedical Informatics Program at Stanford's School of Medicine.  Joining Harry were Aria Pharmaceuticals co-founder and CEO Andrew Radin, BigHat Biosciences co-founder and chief scientific officer Peyton Greenside, and Inflammatix co-founder and CEO Tim Sweeney. The conversation covered how each company's work to advance healthcare and therapeutics rests on data and  computation, and how the ideas, skills, connections each entrepreneur picked up at Stanford have played into their startups and their careers.Radin's company, formerly known as twoXar, models pathogenesis computationally to identify potential drug molecules, shaving years off the drug development process. Radin developed Aria's core technology, a collection of proprietary algorithms for discovering novel small molecule therapies. The algorithms incorporate system biology data, disease-specific data, chemistry libraries, and more than 60 separate AI methods to sift through molecules with known chemistry to find those with novel mechanisms of action and favorable safety profiles absorption properties. Whereas traditional drug discovery methods have a 1-2% success rate after 4 years, Aria claims its approach has a 30% success rate after just 6 months. It has a pipeline of at 18 drug candidates in areas including kidney, lung, and liver diseases, lupus, cancers of the liver and lung, glioblastoma, and glaucoma. Radin holds MS and BS degrees in computer science from Rochester Institute of Technology, studied computational biology and medicine through the Stanford Center for Professional Development, and was formerly an advisor to several venture capital firms and startup accelerators. Greenside started BigHat to combine wet-lab science and machine learning with the goal of speeding up the design of antibody therapies. BigHat's lab consists of numerous “workcells,” each of which cycles through multiple tests of a given set of antibodies synthesized from in silico designs. Assays characterize each antibody variant for traits such as yield, stability, solubility, specificity, affinity, and function. Machine learning algorithms determine how mutations affected each of these properties and feed this learning back into a new set of designs for the next round. The company says this approach allows it to identify therapeutic-grade antibodies faster than traditional bulk screening techniques (in days rather than weeks or months). Greenside is a computational biologist with a PhD from Stanford, an MPhil from Cambridge University, and a BA from Harvard. Silicon Valley Business Journal named her to its 2021 list of “Women of Influence in Silicon Valley.”Sweeney co-founded Inflammatix to develop a new class of diagnostic tests that—rather than searching for a specific bug—“read” the host response of a patient's immune system for clues about the cause and severity of an infection. The problem, as Sweeney originally saw it, is that traditional tests can only detect infections once a pathogen has spread to the bloodstream, meaning that doctors often guess incorrectly about whether a patient needs an antibiotic, or which one they need. Inflammatix is built around the idea that the human immune system has evolved targeted responses to different kinds of infections and other diseases. These responses are complex and vary according to age and setting, but by analyzing mRNA samples from multiple, diverse cohorts, the company believes it can identify a “reproducible signal in the ‘noise' of multiple datasets.” Inflammatix is developing a cartridge-based system called Myrna for use in emergency rooms, urgent care clinics, and outpatient clinics that can screen for acute bacterial infections, viral infections, and sepsis in 30 minutes. Sweeney is a physician and data scientist who earned an MD/PhD from Duke and then trained as a general surgery resident at Stanford.Please rate and review MoneyBall Medicine on Apple Podcasts! Here's how to do that from an iPhone, iPad, or iPod touch:1. Open the Podcasts app on your iPhone, iPad, or Mac. 2. Navigate to the page of the MoneyBall Medicine podcast. You can find it by searching for it or selecting it from your library. Just note that you'll have to go to the series page which shows all the episodes, not just the page for a single episode.3.Scroll down to find the subhead titled "Ratings & Reviews."4.Under one of the highlighted reviews, select "Write a Review."5.Next, select a star rating at the top — you have the option of choosing between one and five stars. 6.Using the text box at the top, write a title for your review. Then, in the lower text box, write your review. Your review can be up to 300 words long.7.Once you've finished, select "Send" or "Save" in the top-right corner. 8.If you've never left a podcast review before, enter a nickname. Your nickname will be displayed next to any reviews you leave from here on out. 9.After selecting a nickname, tap OK. Your review may not be immediately visible.Full TranscriptHarry Glorikian: I'm Harry Glorikian, and this is MoneyBall Medicine, the interview podcast where we meet researchers, entrepreneurs, and physicians who are using the power of data to improve patient health and make healthcare delivery more efficient. You can think of each episode as a new chapter in the never-ending audio version of my 2017 book, “MoneyBall Medicine: Thriving in the New Data-Driven Healthcare Market.” If you like the show, please do us a favor and leave a rating and review at Apple Podcasts.Harry Glorikian:Home base for MoneyBall Medicine is the Boston area. It's one of the world capitals for biomedical innovation and the digital revolution in healthcare. So I don't have to venture far to find great guests.But obviously Boston isn't the only capital for biosciences innovation. This summer, during the brief break between surges in the coronavirus pandemic, I escaped to the San Francisco Bay area. And while I was there, I got a lesson about the considerable impact created by one particular Bay Area institution. Namely, the Stanford School of Medicine's Biomedical Informatics program, or BMI for short.BMI trains students how to use and adapt computational methods like machine learning to solve hard problems in biology and medicine. And a remarkable number of BMI alumni have fanned out into the world of life science startups. On today's show you'll hear from three of them. We'll talk about the work their companies are doing now and how the skills and connections they picked up at Stanford have played into their careers.The first guest, and the person who helped to organize the group interview, has actually been on the show twice before. His name is Andrew Radin, and he joined me in November of 2018 and again in August of 2020 to talk about his Palo Alto-based company Aria Pharmaceuticals, formerly known as twoXar. Aria uses a collection of proprietary AI algorithms to discover new small-molecule drugs for a range of diseases. In traditional drug discovery, years can go by between the identification of a new drug candidate and testing the drug in animals. Radin says Aria's AI can reduce that time to just weeks.Andrew kindly recruited two of his fellow Stanford BMI alumni for our conversation. One is Peyton Greenside, the co-founder and chief scientific officer at BigHat Biosciences in San Carlos, California. The company combines wet-lab science and machine learning to make it easier and faster to design new antibody therapies. And again, the leap forward is that BigHat's rapid cycle of antibody design, synthesis, and characterization vastly speed things up, reducing the time required to identify new therapeutic antibodies from months to just days.And our final guest is Tim Sweeney. He trained as a surgery resident at Stanford and then founded a company to tackle one of the biggest problems in acute care, namely how to diagnose infections faster and more accurately. The company is called Inflammatix, and it's building a device that emergency departments and outpatient clinics can use to rapidly analyze messenger RNA in patients' blood to screen for sepsis and other kinds of infections.All three of these companies are benefiting in different ways from the computational methods their founders studied at Stanford. And they've got some great stories to share about how their time at BMI convinced them that future progress in medicine and drug discovery would depend on data above all else.We originally planned to meet up in person for this interview. But we switched to Zoom at the last minute out of concerns over the Delta variant. So without further ado, here's my talk with Andrew Radin, Peyton Greenside, and Tim Sweeney.Harry Glorikian: Well, hello everybody. And welcome to today's show. Tim Sweeney: Thank you. Peyton Greenside: It's great to be here. Harry Glorikian: Yeah, it's, it's great to have all of you here. For everybody listening and watching, we were actually supposed to do this in person, but unfortunately the Delta variant sort of threw a monkey wrench in that whole process. So I reserve the right that we can do this in the future and actually get together when this whole thing is over, like normal human beings. Each of you are working on super exciting things. Different companies, focusing in different areas. And I know you all know each other, so I'm going to step back one second and say, if you had to give a brief description of your company or pretend you don't know each other, where we're at a cocktail party and you're going to give me two or three sentences about what you're doing and why it's interesting, how would you sort of do that? And Andrew, since you're the ringleader that sort of helped bring this group together, I'll throw it out to you first to sort of get going.Andrew Radin: Well, that's a lot of pressure, but certainly like, our description I think is pretty simple. We are a preclinical stage pharmaceutical company. And we happen to have a proprietary artificial intelligence platform that's discovered all the assets that we have under development. And these days we have 18 programs, 18 different disease areas where we've got new experimental medications and we are working on progressing those new inventions to the clinic and ultimately to FDA approval.Harry Glorikian: Peyton?Peyton Greenside: Hi everyone. I'm Peyton and one of the co-founders of Big Hat Biosciences, and our mission is to improve human health by making it easier to design advanced antibody therapeutics. So we actually do that through a combination of a high-speed wet lab and machine learning techniques in order to very iteratively design and improve antibodies until they meet unmet patient need. And it's been a lot of fun. Then we've been founded since 2019.Harry Glorikian: And finally, Tim. Tim Sweeney: thanks for the opportunity, Harry. Inflammatix was founded about five years ago, spun out of Stanford along with, of course, Aria and Big Hat. We are designing novel diagnostics focused on acute care and critical illness needs. So we basically have a data analytics platform that allows us to decode certain signals of gene expression within the immune system. And then for those of you watching, I'll show you, we have a cartridge that allows us to sort of implement that in a 30 minute point of care diagnostic setting.So our particular focus is basically bringing precision medicine into acute care settings, the hospital, the clinic, the ICU, where sort of historically there hasn't been a lot of diagnostic innovation. Harry Glorikian: Interesting. That's funny because I actually, I wrote a a textbook on how to commercialize novel diagnostics a few years ago. Because you know, unless you've been through the ringer, you may not know all the different pieces.But you guys now all know each other right? Now, that may not surprising because we're in Silicon Valley, and I'm actually in Berkeley right now, but that's close enough. And drug discovery companies and tech companies are all swimming around each other. But your connection is a little bit deeper. I mean, you guys all went to Stanford together. So this is not necessarily a commercial for Stanford, but it's, that's pretty interesting that three CEOs of data-driven, you know, healthcare companies out of the same class, whoosh, come out of Stanford. So how did you, how did you guys meet at first?Andrew Radin: Well, and I would say we're not the only ones to—it's just, you know, the people that happen to be in front of you today. It was funny. So, right before this, I sent a panicked email, because I didn't want to say something that wasn't true. I was like, Peyton, you were in this class, weren't you? Peyton Greenside: Yeah. I don't know if I was Andrew's TA or if we'd all actually been in the same class. But I think our Stanford journeys all started, it sounds like, the same year. Same time. And we all were taking translational bioinformatics, which was a course taught by, I believe, Atul Butte who I think, you know, really brought to fame the idea of big data for biology, what you can draw out a very large data sets and drawing insights. So we were all in the same class and with many other people, as Andrew said, and it was a lot of fun. And I think it was the start of long journeys for all of us than in a similar vein. Andrew Radin: And it was a place for…I think what was awesome about that class, again, not to be an advertisement for the coursework, but it was kind of my characterization of the class was, you basically learned how other people use data science to solve some medical mystery, like across the spectrum. And so the, the purpose of learning all that was to just kind of fill you full of ideas of things that you could do. And then the kind of the capstone of the class was a final project where you basically had to come up with something, right? And so you were just sort of primed with all this like super interesting sort of research on how other people had approached very different problems in the space. And for me, it was just the source of lots of interesting ideas that then, you know, helped me ultimately create what's the technology behind our company today. Tim Sweeney: It is remarkable how much came out of Stanford biomedical informatics. Though, I mean, to Andrew's point, there are, there are a number of other CEOs that came through in that sort of in maybe a five or seven year stretch, all out of the same program. And I think a lot of it had to do with that, yes, this one particular class had all the different applications of data science sort of across the spectrum of life sciences, but they also attracted people like that. Right? I mean, everyone on this call has a very different background before Stanford BMI. And I think that was part of what made that culture so special is that it ended up being a real team sport, whether your background was medicine or business or math or computer science or bio-engineering or anything else, learning a technique from A, and applying it into area B, I think, was a pretty successful way to grow innovation. Harry Glorikian: I feel like as a venture guy, I should be standing at the exit door and just sort of saying, you know, “What's your idea, what's your idea,” screening as they're coming out the door.Peyton Greenside: Well, you know, some folks have also become venture capitalists. Harry Glorikian: That's true. Peyton Greenside: Yep.Harry Glorikian: So was there anything in particular that you guys, interests or questions or discussions that you sort of bonded over that sort of brought you together? I mean, even, even as just friends that decided to keep in touch? Andrew Radin: Well, I think it's probably different for different people. I think the first real interaction I had with Tim, you know,the details escape me, because this is almost 10 years ago now, but I remember, he's a medical doctor, right? He's got a MD and a PhD if I'm, if I'm not mistaken. And so my, you know, I'm a hardcore computer scientist. That's my background. And so back in those days, I was rapidly learning all I could about medicine and biology. And I don't remember the topic, but I do recall him helping me after class was something that wasn't just quite, you know, sitting in my head correctly. And I remember thinking like, what a nice dude, to, like, you know, kind of take some time and give me like, you know, a little private tutoring. And then and then if I recall afterwards, you said, yeah, so I'm trying to do this stuff with some clinical data. Can you help me with this sort of stuff? Which if I remember correctly, I never actually helped you. I was talking about, oh, I might be able to help you. And then eventually you said, “I figured it out. I don't need you”Tim Sweeney: I said I needed to build a web scraper. And I said, I have no idea how to.Andrew Radin: Oh yeah, I have totally done that. Lots of times. So yeah, something like that. That's how the conversation started with Tim, which was sort of to the point about having very different backgrounds, You know, with Peyton, I don't really recall the first interaction. I remember we were in a journal club, maybe with Russ and you were talking about some stuff, but I think the more I got connected to her was around the time she was working on her defense and I actually went to her PhD defense. And I have this BS detector that sometimes go off a little early, right? When people make a statement, I'm like, “I don't know about that.” We're sitting in her defense and every time she said something that made me, do one of these, like, “Wait a minute,” she instantly resolved that in the next sentence. I was like, “Okay. All right. That's cool.”Peyton Greenside: Okay, that feels good. Fortunately, fortunately. Andrew Radin: You don't have to pass my scrutiny obviously, but yeah, I think that led to a number of kind of interesting conversations as she was contemplating, you know, what to do next. She was moving through her career, but yeah, I think that the interactions are very, very different for each person. At least that's my view, but I don't know if you guys have different memories. Peyton Greenside: Yeah, I think what's, what's interesting, I mean, just generally I agree with that. And I think one of the most interesting parts of BMI, as Tim said, is just the backgrounds that everyone has. And I also come from the kind of applied math, computer science background, and there's this kind of fascination of what you can do with computational skills in biology. I think to me, a lot of the conversations were around where do I even apply this to? I think people sort of think of computational biology as a, maybe sort of a niche, small field at the intersection of maybe somewhere where biology meets, I guess, you know, statistics, computer science and math. But it's so broad and it's so vast. And I think most of the, I say the most exciting conversations I've had are, you know, we work in immunology, you know, you're a clinician, you work with clinical data. How do you apply these tools? The most daunting but fun task upon showing up at Stanford with such an incredible ecosystem here is, where do you even focus your attention? Where should you work? There's too many exciting opportunities to pick. And I think some of the fun conversations I remember also having a Tim, with a more clinical background, is what's actually useful? You know, I want, I want to do something useful and sort of try to figure out, you know, where this, you know, where are you can actually kind of apply your time to the most impactful problem. It was a lot of fun. Andrew Radin: And I think, Tim, it'd be great for you to share. I mean, when we first met, I'd asked you kind of like, what were you doing there? What your story was? I can't remember the words back then. But you basically said like, “Look, I'm a surgeon,” if I recall, “I'm trying to save people's lives and I'm just thinking like, is there a better way? Can I like just, you know, do something that's going to have a much larger impact? And I don't know what that is yet.” I know I'm wildly paraphrasing what you said, right. But I'm thinking about like what that could be. And I think. You know, when I met you, you were sort of on the hunt for figuring out where to apply, you know, kind of the, the skill set.Tim Sweeney: I think that the everyone shows up with their strengths and weaknesses. Mine certainly was the summer before the program actually started, I had to take, you know, basic courses in computer science and linear algebra. And I remember, I mean, I literally went from my last overnight call at Santa Clara Valley Medical Center, running two ICUs, to the next morning CS 106x. Which, because it was the summer, was filled with all the high school students that are just total whiz kids, like 16 year olds, and they're like, you know, we're learning like order of operations or something and they're raising their hands and I'm like desperately trying to write down like, oh, if n means....You know, and obviously Andrew and Peyton were among the folks that sort of helped me on the basic science side of things. But I think that the story about sort of getting the question right is absolutely correct. And I remember actually the time that I knew I was in the right program was maybe two or three months in to training. They used to have these like sort of work in progress talks, and it was like, you know, Wednesday or Thursday or something, you bring a lunch. And somebody was talking about this thing that sounded very, very cool to me. It was all about how you could, you could program a system to learn new knowledge on its own. And it was like, you know, generalized AI for health data. And I was incredibly impressed. And, and the first example that was given was like, you know, so we've sifted through all of the billions of data points. And I have discovered—he stumbles over the drug name—I've discovered that plopacapagril, by which he meant clopidogrel, is associated with bleeding events. And everyone goes, “oh.” And I put my hand up, like, “That's an anti-platelet medication.” And he looks at me and I'm like, “the point of that is that it thins the blood.” He looked at me and was like, “So bleeding is a known side effect?” Totally crestfallen that people knew this already. Like, he had no idea. I was like, I do have something to contribute, so it's good. It's a good merge.Harry Glorikian: Yeah. So, you know, Tim, you're running a diagnostics company you know, Peyton and Andrew you're running what I'll lump together as drug discovery companies in different markets, different regulatory processes. You know, I'm sure there are common challenges to life science startups in the valley. What are some of the biggest challenges that you guys see? Is it scalability? Is it finding the right people? Is it finding the right investors? Where do you guys see your challenges?Andrew Radin: And I would just say for a little clarification to Peyton's point about there's so many different problems. Even though Peyton and I are both in the business of creating new medicines, we couldn't be any more different. We're a small molecule company. She's a large molecule company. If you know what that means. You know, I'm making motorcycles, she's making trucks. Like, we're just, we're just, we're just doing completely different things. To your question about like, kind of what are the very similar things, we're not really even competing with one another from that perspective.But I think, to answer your question, at least from my viewpoint, you kind of have to do all those things. I think, you know, in startups, everything has to work. You can't sort of have any one thing that doesn't function and whether that's the science or the fundraising or the team or all of those things, if you've got a problem in any one of those areas, it can be life-threatening to the company.And so I think part of the experience for the entrepreneur is sort of, you know, because your time is limited and your resources are limited is sort of finding a best fit to try to solve, you know, or, or to maximize all of those problems simultaneously. And I would say all the things that you've listed, they all at various points in the company, they've been critical and it's more of a juggling act rather than “Geez, all you need to do is just knock it out of the park, on, you know, financing and who cares about anything else?” We know lots of stories where that hasn't gone well. Or you knock it on the park on an exceptional team, and the other things don't come together. So, you know, from my standpoint, all of that stuff has to work. Peyton Greenside: I think my answer continues. I think one of the things I, and what many people who just find, I would say many scientific, inquiries fascinating, is just what to work on that. And I have the same problem now, you know, I think it happened when I went to Stanford and happened you know, postdoc and have it happened now.And, in the context of my company, wo we basically have a platform that can work on engineering any protein. We work on antibodies, but really can be anything. So, you know, we have this landscape. There are tons of diseases with unmet need. There's sort of tons of opportunities for the type of therapeutic protein you would use, whether that's a standard antibody, monoclonal IgG, sort of a next generation antibody. And so we always have to decide, you know, what, what are the programs gonna be? What are you going to go after? What's the modality? And I think at the crux of it, like you know, for a drug discovery company, is what is the shape of your company. But our platform is so broad that basically we can work on so many things. And I, once again, by myself faced the same problem, which is okay, like, you know, where should we focus our attention? And that's been really fun. This is getting maybe more of Tim's background, but so we're learning more about the clinical side of things and where that need is and where that pairs with our technology. But I agree with what Andrew said, nothing really can go shortchanged, but that's been the same theme, I would say just now in a different vein. Harry Glorikian: Yeah. I mean, I think about this as a balance of dynamics where you're at different stages at different points, depending on where you are in the development cycle. And you need different people and different issues become a problem at different points or maybe become more acute at different points. But you know, all of you guys have one theme in common, which is why we're on the show together. It's data and some form of machine learning or other, you know, part of artificial intelligence that's being applied to find something valuable or identify some valuable piece of information that can make something actionable. It's sort of a big question, but how do you employ machine learning and AI in what you're doing in each of your businesses? Because I think of these things as like I have a toolbox and then I have to apply that tool in a very specific way with a specific set of knowledge that can feed it, where I can get an output that I'm looking for. And so each one of you, like you said, Andrew, you're, you're working on the motorcycle, she's working on the big truck, and he's trying to make sure that everybody gets diagnosed and not, not ends up in worse than they already are. So how are you each of you thinking or approaching this in your own unique way? If you can summarize. Tim, why don't you go first?Tim Sweeney: Our tests work by measuring a discrete number of genes within the body. It's their expression levels. So for instance, for our flagship test inset, we look at 29 different gene expression levels from, from blood. And then of course we have to somehow integrate  29 different levels into actionable information. And so the backend of that is the data science part, the machine learning. So step one is actually choosing what to measure. And then after you've chosen what to measure, then it's training hardened algorithms that turn 29 different things into a score that says, “This person has a bacterial infection.” And then of course doing that repeatably, doing it in a way that is traceable and verifiable. And then all of the post hoc, you know, how is it affected by different demographics? And how has it, in the actual context of care, and of course in the coming years when actually implemented in a health system, how does it impact patients and providers and does it save costs and improve outcomes?And maybe just since I didn't get a chance to answer, I think one of the questions about challenges is a lot of times it changes with the application that you're taking farther. Right? One of the things that we all have in common, I think is that we're all platform companies. And to, to Peyton's point, like you can apply that data science platform to a lot of different areas, but each one of those areas has to be taken through a very long development process to actually help a person and the challenges totally change along that development life cycle. Harry Glorikian: And just for everybody listening—so you developed this product. What is the, so what, what is the impact? Tim Sweeney: In our case, we decided that we wanted to go after one first indication that would be a big enough hit to make the business matter. We've got lots of things we'd like to do in the long run, but sepsis is an area of outstanding unmet need. And the “so what” is right now, if you go in and you're feeling sick and you see a doctor and you want to know, Hey doc, like, do I need antibiotics? There is literally no test that can answer that question. It's a guess. So it's not to say that antibiotics aren't administered quickly, but as a physician myself, I can tell you that that is it's a guess at first, and then you have to wait for tests to come back and those tests themselves are imperfect. And so something like 40% of antibiotics are probably misprescribed. And if you knew in 30 minutes, Hey, this person has a bacterial infection or no, you could greatly simplify care and really improve outcomes. And that's the premise. But the challenge of course is that beyond the data science, there's so much that goes into building the product and proving out the clinical data and get it through FDA and then getting it reimbursed and, and, you know, getting it rolled out more broadly, if you want to get to the point where you've actually helped a number of people and built a solid business. Harry Glorikian: When I, in my last company, before I moved on to venture, I, we had a strategy consulting firm and we did a lot of digging into sepsis. That was a big problem, a nut that people were trying to crack, and, you know, if you could crack it, the opportunity is quite significant.So Peyton, Andrew, how do you guys think about it? Because I'm, I'm thinking manipulating an antibody and sort of tweaking little parts of it until you find the exact fit. [It requires] supercomputing or massive computing. Peyton Greenside: It's funny. I actually think that the context in which we all met, which is you know, when I think big data was becoming really popular in medicine is actually a great context, I think, for where Big Hat ended up, and it's funny, because it's going to been kind of a long journey—it always happens when I look back, I'm like, yeah, that makes, that makes sense. Right? Based on where I was. We actually put a lot of our attention into integrating the wet lab with the dry lab. And this is actually, you know, with a goal of making big data into what I might call sort of smart data or agile data, which is that the idea of back in the day when first, I would say you got tons and tons of really large data sets. And you can sort of mine them, or you can look for trends. You can sort of just figure out something, you know, interesting relationship between gene expression and patient outcome. And I kept throughout my career feeling frustrated by being handed the dataset and sort of having to just mine it and not having kind of, you know, ownership of being able to say, “I want to look here, I want more data here.” Right? You're sort of handed a really large data set and you're, a passenger in this dataset that has already been generated. You cannot modify it. That's kind of the fixed dataset. And, you know, as a computational person, that, that you're often the second person, like a wet lab or experimental lab is making the data, then you kind of get it right. And so, you know, throughout I would say, especially in my time at Stanford this was very much the case, where I was felt kind of trapped in being given a data set that I didn't actually design, but I could sort of mine. And so at Big Hat we're basically trying to now put computation in the driver's seat and kind of change that paradigm. We're actually now, instead of just getting one large data set that you design up front, you acknowledge that biology and the science are very iterative, right? As as you said, you sort of start with an antibody sequence, but, you know, would you stop there? If you could just make one tweak, maybe you'd make it, you know, 10x better, 100x better with two. So how do you enable it? How do you want to enable that very rapid cycling? And so we view this as kind of the intersection of how closely can a lab and the computational side interact and how can they inform each other? How can you one learn from the other? And so we actually enabled a computational person to design an antibody on Monday and in a few days you synthesize, purify, characterize the antibody and kind of understand, are you moving in the right direction or are you not? And repeat, and then repeat it and repeat and repeat. So you don't get kind of stuck in the fixed data set again. So it's really attractive for a lot of ways, right? There are a lot of reasons you kind of can end up in a really good regime and it's big data or sort of area, but, you know, there's kind of a lot of lost opportunity in terms of being able to kind of be very agile and move toward something that looks promising and then iterate more. And the goal is that that will allow us to enable types of antibodies they don't even exist today because you can't engineer them that easily. You're kind of are stuck with a fixed format. So that's been really fun. And so we've been spending a lot of time designing the wet lab to kind of support the machine learning side and data science side from the ground up and, and vice versa.And so it's a pretty unique sort of set up. And I think I like to think of it as sort of smart data, right? You're thinking really closely about what should I generate that will be helpful and can use that to inform how you redesign the next dataset and improve your antibody every time in our case.Andrew Radin: Yeah, it's interesting to hear the different stories. You know, I think all of us are kind of taking the approach that, you know, what data sources and what artificial intelligence allows you to do is to take real world data and then make some prediction under uncertainty. You know, with the expectation that prediction is potentially better than what you could, what you could do with other methods.And so, you know, kind of tying this back to when I was student and thinking about where are the places I can make a big impact, it was very interesting to me that with very complex diseases there was really no single biomedical measurement that would help kind of unravel the mystery of the biology behind that disease. And therefore could, you know, explain something about pathogenesis that would lead to a new discovery or a new medication as a result. And, you know, part of that coursework in 2.17 was this concept of integrative genomics. This idea of using, you know, different data sources that are all keyed to the same thing, maybe a, a gene or a gene product, and kind of looking for that overlapping evidence.And there were some great papers that were shown. There was one, I think, by, by Eric Lander in particular, where he was using, GWAS and proteomics and maybe some gene expression microarray data, each of which would give you, you know, like hundreds of quote-unquote “answers” and the real answers in there buried with a bunch of false positives. But ultimately what would happen in this paper is he showed that there was one overlapping gene in all three of these datasets and he ran some assays and determined, indeed that was the key to unlock this mystery. And that certainly worked well if all of your data sets are sort of keyed to the same thing, but that's not the reality of biomedical data sets. There's genomics measures, there's chemistry measures, there's phenotypical measures, there's different patient measures. And unless you're conveniently measuring them all from the same patient population over time, which is very expensive and very, very time consuming to do, there's really no easy way to sort of key all these things together. And my thought was like, “Hmm, maybe, maybe there, there is a way.” And so the technology that I created and ultimately has been expanded upon is taking this concept, the concept that the answer to a very complex disease doesn't necessarily live in any one measurement or anyone biomedical data set. And if you have the ability to ultimately pull in lots of very diverse—and by diverse I mean statistically independent—data sets across a wide range of biomedical measures and integrate them as a single processing unit, you can ultimately uncover things that other people essentially haven't noticed before. And then use that, in our case, you know, to do lots of things, but in our case specifically to develop new therapeutics. So in all of our disease areas, ultimately what this means is we are working on new mechanisms of action. These are, these are new, if you will, new concepts or new understanding of biology in these disease areas and therefore what it means or what the impact is—to your earlier statement—is, we're going after biology that potentially has a disease modifying effect that others have not approached before. And therefore the promise of the opportunity is to make a significant dent in these very complex diseases. And so that's a kind of a high level view of what we do, but ultimately it's all about, you know, integration of these very different datasets. And then using that to ultimately come up with new experimental medicine that we would explore and experiment with and see what it can mean for patient impact.Harry Glorikian: Yeah. I think that's one of the most exciting parts of when I talk to everybody. Assuming the system is designed well, and the data going in is actually good, it's like, “Wow, I didn't notice. I didn't know that that happened. I didn't know that pathway was involved or this little tweak could make this difference.” And so that's what I see when I talk to different people that are working in this area. “I just didn't know,” or “None of the papers talked about this,” or “That's not what I learned in school.” And so that's the most fascinating part of these systems where you can identify things faster, hopefully and more accurately, hopefully than you might normally do with a human being. No knock to human beings, all of them are valuable, but it seems the systems move at a different pace and can handle a much broader level of data being input into them. And so that brings me to the question that Andrew, you and I have talked about. If you had to put a timeframe around it or something is, is this shortening the time to discovery? And I think you and I, the last time we talked, you said to about three years where I can shave off on the front. And then at some point when I have to get to a mouse, I have to follow the normal trajectory of that mouse. But if that's changed and you you've, you're finding other areas, I'd love to hear it. But Peyton and Tim, where do you see the aha the speed or the financial impact of what you're doing? You're doing it because it's moving at faster or you're able to identify something that you haven't, but it's better than X or Y that's already being done in the marketplace.Peyton Greenside: For us actually, this is, I mean, we do do things faster. We do improve on a lot of metrics. But it's actually, at least for my companyl about designing antibodies that couldn't otherwise exist. So for example, the standard monoclonal IgG, there are many tools out there to sort of discover initial molecules and optimize them, but you start getting into these kinds of next-generation or kind of Frankenstein antibodies, antibodies that are a tenth of the size, or SCRBs which are these fragments that are part of car T therapies or other formats.They become more complex and people have trouble engineering them, and you can kind of run your imagination and say, well, if I had the ability to engineer things, what other formats would I conceive? Would I consider, tiny antibodies like cell-penetrating peptides that can get into cells and sort of have all sorts of characteristics? But they're difficult to engineer.And so we actually, instead of sort of doing the same thing faster we actually think more about how can we expand the universe of what could be a potential therapeutic protein and how would that solve current patient needs in ways that existing therapeutics do not. And we do that by doing things faster, sort of, and cheaper and, sort of. More smartly. But hopefully that's what we really care about. Tim Sweeney: I'd answer probably somewhat like Peyton's. But if you look at a diagnostics and biomarkers in particular, a lot of diagnostics are about, “Hey, you know, we found that if you measure this one protein that's useful for health.” So it's just a very slow process and it's not optimized. You tend to study things that are obvious because they're easy to measure. Or like in our field, there's one protein called procalcitonin that's sort of the current closest biomarker for whether or not somebody has a bacterial infection, but PCT, as procalcitonin is abbreviated, was discovered 30 years ago and it was originally basically by accident that someone even measured it in someone with bacterial infections, and then it worked pretty well. And you know what I mean, it's a sort of based on serendipity and it can't be improved upon it has. However good procalcitonin was yesterday, that's how good it's going to be tomorrow and how it's going to be the day afterwards.I think the benefit of data science and in diagnostics was really began with cancer, when you had sort of the wonderfully successful tests like Oncotype showing how you could measure signals across complex diseases by integrating things from multiple biomarkers. And a lot of those were designed and there, again, the problem was that they took a long time to develop. And of course they take a long time to actually run, right? I mean, most of them, if you've ever had one of those tests done, it's like a week to send out, you know, you send some tissue to a company, it gets processed. You get your answer seven days later. So one of the things we're doing differently, one, it has to do with the way that we gather and integrate data sets to empower faster discovery.And that's kind of like Andrew. The other is basically the ability to build new answers that haven't yet existed, sort of more like Peyton. And ultimately the hope is to create a feedback loop where you know, better and better versions of the tests can be slowly released. And so over time, it's not just that you're sort of stuck with, “Hey, you know, procalcitonin is as good as it is [going to get].” It's like, you know, you're on Insept version five in 2030, and it's now X percent more accurate. And I think that's a real benefit to patients.[musical transition]Harry Glorikian: I want to pause the conversation for a minute to make a quick request. If you're a fan of MoneyBall Medicine, you know that we've published dozens of interviews with leading scientists and entrepreneurs exploring the boundaries of data-driven healthcare and research. And you can listen to all of those episodes for free at Apple Podcasts, or at my website glorikian.com, or wherever you get your podcasts.There's one small thing you can do in return, and that's to leave a rating and a review of the show on Apple Podcasts. It's one of the best ways to help other listeners find and follow the show.If you've never posted a review or a rating, it's easy. All you have to do is open the Apple Podcasts app on your smartphone, search for MoneyBall Medicine, and scroll down to the Ratings & Reviews section. Tap the stars to rate the show, and then tap the link that says Write a Review to leave your comments. It'll only take a minute, but it'll help us out immensely. Thank you! And now back to the show.[musical transition]Harry Glorikian: So you guys have been doing this for a while. Do you see the promise of big data and AI playing out the way that you thought and or is, or is it different than you thought now that now that you like jumped into the pool and you've been swimming in it for a while? Is it fulfilling the dream you had, is it more exciting than you thought?Andrew Radin: It's a funny question. Coming from very different industries, you know, looking at where I was 10 years ago, I think I was very naïve about what it actually takes to bring a drug to market. And I think in the very early days of the company, you know, my prior startups, you know, one of them I was in and out in a year and it exited. And there's no such thing in this industry, to do anything like that. And so, you know, part of it was biased by my prior experience, but I think part of it as well is, sometimes I think it's also hard to see how far things have moved along. And I think even in Tim's description is he was sort of talking about, well, you know, this, this was state-of-the-art science, you know, in decades past you know, the work he's doing today was impossible back then. So, you know, there's sort of these steady, incremental improvements.And I, and I think part of what really is happening in the industry is that the things to solve essentially are becoming exponentially harder. For example, for high throughput screening, which is maybe the old way of doing things, to find a hit is exponentially harder. For diagnostic tests or blood tests to sort of detect these nuances, you sort of have to bring in these technologies and these capabilities that are exponentially better at solving those things.And so I think what happens is, you can therefore characterize it in a different way, you know, is the time faster compared to the old way? Well, of course, because those old ways just don't have a chance of being able to do these things. Like, is it cheaper? Well, yeah, because those old ways, again, just don't have a chance. But I think part of it is what is the pace of innovation? And that's, I think kind of where the rubber meets the road and what is actually possible and what it's capable of. And so today, you know, we're, we talk about having, you know, 18 concurrent disease programs and we've got a very small team and we haven't raised very much money. You know, that would just be flat out impossible 10 years ago. And we still like raise some eyebrows around that, but now, it's okay. We recognize software is doing a lot of what used to happen in the wet labs. So this, you know, sort of fits within the expectation of what a modern technology company would do in this space.So I think there's that other angle of where expectations are kind of catching up with what's actually been produced. And therefore, you know, at, at some point we become the old technology. Thirty years from now, some next generation we'll be talking about, oh, those, those slow, painful people that, you know, tried this in the past kind of stuff. And so it's, you know, each, I think each iteration of innovation has its moment in the sun, if you will. And this is definitely the time for the work that we're collectively doing.Peyton Greenside: I think the promise is ahead of us. We're in an amazing time where I think things are starting to gain traction. We're starting to get tools and infrastructure, but if I were to say my conception of what machine learning and data science and generally computational power is going to do in biology and medicine, I think it's just starting.So I'm excited to see things like AlphaFold. I'm excited to see a lot of these kind of tools and capabilities to be unlocked. But I think, you're solving a complex problem, right? That protein that you're affecting is in a cell, it's part of the tissue, and it's part of a human, and there's so many more layers, I think, to consider.Yeah, we're making great progress. And I still certainly believe in the potential. That's why I'm here. But I do like to say, I think we're at the very, very early days. And as Andrew said, I think it's going to be fun to see what happens in 30 years. So I'm still very excited, but I wouldn't say we're at the accomplishments that I would consider as sort of really demonstrating the cornerstones of machine learning in, in biology and medicine.Tim Sweeney: I have to agree with Peyton, I think the best is ahead of us. So one of the courses we had to take at Stanford BMI, and I don't know if you two remember this, was Marc Musen taught this course on ontologies, but part of it had to do with sort of like the history of applications of sort of clinical data systems. And the oldest one, I forget the details, but it was in like, the '70s. And it was around sort of you know, clinical decision support for therapeutic prescribing. Obviously that system isn't around today and failed for its own reasons and he sort of walked through all of the failures of systems since then.And maybe one of the most remarkable things is how, how little AI and machine learning is actually employed in most clinical practice. You know, for all the buzz around computer vision, the AI that radiologists use most is probably their dictation. I mean, it isn't yet commonplace to have machine assisted radiography reads. And so will that be coming? Absolutely. But the interesting challenges in each successive generation of like, oh, you know, we got pretty close, but it turned out that X wasn't good enough, or it wasn't built in the right way to be integrated with workflow or is coming soon, but still needs some regulatory work or whatever else. There's plenty left to do. Peyton Greenside: I, I think that's probably one thing we all experience actually transitioning from academia to industry is, what's exciting in academia is not necessarily what's going to be reliable when you really want to make a good drug. So what you might think about it, you'd be like, “Oh man, that's a really cool model. I'd love to try that, you know, that's great.” And you kind of go right into industry and you're like, okay, well this is going to matter. This is, this is going to go to patients. It has to work multiple times. I think it is a very different standard. Right. And so I actually think it's the right thing. Just because you find something to be very, very cool and kind of, you know, I would say cutting edge, you really want it to work and want it to work over and over again. I think there's an unappreciated gap between when something is first proposed or conceived of or demonstrated and when you can really make it work at scale, over and over again in areas that matter.So I think we're basically in that transition, for, I would say, a lot of these techniques in biology and medicine. Now let's get to work and practice. Let's get to work and practice reliably. And now we can start sort of really seeing where we're going with the needle on really impactful problems. But it's funny, because I do think that's an important divide between sort of where we all started together.Andrew Radin: Yeah, no, I would, I would agree with that. I mean, look, most of our focus, these days is not on discovery. It is actually in the development of the therapeutics. It is about, you know, preparing for IND filings. It's all the regulatory work we need to do there. It's medicinal chemistry. It's a whole bunch of things that are outside of the discovery process. And as we proceed to the clinic, more and more of our overall effort as an organization has less to do about the core innovation that created all of these assets and more about the heavy lifting you have to do to ultimately get that product to market.And I think, to kind of tie it back to my previous comments, I think there's been a new generation of capabilities that has been created. To what these guys just said, it's gonna be a while until we actually see those things in the clinic. And to Tim's point about, you know, computer vision and radiology, like there's, there's a lot of good science that's already there and has been shown, experimentally to do a better job than obviously the, the human looking at those images. But yeah, it it's gonna take awhile until that becomes the standard. I am, you know, my daughter was born almost five years ago now, but I was shocked to observe, even back then, which is only five years ago, that medical records were being passed from clinic to clinic with a fax machine. It just blew my mind. Like you gotta be kidding me, a fax machine? I don't think I've seen a fax machine in all these years. And so, yeah, I think part of it is, if you want to take the place where innovation moves the slowest it's certainly got to be, you know, government, healthcare, or education. I'm not sure which of those might be the slowest, but there is a time for these new technologies to permeate the industry. And that is going to take time. And I think that's when, ultimately, patients and the people that are on the receiving end of all this innovation, like that's, when they're going to see that difference. And it is going to take many years for this stuff to kind of make its way through the process and ultimately into the hands of providers and ultimately to patients. And that big benefit is going to come in the years to come. It's obviously not in front of patients in many cases.Harry Glorikian: Yeah, well, maybe my brain is wired towards risk or innovation because I'm like, “well, if you're, if you wait till it's done to get involved, you're way too late,” right. You're going to be a dinosaur or you're going to be obsolete. And we've seen that in a lot of areas of tech compared to, you know, old standard industry.There was a great piece the other day about this engineer at Ford who had been working on the gas engine for 40 years and then wakes up one morning and he's like, I need to take early retirement because software and electric EV is the way it's going to go. And now I'm just in this sort of maintenance mode of what I'm doing.And I think about healthcare and I'm like any institution that isn't at least dabbling in using image analytics. for radiology or something and starting to  get used to this, I think they're way behind where they may want to be in the next five years, because technology doesn't follow just a slow curve on the way up. It has a way to go straight up at one point it before moving into an exponential curve. And I think the same for you guys. I mean, those companies that are not involved are partnering, investing in entities like you guys is, if you wait till it's finished, you're, it's already too late. Because Andrew, your system will keep kicking out new molecules and Peyton, you'll be making new antibodies and it'll be a little too late to catch up. I mean, that's, that's the way I think about it. Andrew Radin: I would temper that a little bit and the reason I would say that is because the companies that have been successful in the past in creating diagnostics and therapeutics…Products are on patent. They have long life cycles and they generate lots and lots of cash. And so, you know, big pharma, big diagnostics companies, they can kind of wait around and sort of see how things shake out with different younger companies and simply, buy or acquire, assuming that the companies are willing to be acquired. And so I think, large firms have been very successful in becoming, you know, acquisition and essentially manufacturing and marketing machines. So I don't necessarily think that some of these larger and established players that they're necessarily, their livelihoods are threatened. I think they will continue to acquire the best of the best with their, with their large cash reserves. I think some companies in this space will gather the momentum and break out. And I think in time we might see some changes over time as to what the big, you know, sort of players are in this space. But it's unlike other industries. Certainly software. It's like MySpace disappears and Facebook reappears the next day. And that's because you can deploy new technology and move users over in the course of an afternoon. And from a therapeutic perspective or a diagnostics perspective, that's just not that the pace at which those things move.So there's, there's lots of room for that. You know, and maybe similar in the automotive industry, you kind of have to build a factory and build some cars. It takes some times, right? So, so maybe there's some parallels there, I think in some cases, but. I don't see like a wholesale change happening overnight. At least from where I stand. Harry Glorikian: Not overnight, but we definitely have to have dinner and like have a discussion around this topic. Because I would love to bring some examples to the table about how I see things. Once you digitize something, the model itself doesn't have to stay the same way as it used to be. It is up for change. So I think those are the shifts that may change the dynamics of the market.But I'd love to have that discussion with a wonderful glass of wine. After having come from Napa this week, I can show up with a few nice bottles. Thank you so much for taking the time. Andrew, thank you for bringing this group together. Peyton, Tim, it was wonderful to meet both of you. I hope that we stay in touch and I'll keep watching the companies as they, progress. And I wish you guys incredible success. Peyton Greenside: Thanks so much. Tim Sweeney: Thank you Harry. Andrew Radin: It was our pleasure.Tim Sweeney: Andrew, Peyton, good to see you as always.Andrew Radin: Absolutely. Peyton Greenside: You too.Harry Glorikian: That's it for this week's show. You can find past episodes of MoneyBall Medicine at my website, glorikian.com, under the tab “Podcast.” And you can follow me on Twitter at hglorikian.  Thanks for listening, and we'll be back soon with our next interview.

Dr. Rick Baehner, MD, Chief Medical Officer of Precision Oncology at Exact Sciences discusses the Oncotype MAP™ Pan-Cancer Tissue test for patients with advanced, metastatic, refractory, or recurrent cancer. This rapid genomic tumor profiling test, previously known as PCDx, allows physicians to understand patients’ tumor profiles and effectively recommend targeted therapies or clinical trials based on the biology of their patients’ cancers. He also talks about the broader Oncology Business Unit at Exact Sciences.

Talcum powder, FLAURA, Oncotype and LRR, Vegetables & Prostate Cancer, "Flu Shot", WBRT for Alzheimer's, FLASH quadshotnews@gmail.com @QuadShotNews

An interview with Dr. Lynn Henry from University of Utah Huntsman Cancer Institute on "Role of Patient and Disease Factors in Adjuvant Systemic Therapy Decision-Making for Early-Stage, Operable Breast Cancer: Update of the ASCO Endorsement of CCO Guideline." This guideline update includes data from the MINDACT and TAILORx trials to clarify the recommendations for patients with hormone receptor-positive, HER2 not overexpressed, axillary node-negative early breast cancer. Read the full guideline at www.asco.org/breast-cancer-guidelines  TRANSCRIPT 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. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Hello and welcome to the ASCO Guidelines Podcast Series. My name is Shannon McKernin. And today, I'm interviewing Dr. Lynn Henry from the University of Utah Huntsman Cancer Institute, lead author on "Role of Patient and Disease Factors in Adjuvant Systemic Therapy Decision-Making for Early-Stage, Operable Breast Cancer: Update of the ASCO Endorsement of CCO Guideline." Thank you for being here today, Dr. Henry. Thank you very much for the invitation. So this guideline was updated to incorporate new data from the TAILORx and the MINDACT trials. So can you give us an overview of these trials and their results? Sure. So patients with hormone receptor-positive, HER2 negative breast cancer, are generally treated with anti-estrogen treatment and are sometimes also recommended to have chemotherapy. Since these tumors don't always respond well to chemotherapy, tests have been developed that provide more information about how much benefit, in terms of reduction of the likelihood of cancer coming back, an individual patient is likely to get from treatment with chemotherapy. It is important that the benefit of a treatment outweighs the risk of toxicity from the treatment. Two of those tests are called Oncotype DX and MammaPrint. And they have recently been tested in large clinical trials. So TAILORx is a large prospective trial that tested the Oncotype DX assay. In the Oncotype DX assay, a tumor is tested to get more information about how likely a cancer is to return and how much benefit the patient is likely to get from chemotherapy. Scores on this assay can range from 0 to 100. Previously, a study showed that patients whose tumors had scores of 10 or less, and who received five years of anti-estrogen treatment, were very unlikely to have their tumors return. So chemotherapy is not recommended for them. For patients with higher scores, above 30, we also already knew that chemotherapy is likely to decrease the chance of cancers in those patients, and, so, therefore, we generally recommend chemotherapy for women with higher scores. In the TAILORx trial, the recently reported trial, more than 6,700 women with hormone receptor-positive, HER2 negative, lymph node-negative breast cancer had their tumors tested and were found to have Oncotype DX recurrent scores between 11 and 25, which is in that intermediate range or at the higher end of the low range. Before this trial was conducted, many people with tumors like these, in the intermediate range, were treated with both chemotherapy and endocrine therapy because we weren't sure how much benefit they would obtain from chemotherapy, and we didn't want to leave out a potentially helpful treatment. In this trial, patients were randomized, or randomly assigned by a computer, to treatment with chemotherapy followed by endocrine therapy or to treatment with endocrine therapy alone. The trial was mainly looking at whether leaving out chemotherapy would increase the likelihood of invasive cancer returning. And, luckily, overall, the trial showed that the likelihood of cancer returning in those patients who got endocrine therapy alone, without chemotherapy, wasn't significantly different compared to those who were treated with chemotherapy followed by endocrine therapy. They also looked, specifically, at the group of women who were 50 years of age or younger. So mostly premenopausal women. Now, this was an exploratory question, meaning it provides information that may be correct, but it hasn't been as fully tested as the main question about what do we do for all women? In these younger women, there appeared to be some benefit from chemotherapy in those whose tumors had scores from 21 to 25, and, also possibly, in those whose tumors had scores from 16 to 20. Therefore, we still consider giving chemotherapy to younger women with Oncotype DX scores in the middle range, from 16 to 25, but not to women over age 50. So that was the TAILORx trial. The MINDACT trial was a bit different. It was testing the MammaPrint assay and the trial also included primarily women with hormone receptor-positive, HER2 negative breast cancer. But in this case, most women's sorry lymph nodes were negative, although a few women had up to three lymph nodes involved. In that trial, patient's risk of disease recurrence was assessed in two ways. First, it was assessed based on clinical factors. So the size of the tumor, how many lymph nodes were involved, and the estrogen receptor, progesterone receptor, and HER2 receptors. Second, it was assessed based on genomic factors-- that was using the MammaPrint test. So if patients were low for both clinical factors and genomic factors, they only were treated with anti-estrogen therapy. If they were high for both clinical factors and genomic factors, then they were treated with chemotherapy followed by anti-estrogen therapy. However, if they were high for one and low for the other, then they were randomized to either endocrine therapy alone or chemotherapy followed by endocrine therapy. So it was a little bit of a confusing trial. In the MINDACT trial, those patients who were thought to be high risk based on their clinical risk, so the size of the tumor, the number of lymph nodes, but then found to be low risk on the MammaPrint assay. They found that there was no benefit to treatment with chemotherapy in terms of how likely a woman was to develop distant metastatic disease. And if they were low risk, based on the clinical assessment, then there didn't appear to be a benefit of actually doing the test, the assay, because chemotherapy wouldn't be recommended for the patient, regardless of the results. So that was the MINDACT trial. So what are the new and updated recommendations for the guideline? Yes, so in this guideline, we, based on the TAILORx trial, we made new recommendations for use of the Oncotype DX results. All of these results apply to women with hormone receptor-positive, HER2 negative, lymph node-negative breast cancer. So for women older than age 50, if they have an Oncotype score of 25 or lower, then clinicians may offer endocrine therapy and no chemotherapy. However, for women age 50 or under, if they have an Oncotype score of 15 or lower, 15, then, clinicians may offer endocrine therapy and no chemotherapy. But if the score is 16 to 25, then chemotherapy can be considered in addition to endocrine therapy. So it made a difference in that gray area in the middle. For all women with score 26 to 30, chemotherapy may be considered. And for scores above 30, chemotherapy should definitely be considered. The data from the MammaPrint trial actually aren't that new. Results from that trial were originally published in 2016. However, that was after the original guideline was published, so we wanted to add these results to these updated guidelines for completeness. For a patient with hormone receptor-positive, HER2 negative, node-negative breast cancer, who is thought to be at high clinical risk of breast cancer recurrence, if the MammaPrint assay shows low genomic risk, then treatment with chemotherapy can be avoided. If a patient is thought to be at low clinical risk, the MammaPrint should not be used as chemotherapy can be avoided regardless. And for a patient with hormone receptor-positive, HER2 negative breast cancer, but who has one to three positive lymph nodes, who is thought to be at high clinical risk of breast cancer recurrence, if the MammaPrint assay shows low genomic risk, then it is possible that chemotherapy could be avoided, especially if only one lymph node is involved. So I think the bottom line for this part is that both of these tests-- there are now women who previously would have been recommended to have chemotherapy that maybe now we can avoid chemotherapy based on using these assays on their tumors. So why are these changes so important and how will they affect practice? Yes, that's a good question. Before the publication of the TAILORx trial, we had good information about how to treat patients who had either very low or very high Oncotype scores. But we really weren't sure how best to treat those patients who scores fell in the middle. Now, we have important information to guide decisions about chemotherapy for patients with intermediate scores. For many patients with scores in this range, these new results mean they will be able to avoid chemotherapy and just get endocrine therapy. While these results don't give us answers for every patient, they do provide more information that oncologists can use when having discussions with patients about the benefits and risks of chemotherapy. And what does this mean for patients with early-stage invasive breast cancer? And what should they talk to their doctors about? So as a result of both of these trials, we now have additional tools that can help oncologists provide more individualized treatment recommendations for patients and really assess whether or not chemotherapy, in addition to endocrine therapy, is likely to provide benefits. Knowing which patients' tumors will respond to chemotherapy can help some patients avoid unwanted side effects from a treatment that's not likely to actually give them much benefit. Now, these tests aren't appropriate for everyone and don't provide all the answers, but they are an important step in the right direction for providing more personalized treatment for women newly-diagnosed with certain types of breast cancer. Patients should talk with their doctors about whether these tests are right for them when they're making important decisions about whether or not they should receive treatment with chemotherapy. Great. Thank you, Dr. Henry, for this informative overview of the guideline. Keeping these clinical practice guidelines updated is really crucial and it takes a lot of careful thought to ensure these recommendations represent the evidence. So thank you for coming on the podcast to discuss the "Role of Patient and Disease Factors in Adjuvant Systemic Therapy Decision-Making for Early-Stage, Operable Breast Cancer: Update of the ASCO Endorsement of CCO Guideline." Thank you very much for the opportunity to talk with you today. And thank you to all of our listeners for tuning into the ASCO Guidelines Podcast Series. To read the full guideline, go to www.asco.org/breast-cancer-guidelines. And if you've enjoyed what you've heard today, please rate and review the podcast and refer the show to a colleague.

An interview with Dr. Lynn Henry from University of Utah Huntsman Cancer Institute on "Role of Patient and Disease Factors in Adjuvant Systemic Therapy Decision-Making for Early-Stage, Operable Breast Cancer: Update of the ASCO Endorsement of CCO Guideline." This guideline update includes data from the MINDACT and TAILORx trials to clarify the recommendations for patients with hormone receptor-positive, HER2 not overexpressed, axillary node-negative early breast cancer. Read the full guideline at www.asco.org/breast-cancer-guidelines  TRANSCRIPT 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. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Hello and welcome to the ASCO Guidelines Podcast Series. My name is Shannon McKernin. And today, I'm interviewing Dr. Lynn Henry from the University of Utah Huntsman Cancer Institute, lead author on "Role of Patient and Disease Factors in Adjuvant Systemic Therapy Decision-Making for Early-Stage, Operable Breast Cancer: Update of the ASCO Endorsement of CCO Guideline." Thank you for being here today, Dr. Henry. Thank you very much for the invitation. So this guideline was updated to incorporate new data from the TAILORx and the MINDACT trials. So can you give us an overview of these trials and their results? Sure. So patients with hormone receptor-positive, HER2 negative breast cancer, are generally treated with anti-estrogen treatment and are sometimes also recommended to have chemotherapy. Since these tumors don't always respond well to chemotherapy, tests have been developed that provide more information about how much benefit, in terms of reduction of the likelihood of cancer coming back, an individual patient is likely to get from treatment with chemotherapy. It is important that the benefit of a treatment outweighs the risk of toxicity from the treatment. Two of those tests are called Oncotype DX and MammaPrint. And they have recently been tested in large clinical trials. So TAILORx is a large prospective trial that tested the Oncotype DX assay. In the Oncotype DX assay, a tumor is tested to get more information about how likely a cancer is to return and how much benefit the patient is likely to get from chemotherapy. Scores on this assay can range from 0 to 100. Previously, a study showed that patients whose tumors had scores of 10 or less, and who received five years of anti-estrogen treatment, were very unlikely to have their tumors return. So chemotherapy is not recommended for them. For patients with higher scores, above 30, we also already knew that chemotherapy is likely to decrease the chance of cancers in those patients, and, so, therefore, we generally recommend chemotherapy for women with higher scores. In the TAILORx trial, the recently reported trial, more than 6,700 women with hormone receptor-positive, HER2 negative, lymph node-negative breast cancer had their tumors tested and were found to have Oncotype DX recurrent scores between 11 and 25, which is in that intermediate range or at the higher end of the low range. Before this trial was conducted, many people with tumors like these, in the intermediate range, were treated with both chemotherapy and endocrine therapy because we weren't sure how much benefit they would obtain from chemotherapy, and we didn't want to leave out a potentially helpful treatment. In this trial, patients were randomized, or randomly assigned by a computer, to treatment with chemotherapy followed by endocrine therapy or to treatment with endocrine therapy alone. The trial was mainly looking at whether leaving out chemotherapy would increase the likelihood of invasive cancer returning. And, luckily, overall, the trial showed that the likelihood of cancer returning in those patients who got endocrine therapy alone, without chemotherapy, wasn't significantly different compared to those who were treated with chemotherapy followed by endocrine therapy. They also looked, specifically, at the group of women who were 50 years of age or younger. So mostly premenopausal women. Now, this was an exploratory question, meaning it provides information that may be correct, but it hasn't been as fully tested as the main question about what do we do for all women? In these younger women, there appeared to be some benefit from chemotherapy in those whose tumors had scores from 21 to 25, and, also possibly, in those whose tumors had scores from 16 to 20. Therefore, we still consider giving chemotherapy to younger women with Oncotype DX scores in the middle range, from 16 to 25, but not to women over age 50. So that was the TAILORx trial. The MINDACT trial was a bit different. It was testing the MammaPrint assay and the trial also included primarily women with hormone receptor-positive, HER2 negative breast cancer. But in this case, most women's sorry lymph nodes were negative, although a few women had up to three lymph nodes involved. In that trial, patient's risk of disease recurrence was assessed in two ways. First, it was assessed based on clinical factors. So the size of the tumor, how many lymph nodes were involved, and the estrogen receptor, progesterone receptor, and HER2 receptors. Second, it was assessed based on genomic factors-- that was using the MammaPrint test. So if patients were low for both clinical factors and genomic factors, they only were treated with anti-estrogen therapy. If they were high for both clinical factors and genomic factors, then they were treated with chemotherapy followed by anti-estrogen therapy. However, if they were high for one and low for the other, then they were randomized to either endocrine therapy alone or chemotherapy followed by endocrine therapy. So it was a little bit of a confusing trial. In the MINDACT trial, those patients who were thought to be high risk based on their clinical risk, so the size of the tumor, the number of lymph nodes, but then found to be low risk on the MammaPrint assay. They found that there was no benefit to treatment with chemotherapy in terms of how likely a woman was to develop distant metastatic disease. And if they were low risk, based on the clinical assessment, then there didn't appear to be a benefit of actually doing the test, the assay, because chemotherapy wouldn't be recommended for the patient, regardless of the results. So that was the MINDACT trial. So what are the new and updated recommendations for the guideline? Yes, so in this guideline, we, based on the TAILORx trial, we made new recommendations for use of the Oncotype DX results. All of these results apply to women with hormone receptor-positive, HER2 negative, lymph node-negative breast cancer. So for women older than age 50, if they have an Oncotype score of 25 or lower, then clinicians may offer endocrine therapy and no chemotherapy. However, for women age 50 or under, if they have an Oncotype score of 15 or lower, 15, then, clinicians may offer endocrine therapy and no chemotherapy. But if the score is 16 to 25, then chemotherapy can be considered in addition to endocrine therapy. So it made a difference in that gray area in the middle. For all women with score 26 to 30, chemotherapy may be considered. And for scores above 30, chemotherapy should definitely be considered. The data from the MammaPrint trial actually aren't that new. Results from that trial were originally published in 2016. However, that was after the original guideline was published, so we wanted to add these results to these updated guidelines for completeness. For a patient with hormone receptor-positive, HER2 negative, node-negative breast cancer, who is thought to be at high clinical risk of breast cancer recurrence, if the MammaPrint assay shows low genomic risk, then treatment with chemotherapy can be avoided. If a patient is thought to be at low clinical risk, the MammaPrint should not be used as chemotherapy can be avoided regardless. And for a patient with hormone receptor-positive, HER2 negative breast cancer, but who has one to three positive lymph nodes, who is thought to be at high clinical risk of breast cancer recurrence, if the MammaPrint assay shows low genomic risk, then it is possible that chemotherapy could be avoided, especially if only one lymph node is involved. So I think the bottom line for this part is that both of these tests-- there are now women who previously would have been recommended to have chemotherapy that maybe now we can avoid chemotherapy based on using these assays on their tumors. So why are these changes so important and how will they affect practice? Yes, that's a good question. Before the publication of the TAILORx trial, we had good information about how to treat patients who had either very low or very high Oncotype scores. But we really weren't sure how best to treat those patients who scores fell in the middle. Now, we have important information to guide decisions about chemotherapy for patients with intermediate scores. For many patients with scores in this range, these new results mean they will be able to avoid chemotherapy and just get endocrine therapy. While these results don't give us answers for every patient, they do provide more information that oncologists can use when having discussions with patients about the benefits and risks of chemotherapy. And what does this mean for patients with early-stage invasive breast cancer? And what should they talk to their doctors about? So as a result of both of these trials, we now have additional tools that can help oncologists provide more individualized treatment recommendations for patients and really assess whether or not chemotherapy, in addition to endocrine therapy, is likely to provide benefits. Knowing which patients' tumors will respond to chemotherapy can help some patients avoid unwanted side effects from a treatment that's not likely to actually give them much benefit. Now, these tests aren't appropriate for everyone and don't provide all the answers, but they are an important step in the right direction for providing more personalized treatment for women newly-diagnosed with certain types of breast cancer. Patients should talk with their doctors about whether these tests are right for them when they're making important decisions about whether or not they should receive treatment with chemotherapy. Great. Thank you, Dr. Henry, for this informative overview of the guideline. Keeping these clinical practice guidelines updated is really crucial and it takes a lot of careful thought to ensure these recommendations represent the evidence. So thank you for coming on the podcast to discuss the "Role of Patient and Disease Factors in Adjuvant Systemic Therapy Decision-Making for Early-Stage, Operable Breast Cancer: Update of the ASCO Endorsement of CCO Guideline." Thank you very much for the opportunity to talk with you today. And thank you to all of our listeners for tuning into the ASCO Guidelines Podcast Series. To read the full guideline, go to www.asco.org/breast-cancer-guidelines. And if you've enjoyed what you've heard today, please rate and review the podcast and refer the show to a colleague.

Rachel Freedman, MD, MPH- Assistant Professor, Medicine, Harvard Medical School, Dana-Farber Cancer Institute presents a self-assessment question from an ASCO University course focusing on the treatment breast cancer.  AUDIO TRANSCRIPT Welcome to the self-evaluation episode of the ASCO University weekly podcast. My name is Rachel Friedman, and I'm a medical oncologist and clinical researcher in the Breast Oncology Center at Dana-Farber Cancer Institute. Today, we feature a self-evaluation question on the treatment of early stage breast cancer. We begin by reading the question stem. A 75-year-old woman with a past medical history of coronary artery disease and diabetes, with an ECOG performance status of 2, has been seen in the medical oncology office following a partial mastectomy for a 1 centimeter invasive breast cancer. The margins were clear and hormone receptors are reported as positive. The HER2/neu status is reported as negative. An Oncotype recurrence score is reported as 5. Which of the following is the best adjuvant therapy for this patient? Choice A, doxorubicin, cyclophosphamide, and weekly paclitaxel, followed by an aromatase inhibitor. B, docetaxel and cyclophosphamide for four cycles, followed by an aromatase inhibitor for five years with radiation therapy to the breast. C, radiation therapy to the breast and axilla, followed by an aromatase inhibitor. D, aromatase inhibitor. E, tamoxifen. The correct answer to this question is D, aromatase inhibitor. This patient has a poor performance status and high co-morbidity burden, with a higher likelihood of non-breast cancer deaths over breast cancer death, over time. The cancer is low risk, with a low likelihood for local and distant recurrence. Radiation and chemotherapy are unlikely to improve her outcome and will increase her toxicity risk. Further, we have multiple randomized trials to support safe omission of radiation and the setting of older age and stage 1 hormone receptor positive disease. Briefly, the benefit of adjuvant chemotherapy is anticipated to be negligible, and even harmful, in the setting of her low risk disease, advanced co-morbidity, poor functional status, and Oncotype score of 5. Chemotherapy should be avoided in this setting, making answers A and B incorrect. Although radiation should be considered and administered in most patients with invasive breast cancer, undergoing breast conservation, as mentioned earlier, we have prospective randomized controlled trial data, supporting omission of radiation in this clinical scenario, making option C also incorrect for this reason. Further, there is no indication for radiation to the axilla in a low risk breast cancer, such as the one described here, making option C incorrect for that reason as well. Option E, tamoxifen, is also a treatment option here, but may be less appealing in an older patient who lives a more sedentary lifestyle who may be at more risk for adverse events on tamoxifen, such as thrombosis, and where the use of aromatase inhibitors may be of a small incremental benefit over tamoxifen, with regard to risk for recurrences over time. Thank you for listening to this week's episode of the ASCO University weekly podcast. For more information on the treatment of breast cancer, including opportunities for self-evaluation and for a review, please visit the comprehensive eLearning center at university.asco.org. 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. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.

Einstein Perspectives recently spoke with Dr. John Leighton, Division Chair of Hematology and Medical Oncology at Einstein Healthcare Network in Philadelphia, for his interpretation of this game-changing New England Journal of Medicine study.