Podcasts about nf1

In today's episode, supported by SpringWorks Therapeutics, we spoke with Christopher L. Moertel, MD, about the evolution of treatments for neurofibromatosis type 1 (NF1)–associated plexiform neurofibromas (PN). Dr Moertel is a professor and the Pediatric Neuro-Oncology Fellowship Program director in the Division of Pediatric Hematology/Oncology, a faculty member in the Department of Pediatrics, medical director of the Pediatric Neuro-Oncology and Neurofibromatosis Programs, co-medical director of the Katie Hageboeck Children's Cancer Research Fund Clinic, clinical neuro-oncology leader of the Brain Tumor Program, and the Kenneth and Betty Jayne Dahlberg Professor at the University of Minnesota School of Medicine in Minneapolis. In our exclusive interview, Dr Moertel discussed the expansion of the NF1-associated PN treatment paradigm to include the MEK inhibitors mirdametinib (Gomekli) and selumetinib (Koselugo); the benefits of offering treatment options in oral formulations; the toxicities associated with MEK inhibitors; the importance of managing these adverse effects to ensure long-term treatment adherence; and the need for continued oncology education to optimize treatment outcomes for this population.

This week Monique chats with Sienna Macalister (they/them), who listeners may know by their Instagram handle @sienna.stims, about being an Autistic person with high support needs. Sienna is a non-binary, ‘unreliably speaking’ Autistic advocate, diagnosed with Autism Level 3. They are multiply neurodivergent and have a number of co-occurring health conditions, including Ehlers Danlos Syndrome (EDS), Postural Orthostatic Tachycardia Syndrome (POTS), and Neurofibromatosis Type 1 (NF1). Sienna is passionate about creating a world where Autistic people are not just accepted but celebrated, with a deep affinity for exploring neurodivergence with nuance. Monique and Sienna cover: What does ‘unreliably speaking’ mean? What neurodivergence means to Sienna and the importance of understanding the term to mean more than just Autism and ADHD. Sienna’s experience of early diagnosis of Autism and the diagnostic overshadowing this led to, particularly around diagnosis of their health conditions. The evolution of Sienna’s neurodivergent identity. Sienna’s experience of using mobility, communication, and health and wellbeing supports. Support needs, disability, and therapeutic intervention as a valid part of the neurodivergent experience, and the difference between affirming and non-affirming therapies. The role of lateral violence and internalised ableism in excluding people with higher support needs from the cultural conversation on Autism. Sienna’s suggestions to increase inclusion and representation for Autistic people with higher support needs. Sienna’s current special interest – budgie breeding! Find Sienna on TikTok and Instagram @sienna.stims, on their professional Instagram @sienna.macalister_media, or on YouTube @sienna_stims. Sienna’s writing is features in the anthologies Someone Like Me, edited by Clem Bastow and Jo Case, and Hyperfocus, edited by Spectrum Writing. Got questions for us?? Come along to our LIVE Q&A event! Held online on 27th June (with replay available to all ticket holders). Grab a ticket here and submit your question! Enjoyed the episode and want to support us further? Join our Patreon community! Patreon subscribers receive ad-free episodes, basic episode transcripts from Season 4 onwards, access to a monthly live zoom hang out, 50% off our episode articles, plus bonus monthly content (depending on subscription tier). Check out our Patreon page to support us, as we aim to make quality mental health care information accessible to everyone: www.patreon.com/ndwomanpod. Want polished copies of our episodes in beautiful and readable pdf article format? Grab them here. Contact us at ndwomanpod@gmail.com, or visit our website: www.ndwomanpod.comSee omnystudio.com/listener for privacy information.

Featuring an interview with Dr Christopher L Moertel, including the following topics: Overview of neurofibromatosis type 1(NF1) (0:00) Cancer in NF1 (8:38) Dermatologic manifestations of NF1 (16:57) Treatment options for NF1 (20:43) Malignant peripheral nerve sheath tumors (MPNST) (25:14) FDA-approved MEK inhibitors for NF1 plexiform neurofibromas (28:36) Specializing in NF (44:44) CME information and select publications

Featuring a slide presentation and related discussion from Dr Christopher L Moertel, including the following topics: Overview of neurofibromatosis (0:00) Common clinical manifestations of neurofibromatosis type 1 (NF1) (14:13) Role of MEK inhibitors in the management of NF1 plexiform neurofibromas (29:30) CME information and select publications

Grab a cafe au lait and settle in for a nerve-rackingly good conversation with Dr. Carlos Prada, Pediatric Genetics specialist at Northwestern University's Lurie Children's Hospital. Dr. Prada walks us through the most common presentations of NF1, the recently updated diagnostic criteria, and important follow-up screening exams and treatment options. It's an episode so good, even your nerves will be on edge!

Dermatology Snapshots is sponsored by a educational grant from Abbivie. Feedback always welcome. 1)    12 SQ-HDM SLIT for treating allergic rhinitis and allergic asthma caused by house dut mites NICE2)    Combination of Janus kinase inhibitor and biologic for recalcitrant severe atopic dermatitis3)    Demodicosis4)    Selumetinib in adults with NF1 and inoperable plexiform neurofibroma: a phase 2 trial5)    Analysis of health outcomes in women on oral 5 alpha reductase inhibitors: a single centre retrospective cohort study6)    Paediatric Bier anaemic spots, cyanosis, and urticaria like eruption syndrome (BASCULE) in 42 patients: a peek intodysautonomia.7)     Isla Galpin. Violin Sonata in G minor, 1st and 2nd movement by Eccles

I sit down with Katie, who has been living with Neurofibromatosis Type 1 (NF1), a rare genetic condition known for its tumor-growing tendencies. Diagnosed at a young age, Katie's journey with chronic illness began at just four years old. By the time she was 12, her spine had crushed her spinal cord, leading to a life-altering spinal cord injury. Alongside NF1, Katie also manages Scoliosis, chronic pain, and fatigue, challenges that have shaped her life in profound ways.We dive into Katie's medical journey, from the surgeries and treatments she's undergone to manage mobility and pain, to the therapies that have helped her navigate daily life. She shares the emotional and mental toll of living with chronic illness, how she has learned to advocate for herself within the medical system, and the evolution of her relationship with her body.Katie also opens up about the feelings of being a burden that many with chronic illness experience, and how she counters these thoughts with self-love and self-care. Whether you're facing a similar diagnosis or simply seeking insight into resilience and self-advocacy, Katie's story is one of strength, perseverance, and hope!Find Katie :Instagram

Dr Moertel discussed the significance of this approval, key efficacy and safety data from the phase 2 ReNeu trial (NCT03962543), and considerations for integrating mirdametinib into clinical practice for patients with NF1-associated PN.

A Different Man This week we are looking A Different Man, at a film that takes some pretty bold and experimental swings at a subject that many would be uncomfortable with; facial difference and the experiences of the people who live with it. Sebastian Stan takes on the role of Edward; a shy actor who has facial difference (it is not mentioned but it seems to be Neurofibromatosis type 1 or NF1). His life is upended when he tries an experimental procedure and suddenly his face is no longer different. It's multi layered, complex and very very odd. The whole team is in for this one and there's plenty to talk about here. Enjoy! Synopsis An aspiring actor undergoes a radical medical procedure to drastically transform his appearance. However, his new dream face quickly turns into a nightmare as he becomes obsessed with reclaiming what was lost. https://youtu.be/sIK2LCOmz8o A huge thank you to all our wonderful weirdos who tune into to each episode of the show, especially those of you who have facial difference or in fact, any kind of difference... who join in on the live-chat during the Twitch stream this week (and every week!). If you haven't done so before join us next week for our live show 7:30pm next Tuesday! Special love and thanks goes to those who have financially bolstered this podcast via dropping their typewriter into our Ko-Fi cup and now also by subscribing on Twitch! Your generosity is always appreciated! If you feel so inclined drop us a sub! The more subs we get the more  emotes, you get! Every bit of your support helps us to keep the show on the air! Don't fret if you can't be there for the recording though as you can catch them on Youtube usually later that very night. Make sure to subscribe so you don't miss them! https://youtu.be/_9CmC5Rmsdw?si=Tbk2Y8rJnDDbR7Dz WE WANT YOUR FEEDBACK! Send in voicemails or emails with your opinions on this show (or any others) to info@theperiodictableofawesome.com Please make sure to join our social networks too!  We're on: Youtube: https://www.youtube.com/user/TPToA/ Twitter: www.twitter.com/TPToA Facebook: www.facebook.com/PeriodicTableOfAwesome Instagram: www.instagram.com/theperiodictableofawesome/

The Promise of Discovery Season 5, Episode 3 Neurofibromatosis Type 1 (NF1) is a neurodevelopmental disease which affects about 100,000 people in the US. Around 80% of these patients experience cognitive and intellectual impairments which are unaffected by currently approved therapies for NF1. A recent genetic study from our lab identified an association between the NF1 disease and a receptor protein called metabotropic glutamate receptor 7 (mGlu7). This project investigates how using small molecules to augment mGlu7 function could help identify new therapies for NF1 patients struggling with cognitive impairments. Featuring: Harrison Parent, Ph.D. Candidate- Niswender Lab, Department of Pharmacology, Vanderbilt University School of Medicine Interviewer: Colleen Niswender, Ph.D., Associate Professor of Pharmacology; Director of Molecular Pharmacology, Warren Center for Neuroscience Drug Discovery, and a Vanderbilt Kennedy Center Member

Omkring 2000 personer lever i Danmark med den sjældne genetiske sygdom Neurofibromatose 1 (NF1), der både kan nedarves fra forældrene eller vise sig som en nyopstået mutation. 29-årige Sofie lever med den sjældne gen-sygdom NF1, der blandt andet giver hende en skæv ryg. Da Sofie gik i anden klasse, var ryggen 95 grader skæv og Sofie har gennem sin opvækst været igennem ni rygoperationer for at rette op på den. Sofie lever i dag et godt liv med sygdommen og arbejder dagligt for at hjælpe andre med NF1.Podcasten er produceret af SundhedsTVAfsnitet er sponsoreret af Alexion.

Patients with plexiform neurofibromas (PN) associated with neurofibromatosis type 1 (NF1) experience considerable morbidity, a poor quality of life, and increased mortality. Research efforts have led to earlier diagnosis, new monitoring approaches, emerging treatment options, and considerations for surgical intervention. To this end, it is critical that pediatric oncologists as well as other members of the multidisciplinary team neurologists caring for patients with NF1-PN are up to date on recent advances. In this podcast lecture library, Dr. Armstrong uses a case-based discussion to address the heterogeneity and complexity of this condition as well as considerations for the use of emerging therapies when making individualized management decisions among diverse patients.Launch Date: October 31, 2024Release Date: October 31, 2024Expiration Date: September 30, 2025FACULTYAmy Armstrong, MDAssistant Professor of PediatricsDivision of Hematology/OncologyNeurofibromatosis (NF) CenterWashington University School of MedicineSt. Louis, MissouriThis podcast provides accredited continuing education credits.  To receive your credit, please read the accreditation information provided at this link below prior to listening to this podcast.https://www.practicepointcme.com/CMEHome/neurofibromatosis-type-1-related-plexiform-neurofibromas-improving-diagnosis-and-monitoring-while-integrating-ongoing-updates-in-the-treatment-continuum-1

In the patient populations treated by neurologists, central neuropathic pain develops most frequently following spinal cord injury, multiple sclerosis, or stroke. To optimize pain relief, neurologists should have a multimodal and individualized approach to manage central neuropathic pain. In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Charles E. Argoff, MD, author of the article “Central Neuropathic Pain,” in the Continuum October 2024 Pain Management in Neurology issue. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Argoff is a professor of neurology and vice chair of the department of neurology, director of the Comprehensive Pain Management Center, and director of the Pain Management Fellowship at Albany Medical College in Albany, New York. Additional Resources Read the article: Central Neuropathic Pain Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Full episode transcript available here Dr Jones: This is Doctor Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum Journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Jones: This is Doctor Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today I'm interviewing Dr Charles Argoff, who recently authored an article on central neuropathic pain in the latest issue of Continuum covering pain management. Dr Argoff is a neurologist at Albany Medical College where he's a professor of Neurology, and he serves as vice chair of the Department of Neurology and program director of the Pain Medicine Fellowship Program there. Dr Argoff, welcome. Thank you for joining us today. Why don't you introduce yourself to our listeners?  Dr Argoff: I'm Charles Argoff. It's a pleasure to be here and thank you so much for that kind introduction. Dr Jones: I've read your article. Many of our listeners are going to read your article. Wonderful article, extremely helpful. Closes a lot of gaps, I think, that exist in our field about understanding central neuropathic pain, treating central neuropathic pain. You now, Doctor Argoff, you have the attention of a huge audience of mostly neurologists. What's the biggest point you would like to make to them, or the most important practice-changing advice that you would give to them? Dr Argoff: I think it's at least twofold. One is that central neuropathic pain is not as uncommon as you think it might be, and it occurs in a variety of settings that are near and dear to a neurologist's heart, so to speak. And secondly, although we live in an evidence-based world and we want to practice evidence-based medicine - and I'm proud to have formerly been a member of the Quality Standard subcommittee, which I think has changed its name over time. And so, I understand the importance of, you know, treatment based upon evidence - the true definition of evidence-based medicine is using the best available evidence in making decisions about individual patients. And so, I would urge those who are listening that, although there might not be as robust evidence currently as you'd like, please don't not take the time to try to treat the patient in front of you o r at least acknowledge the need for treatment and work with your colleagues to address the significant neuropathic pain associated with that central neurological disorder. Because it can be life-changing in a positive way to make even a dent and to really work with somebody, even though not clear-cut always what's going to work for an individual patient. Dr Jones: Well said. I'm glad you brought that up. So, to put it a different way, absence of evidence is not an excuse for absence of treatment. Right? Dr Argoff: Exactly. And I think that, I hope that we would agree that especially in neurology, what we do is about as far from, ‘Yep, you've got strep throat, here's that antibiotic that's going to work for you and all you have to do is take the medicine.' I mean, most of what we do is nowhere near that.  Dr Jones: It's complicated stuff. And this is a complicated topic. And I'll tell you, I learned a lot reading your article. I think most of us in neurology and medicine, when we hear the term neuropathic pain, it feels roughly synonymous with peripheral generators of that pain, such as diabetic neuropathy or posttraumatic neuralgia. But as you mentioned, there's central mechanisms for pain generation. How is it defined? What is central neuropathic pain? Dr Argoff: It's defined as pain caused by a lesion or disease of the central somatosensory system . Though neuropathic pain in general is pain associated with the lesion of the somatosensory system; and to your point, that can be peripheral, which of course is outside the spinal cord, or brain or central, which is within the spinal cord or brain. And central neuropathic pain is defined specifically as pain caused by a lesion or disease of the central somatosensory system. That's either brain or spinal cord. But there's an interesting follow-up, and I'm going to ask if you could remind me because I know we're talking about definitions now, but I'll just bring something up and we can come back to it. What's interesting about that is that my - whoever 's listening, that's not to say that they're not connected. And in fact, they are very much connected. And there's very new work, which I included in the article, down at Washington University in Saint Louis, that suggests you can actually affect central neuropathic pain by addressing peripheral input to the central nervous system. If you remember Ken Casey at the University of Michigan at the World Pain Congress in Vancouver, British Columbia many years ago, he ended his talk on pain with a limerick, of which the last line was, Remember, there ain't no such thing as pain without a brain. And so that kind of summarizes that. Dr Jones: Well, and it goes both ways too, right? We know that there's some central sensitization that can happen with peripheral generators, right? So we really have to think about the whole circuit. Dr Argoff: Yes. And that's been sometimes the bane of my existence as a colleague of others and a sometimes debater. Is the pain central? Is it peripheral? Well, it's everything. And it's important to know as many of the mechanisms and many of the targets that you could use for treatment so that you can affect the best outcome for your patients. Dr Jones: Yeah, so - and you mentioned in your article what some of the common causes of central neuropathic pain are. What are the big ones in your experience?  Dr Argoff: So, the biggest ones are spinal cord injury-related pain, MS-related pain - and I'd like to come back to a point and just if I do the third one - and central poststroke pain. And what struck me, I think Tim Vollmer published a survey about the incidence, the prevalence of ongoing pain in patients with multiple sclerosis. And it blew my mind several years ago because it was incredibly high. Like in this survey of MS patients who, you never hear about pain, you hear about these modifying treatments, all the wonderful expanses that have been made. I mean, like seventy something percent of people say they have moderate to severe pain. And when you think about how sensory processing occurs, it makes perfect sense that a demyelinating disorder is going to interrupt the flow of information for a person to feel normal.  Dr Jones: Yeah, I think it's a good example of, there are things that we tend to focus on as clinicians where we worry about deficit and function and capacity. But if we're patient-centered and we ask patients what they care about, pain usually moves up higher on the list. And so, I think that's why we, it's maybe underrecognized with some of those central disorders, right? Dr Argoff: I think so, and I and I think you hit the nail on the head that - and we're also trained that way. I tell this to my patients very often so that they are reassured when I examine them and I say, and I tell them that everything looked pretty OK. It's not a medical term, I understand that. Because what we do in a typical neurological exam, even if it's detailed, doesn't really address all the intricacies of the nervous system. So it's really a big picture and sensory processing and especially picking up sensory deficits; you know, we use quantitative sensory testing and research studies and things like that, but bedside testing may not reveal the subtle changes. And when we don't see overt changes, we often think - that can lead someone to think that everything is OK and it's not. Dr Jones: So, when you when you see a patient who you've diagnosed with a central mechanism, so central neuropathic pain, how do you approach the management of those patients, Dr Argoff? Dr Argoff: I always review what treatments and what approaches have been addressed already. And I see if - a handful of time, we actually just submitted a paper for publication regarding this in a group of patients with pelvic pain who had untreated, difficult-to-treat chronic pelvic pain, seen all the urological kinds, gynecological things. Look, we picked up two patients who had unknown MS. So, it's just interesting when it comes down to that level. And we also picked up some patients who had subacute combined degeneration. So that's another central kind of disorder as well. Again, the neurologist in us says to make sure that we have specific diagnosis that underlies the central neuropathic pain. And so interestingly, of course, for somebody with MS - or even though it's uncommon, it could be more than one. Somebody with MS might have a stroke, somebody with MS might have a cord injury due to cervical, you know, joint disc disease. Not to overcomplicate things. Know the lay of the land, know the conditions, know what you're battling and lay out so that you can treat the treatable; you want to treat whatever you can correct? So, for MS you simply want to have the best disease-modifying treatment on board, tolerable and appropriate for that person, and so on. And then you really want to take a history of past treatments - and your treatments can be everything and anything, including behavioral modification, physical rehabilitative approaches, as well as pharmacologic management. That's - as I think I put in my article, we concentrated in the article on pharmacologic management because honestly, that's what most patients are looking for, is ‘what can we, what can you do to help me now, in addition to what I can do myself.' And that's what we typically think of. There are also some more interventional approaches, invasive options, that have developed over time. And of course, those are the ones, some of them, especially in neuromodulation, that we have the least information about, but it appears somewhat promising.  Dr Jones: No, that's exactly what we need to hear. And you also mentioned something that I think is important. This is a common theme throughout the issue because I think it's true for the management of many different types of pain and interdisciplinary approach. In other words, not just honing in on pharmacotherapy or neuromodulation as a one-size-fits-all magic pill, right? So, that - tell us a little bit more about that interdisciplinary approach and how that's important for these patients. Dr Argoff: So, let me back up and give an example. Let's look at Botox for chronic migraine. So, the pre-M studies that led to the approval of Botox for chronic migraine: two treatment sessions versus two random, two placebo session in different patients. The mean headache frequency was, let's say, fifteen to twenty in each group. It was like seventeen, eighteen, something like that. But the mean pain headache day reduction was somewhere between four and five after two treatments compared to a lesser, a lower number in the placebo group. So, if you think about that, that means that you went from nineteen, let's say, to fourteen, thirteen, or twelve. Want to be generous, eleven or ten. But that means that person, everyone 's happy. We use treatment. We have better data than that because the longer you use it, the better it gets in general, but it means that people are still going to be symptomatic. So that drives home in a different painful disorder the importance of yes, treatment can be effective, but it's not the only treatment that a person is going to likely need. And so, I think that's what's so important about multidisciplinary approach. I- we may affect positive changes, reduction in pain intensity with a particular pharmacologic agent, but we don't anticipate it's like taking an antibiotic or a strep throat, not curative. And so, we want to, early on, to explain that logically, methodically, step by step. There are many options for you and we're going to, you know, systematically go through them. And I may need to call in some colleagues to help because I don't do everything. No one does everything, right? But don't feel as if there isn't any hope because there is. If we were to use intraspinal Baclofen for someone who has painful spasticity following a stroke or a spinal cord injury, combining that with physical therapy might give more effect, maybe synergistic. Some targeted muscles, some local muscles may not respond as well to the intraspinal Baclofen, so is that - what can we do? Well, we could use oral agents or we might be able to target that with botulinum toxin, and so on and so forth. So it's limitless, virtually, in what you can do. Dr Jones: There's kind of setting expectations and letting people know that you, you're going to need a lot of different approaches, right? To sort of get them the best possible outcome. Dr Argoff: Yeah, I think that's so important. And of course, no matter what we try to set out, there are going to be individuals - for those of you who are listening, we all know - who expect to be cured yesterday. That might be challenging for us not only to actually complete, but also, it's challenging for some individuals to appreciate that we're with them, we're going to work with them. It'll be a process, but we've got your back. Dr Jones: Great. And you know, this is a question that I get all the time from patients and from other clinicians is, you know, what about cannabinoids? What's the role of cannabinoids for the management of central neuropathic pain? Dr Argoff: First, I'll say that the short answer to that is we don't know. The second part of my response would be, there is new evidence that it might be helpful in the acute treatment of migraine. And I'm happy to say that the editor of this edition of Continuum is the person who developed that evidence, and it's been recently presented at the American Headache Society. But the challenge and the conundrum that we all face is, everywhere within our nervous system where there's pain being processed, there are endocannabinoid receptors. There also happen to be opioid receptors, but that's a separate issue. And the endocannabinoid system, the peripheral or central, you know, CB1, CB2, is very, very important, but we haven't figured out a way of harnessing that knowledge in developing an analgesic, an effective analgesic. And part of that is that there are so many chemical agents that have cannabinoid properties and there are different… the right balance has not yet been found. But even the legalization, the available of medical cannabis, hasn't led to a standardized approach to evaluating if a preparation does help. And that's part of the conundrum. It's like saying, ‘does medicine work?'Well, yeah, sometimes. But which medicine? Which receptor? How do you harness the right ratio between TBD, THC, other active agents, et cetera? And I think maybe as we go forward in the future, we'll be able to do that with - more precise. I mentioned Dr Schuster's study in which he had defined ratios of THC effect and CBD and was able to clearly show effect based upon that. But the average person going into a dispensary doesn't really get that. We don't get to study that. Each person's an NF1  and it's not very helpful to understand how to do that. I would say, as I'm sure you remember, there was a practice parameter that was published probably over a decade ago about using cannabis symptomatically in different neurological disorders. And I believe that it was what they studied or what they reviewed was helpful in MS-related urinary discomfort and spasticity, but not necessarily pain.  Dr Jones: And we're still in the early days of studying it, right? Dr Argoff: Yes.  Dr Jones: That's part of the point, as we got started late and we're still waiting for high-quality evidence. And I guess, if you look at the horizon, Dr Argoff, or the future of management of central neuropathic pain, what's going to be the next big thing?  Dr Argoff: One of the joys of being asked to get involved in a project like this is that inevitably we learn so many new things because, you know, that's when anyone says, oh, you must be an expert, I say, I don't know anything because I'm always learning something new. One of the reasons why I moved to Albany Medical College about seventeen years ago was to be able to further my interest in studying why people benefit from topical analgesics by working with a scientist at Albany Med who studied keratinocyte neurochemistry and its impact on pain transmission. And that's a separate issue, but it indicates my love for the peripheral nervous system. And one of my thoughts historically, that is, what the central nervous system processes is what it processes and it might get input, as you mentioned earlier, from the peripheral nervous system, so that topical agents could be dampening central mechanisms. And lo and behold, as I was doing research for this article, I learned that people doing peripheral nerve blocks - so blocking peripheral input at the into the spinal cord - at Washington University, Simon Guterian and colleagues, demonstrate that they could give prolonged benefit from central pain by blocking peripheral input. And that's wild because certainly the nervous system is a two-way street. It's an understatement. What I really found amazing was that, again, blocking input helped the injured central nervous system to behave better.  Dr Jones: That is kind of cool to think about. And I'll tell you, as editor of the journal, one of the funnest things is getting to learn all about neurology, including pain and including central neuropathic pain, when in the end you're doing all the work, I just get to sit here and enjoy it. And you're a program director of a pain fellowship. What's the pipeline look like? Are neurologists more interested in pain than they used to be?  Dr Argoff: I'm happy for this. We are seeing more and more applicants from neurology into our pain management programs. I would say… I was going to say tragically. If I say tragically, it's because what specialty better understands how to diagnose, figure out, assess, come to a conclusion? You can't have pain without your brain. It's always amazed me that more neurologists weren't interested, and I understand the background and such. Just like in migraine, it's only advances in understanding mechanisms of migraine that allow neuroscientific advances that are leading to great therapeutics - that's happening and increasing in ‘pain.' Today, as program director, we had our fellowship interviews earlier today and three of the nine applicants that we interviewed were neurologists. Last week, I think we interviewed two or three also. That would not have happened five years ago or six years ago. And if you think about it, we can not only diagnose, quote-unquote figure out what's happening, but we now, with pain management training, we can offer people a variety of both invasive and noninvasive options, all while understanding what we're doing with respect to the nervous system in a way that's different than the other specialties that typically go into pain med. And that's such - for me, it's a beautiful experience and something I really enjoy doing. There isn't a neurological condition in the most part that either doesn't have pain associated with it or doesn't have mechanisms that overlap. If you think about epilepsy, and please don't think I'm crazy, but epilepsy is associated with disinhibited hyper-excitatory behavior, just to put it loosely, among certain neurons. That's what pain and neuropathic pain is about too. And you, in fact, we know that several mechanisms since now what medicines are used for both. But what was interesting since, if I may just go back to another point, one of the advances since I brought up the migraine that's very exciting is the whole story about sodium channels. Dr Harouthounian at WashU and his group used lidocaine injection. Lidocaine's a more generalized sodium channel blocker, but some of the newest treatments for treating neuropathic pain. Our NAV specific sodium channel blocker's trying to match up mechanism to treatment. Not exactly the way that we do with migraine, but still a step forward to not just generally treat but really target different neuronal mechanisms. It's an exciting time.  Dr Jones: So, the pipeline is doing better because we're getting better understanding of disease, and hopefully that pulls in more interest because obviously there are big gaps in caring for patients with pain. And again, thank you, Dr Argoff, for an amazing article. Thank you for joining us and thank you for such a fascinating discussion. I enjoyed the article. I read the article, I learned from our conversation today. So, thank you for joining us to talk about central neuropathic pain. Dr Argoff: Thank you for having me. Dr Jones: Again, we've been speaking with Dr Charles Argoff, author of an article on central neuropathic pain in Continuum 's most recent issue on pain management. Please check it out, and thank you to our listeners for joining today. Dr Monteith: This is Doctor Teshamae Monteith, associate editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at Continpub.com/AudioCME. Thank you for listening to Continuum Audio.

Imagine facing your mortality before you even graduate high school. Gabe Donovan knows this reality all too well. Born with NF1, a rare and complex genetic disorder that affects every part of his body, Gabe's journey has been filled with unimaginable challenges, from painful tumors to feeling completely isolated. In this episode of A Place of Yes, host Heather sits down with Gabe and his mother, Maureen, to discuss how this disease has shaped Gabe's life, the battles they've fought together, and the resilience he's found along the way. It's a raw, eye-opening conversation about strength, vulnerability, and the profound impact of living with a rare illness that constantly tests the limits of the human spirit. Double H Ranch: https://www.doublehranch.org Find Gabe: https://www.instagram.com/the_original_mad_gabe Find Maureen: https://www.instagram.com/maureeneobrien/ Find Heather and Jake's Help from Heaven ❤️ Heather's Instagram: https://www.instagram.com/heathersstraughter/ ❤️ Jake's Help from Heaven: http://jakeshelpfromheaven.org/ ❤️ Jake's Help from Heaven IG: https://www.instagram.com/jakeshelp/ ❤️ Facebook: https://www.facebook.com/jakeshelpfromheaven ❤️ Our YouTube Channel: https://www.youtube.com/@APlaceofYesPodcast Learn more about your ad choices. Visit megaphone.fm/adchoices

In this week's episode I'm chatting with a lovely guest. I've been on her podcast "Chat off the Mat" and I'm happy to return the favour. Welcome to Rose Wippich, Reiki Master, Yoga and QiGong Teacher and Energy Priestess. Rose has a very special and empowering story about Reiki and healing and how everything in her life fell into place as she trusted her Intuition while moving forward in her life. In this episode we talk about: Rose shares her story of hitting a low point in her 30s after a series of relationship breakups. This led her to discover yoga, which helped her feel more grounded and start the healing process. Rose then had a transformative Reiki session where she had a vision of her deceased mother showing her two baby bottles, indicating that she would have twins in the future, even though she did not have a partner at the time. Years later, Rose did get married and became pregnant with identical twin boys, despite being considered a high-risk pregnancy at age 40. When Rose's twin sons were diagnosed with a condition called neurofibromatosis type 1 (NF1) as young children, Rose became a Reiki practitioner herself to help support her sons' health and well-being. Through regular Reiki sessions, her sons were able to manage the condition without major complications. Rose credits her intuition, spiritual practices, and the Reiki energy work as key factors in her personal healing journey and her ability to support her children's health. Rose explains how she uses Yoga, Reiki and Chi Gong and how they complement each other Rose shares her desire to bring those modalities, especially QiGong which is the less known, to more people so they can learn to become aware of energies and heal themselves. Rose offers a special discount for the listeners of Intuitive Queens Podcast for her programme. By entering CODE: ENERGY, you'll get a 10% discount on her programme. CONNECT WITH ROSE Podcast:  Chat Off The Mat.  https://chatoffthemat.buzzsprout.com/ Website: https://www.rosewippich.com Instagram: https://www.instagram.com/rosewippich/ Youtube: https://www.youtube.com/channel/UCT-3xlXAtWCzCeiBaR1BpAA Facebook Group: https://www.facebook.com/rosewippichwellness Email: rose@rosewippich.com Rose's online course: New Energy! New You! Create a new journey towards your most authentic self.   CONNECT WITH ME  https://www.theintuitionqueen.com/ IG: https://www.instagram.com/the_intuition_queen/ SIGN UP TO MY NEWSLETTER TO BE UPDATED ON NEW FREEBIES AND NEW OFFERS:   https://form.flodesk.com/forms/65a1ae45e382a70c005c15ed/submit JOIN MY COMMUNITY Intuitive Queens Network: https://www.facebook.com/groups/theintuitivequeensnetwork WATCH IT ON MY YOU TUBE CHANNEL: https://www.youtube.com/@maramarchesi-theintuitionq3852 FREE RESOURCES: https://www.theintuitionqueen.com/freeresources LEAVE A REVIEW: https://podcasts.apple.com/gb/podcast/intuitive-queens-podcast/id1477108959  

In this episode of the Play Therapy Podcast, I respond to a question from Bailey in Texas about the effectiveness of child-centered play therapy (CCPT) for children with NF1, a genetic condition. Bailey is working with a six-year-old client whose symptoms resemble ADHD, and she's curious about the realistic expectations for therapy outcomes. I broaden the discussion to address how CCPT can benefit children with various disorders or diagnoses, emphasizing that while play therapy may not change the underlying condition, it significantly improves a child's ability to cope, build resilience, and develop crucial emotional and relational skills. I also discuss the importance of shifting the focus away from the condition itself and instead highlighting how play therapy fosters self-trust, problem-solving, and emotional regulation. By reframing the conversation with parents, we can help them understand that the true power of CCPT lies in equipping children to navigate their challenges with confidence and competence, regardless of the condition they face. If you would like to ask me questions directly, check out www.ccptcollective.com, where I host two weekly Zoom calls filled with advanced CCPT case studies and session reviews, as well as member Q&A. You can take advantage of the two-week free trial to see if the CCPT Collective is right for you. Ask Me Questions: Call ‪(813) 812-5525‬, or email: brenna@thekidcounselor.com Brenna's CCPT Hub: https://www.playtherapynow.com CCPT Collective (online community exclusively for CCPTs): https://www.ccptcollective.com Podcast HQ: https://www.playtherapypodcast.com APT Approved Play Therapy CE courses: https://childcenteredtraining.com Twitter: @thekidcounselor https://twitter.com/thekidcounselor Facebook: https://facebook.com/playtherapypodcast Common References: Cochran, N., Nordling, W., & Cochran, J. (2010). Child-Centered Play Therapy (1st ed.). Wiley. VanFleet, R., Sywulak, A. E., & Sniscak, C. C. (2010). Child-centered play therapy. Guilford Press. Landreth, G.L. (2023). Play Therapy: The Art of the Relationship (4th ed.). Routledge. Bratton, S. C., Landreth, G. L., Kellam, T., & Blackard, S. R. (2006). Child parent relationship therapy (CPRT) treatment manual: A 10-session filial therapy model for training parents. Routledge/Taylor & Francis Group. Benedict, Helen. Themes in Play Therapy. Used with permission to Heartland Play Therapy Institute.

Welcome back to Appearance Matters the Podcast! In this episode, we share the recording of our Appearance Matters 10 Conference panel discussion event, titled ‘Beyond the Selfie: Can Social Media Influencers Shape the Appearance Diversity Landscape?' Our panel members include: - Stephanie Yeboah, an award-winning content creator, author and writer. - Amit Ghose, an advocate for the visible difference community and social media influencer with lived experience of neurofibromatosis/NF1. - Phyllida Swift, the CEO of Face Equality International, a charity dedicated to ensuring those with visible differences can live freely without indignity or discrimination. - Dr Amy Slater, a researcher at the Centre for Appearance Research whose work focuses on social media and visible differences. - Mazviona Madzima, a strategic partner manager at YouTube responsible for some of the platforms largest creators. - Antony Genova, a brand manager working in advertising at Google. To find out more about the Centre for Appearance Research, follow us: • On X: twitter.com/CAR_UWE • On Instagram: www.instagram.com/car_uwe/ • On Facebook: www.facebook.com/AppearanceResearch Please share, subscribe, rate and review. It really does mean a lot. Thank you! Music by Sian Evans & John Landau: toplinefilm.com Cover photo by Ivan Samkov from Pexels Episode developed and produced by Abbi Mathews

Welkom bij 'Helende gesprekken' (instagram: @helendegesprekken), de podcast waarin ik (Stephanie Kaars, schrijver en spreker) elke week in gesprek ga met iemand die een bijzonder verhaal te vertellen heeft dat hoop, licht en inspiratie brengt.Deze week praat ik met Puck (15), die de ziekte NF1 (Neurofibromatose) heeft én het Noonan syndroom. Beide aandoeningen kunnen erfelijk zijn, maar bij Puck is sprake van een spontane genmutatie. NF1 zorgt voor ongeremde groei van tumoren: Puck heeft onder andere een tumor in haar kleine hersenen en haar linker hersenslagader is volledig vernauwd. Door het Noonan syndroom heeft zij daarnaast ernstige voedings- en drinkproblemen en is ze afhankelijk van een maagsonde en darmspoelen. Maar Puck is vooral gewoon Puck: een jongedame met toekomstdromen! Op zondag 26 mei aanstaande doet Puck voor de derde keer mee met een sponsorloop: RUNEXPECTED, georganiseerd door Stichting LET'S BEAT NF. De opbrengst komt ten goede aan wetenschappelijk onderzoek (o.a. door het Prinses Maxima Centrum voor Kinderoncologie en het Erasmus MC) en het doel is om NF de wereld uit te helpen en het leven van mensen met NF beter en draaglijker te maken, om te beginnen bij kinderen. Team Puck steunen kan via deze link: https://www.runexpected.nl/teams/team-puckOok benieuwd naar mijn verhaal? Luister dan de tien afleveringen van 'Mijn helende verhaal' op dit kanaal, plus de toegift van mijn dochter Sterre.Laat alsjeblieft een review achter en abonneer je op deze podcast als je niets wilt missen. Liefs, Stephanie (www.stephaniekaars.nl)

This episode features Stephanie M. Morris , MD, is Medical Director, Center for Autism Services, Science and Innovation (CASSI) At Kennedy Krieger Institute, Baltimore. She is a neurologist with special qualifications in child neurology, and is also an assistant professor in the Department of Neurology at the Johns Hopkins University School of Medicine. She works with kids with autism and I/DD and especially genetic conditions such as Fragile X syndrome and Neurofibromatosis Type 1 (NF1). In this webinar, Dr. Morris explains what seizures and epilepsy are, the different types, the high prevalence of seizures in autism, particularly in severe autism, various treatment approaches, and accessing care. Moderated by Jill Escher, president, NCSA For more information, please see NCSAutism.org

29 February marks Rare Disease Day. This day is an opportunity for the rare community to come together to raise awareness of the common issues affecting those living with rare conditions. A rare condition is a condition that affects less than one in 2,000 in the population, and although rare conditions are individually rare they are collectively common. It is estimated that there are over 7,000 rare conditions. Around 80% of rare conditions have an identified genetic origin. In this episode of the G Word, our host Julia Vitarello, Founder and CEO of Mila's Miracle Foundation, is joined by Rich Scott, Interim CEO for Genomics England, and Ana Lisa Tavares, Clinical Lead for Rare Disease Research at Genomics England, as they discuss challenges for those living with a rare condition and the work being carried out across the genomics ecosystem to support them. Julia is the mother of Mila, a young girl who was diagnosed with a rare genetic condition called Batten Disease, and in this episode Julia takes us through Mila's story, and how she hopes to help many more families access treatments for their children.   "So when parents, children, are diagnosed whether it's a fatal or life-longing debilitating or difficult disease, if you know that what's being learned from your child both from just the genomics to the potential treatments that's helping the next child, that helps parents like me be able to continue living."   You can find out more about Mila's story in our previous podcast episode with Rich Scott, Julia Vitarello and Dr Tim Yu.   You can read the transcript below or download it here: https://files.genomicsengland.co.uk/documents/Podcast-transcripts/Rare-Disease-Day.docx  Julia: Welcome to the G Word So my life at that point seemed to just disappear in that moment, all the things that had mattered to me were gone; I knew there was something wrong with my daughter but I had absolutely no idea that a typical child who was outgoing and active and verbal and had friends could suddenly lose all of her abilities and die. My name is Julia Vitarello, and I'm your host for today's episode. Today joining me in conversation is Rich Scott, Interim CEO for Genomics England, and Ana Lisa Tavares, Clinical Lead for Rare Disease Research, also at Genomics England. Today we'll be discussing challenges for those living with a rare condition and the work being carried out across the genomics ecosystem to support them. If you enjoy today's episode, please like, share and rate the G Word on wherever you listen to your podcasts. The 29th of February marks rare disease day. This day is an opportunity for the rare community to come together to raise awareness of the common issues affecting those living with rare conditions. A rare condition is a condition that affects less than one in 2,000 in the population, and although rare conditions are individually rare they are collectively common. It is estimated that there are over 7,000 rare conditions. Around 80% of rare conditions have an identified genetic origin. Before I get into speaking with Rich and Ana Lisa, I wanted to share my story and my daughter, Mila's, story. My life as a mother started really like anyone else's, my daughter was perfectly healthy, her name is Mila. For the first three or four years of her life she was like any other kid. I live in Colorado in the United States, my daughter was a skier, she was a hiker, she was rock climbing, she was incredibly active and singing songs and swimming and riding bikes. But around four years' old she started tripping and falling, she started pulling books and toys up closely to her face; she started being covered in bruises, getting stuck on words and repeating her sentences and I brought her to about 100 different doctors and therapists around the United States to try to figure out what was going on with her. Around four years' old I started speaking with orthopaedic surgeons, with ophthalmologists, with neurologists, with speech therapists and each one of them, you know, told me pretty much that I was a crazy mom and that my daughter was typical and normal and that she would grow out of these sort of strange symptoms that she was having.      By the time that she was six years' old, I had had enough and I was crying on a regular basis, no doctor could help me and I was tired of lugging my daughter, who was now covered in bruises and tripping and falling and stuttering, together with my newborn son at the time, kind of around the country only to be told that I was crazy. And at that point at six years' old I brought her into the emergency room in the Children's Hospital Colorado, near where I live. She was in there for about a week and underwent a battery of tests and at the end of that week I was told that my daughter had a rare genetic condition called Batten Disease and that she would lose all of her abilities and die in the next few years. So my life at that point, first four years of my life seemed to just disappear in that moment, all the things that had mattered to me were gone. I knew there was something wrong with my daughter but I had absolutely no idea that a typical child who was outgoing and active and verbal and had friends could suddenly lose all of her abilities and die. After crying on my closet floor pretty much most of the day for a few weeks I picked myself up. I started to read white papers, I started to go online and learn about other rare conditions. I started to speak with parents that had fought for their children with physicians, with researchers, and did everything I could to kind of figure out if there was even a glimmer of hope. And what I was told at the time at the end of 2016 was that there is almost nothing that could be done and very little was known about my daughter's form of Batten Disease. But that there was a tiny glimmer of hope that we could maybe stop genetic disease, and that's all I needed. I started Mila's Miracle Foundation, which is a non-profit organization. I started telling Mila's story and taking care of my kids by day and trying to fight and learn and raise money by night and I started a gene replacement therapy because it was the only option that I could take on as we didn't know much at all about the disease, and by replacing it, it was kind of the only thing that I could do, but it was going to take many years and millions and millions of dollars and I knew that it wouldn't be in time for my daughter. Along the way, there was something a little bit unusual which was that my daughter had an auto recessive disease which meant that she needed to have a mutation in the same Batten causing gene from her mom, myself, and her father, and they could only find one of these two. That led me to learn about whole genome sequencing, which was kind of the most extensive way of looking at Mila's genome to figure out where this missing mutation was. And in that search I crossed paths with a Dr Timothy Yu at Boston Children's Hospital, and he volunteered with his lab to help me find this missing mutation that no other lab could possibly find. And within a few months and a lot of work, a lot of late nights and weekends and staring at screens, through whole genome sequencing, the team was able to find Mila's missing mutation and finally diagnose her fully with this rare form of an already rare Batten disease. That is where Mila's story changed and turned direction. At that point, a recently approved drug for spinal muscular atrophy was on all neurologists' minds at that moment because it had just been approved in the US by the FDA and in other countries, and it was a game changer, these children were dying and on respirators and in wheelchairs you know at the age of two and with this new drug they were actually living, many of them were living long lives and were active and happy and healthy and going to school. And Mila looking her whole genome sequence was able to kind of fit that same criteria, and so the doctors, including Dr Yu said, “What if we did the same thing for these children? What if we made a drug like this for Mila?” This drug called Antisense Oligonucleotides, or ASO seemed to be a good fit for Mila's mutation. And so a drug was made for Mila and named after her called Milasen and it was a race against time for an entire a year with a team of honestly hundreds of people across academics and industry, I was fighting to try to raise the money and awareness and working with a scientific team. And one year after Mila was diagnosed when she turned seven years' old, we moved to Boston and Mila began receiving Milasen, which was named after her, and only in that moment in time did I realise not only what a big deal this was for me as her mother, but what a big deal this was for science. She was the first person in the world to receive a medicine that was tailored just to one person and it was named after her because there was no-one else in the world they could find that shared that same mutation. When Mila began this, you know, I didn't know what to expect but I knew that she was going to lose all her abilities and die if she didn't receive this. And so once she started receiving this within just a few months, her 30 seizures a day went down to nothing; she had occasional small tiny seizures that were barely visible but her quality of life was incredibly you know improved, not to mention our family's because she was no longer thrashing and smashing her arms and legs up against walls and tables. She had been slumped and could no longer sit up. She could no longer hold her body up and take steps with my support from behind and after Milasen she started being able to do that even walk up the stairs with alternating feet with me supporting her from behind. She also had received a G-tube and was receiving all of her nutrition through the G-tube and after Milasen she started eating by mouth, it wasn't perfect, but she was eating pureed foods, and being able to swallow better and probably most importantly she was able to smile and laugh at the funny parts in the books and the stories that I had been reading and singing to her and that she had kind of really not been responding to as much before Milasen and some of that came back. So, a year into this everyone was quite shocked that Mila had done so incredibly well in this first year despite how progressed she was, progressed her condition was. Unfortunately in the second year it was during COVID and it was unclear whether or not Mila's disease had kind of stopped or whether it was slowly progressing and in the third year Mila started having problems associated with her rare condition and I was faced as a mother with the most horrible decisions anyone should ever, never, never, never have to face to decide what Mila would want if she were able to talk and tell me whether or not this was a life that she felt like she would want to live. And after three years on Milasen, which was three years ago almost this week, Mila died and in many ways my life as I knew it was kind of over. I'm a very positive happy person and I have a son and I continue getting up every day and pushing through the day but I'm not sure how any parent makes it through days, weeks, months and their whole life without their child physically there with them. Ana Lisa: We can really hear the perseverance that you had to get a diagnosis through whole genome sequencing eventually for Mila. Can you tell us a little bit more about that process and what that diagnosis, what did it mean for Mila and for your family? Julia: When Mila was first diagnosed with Batten Disease, one of the missing mutations could not be found by any lab. I did research and found out that whole genome sequencing which at the time was very, very hard to find a lab that would do it or anyone that would do it in the United States, I did learn that that was really what was needed in order to try to really get down to find the underlying genetic cause of Mila's disease and give her a full diagnosis. So once we managed to have Dr Yu's lab at Boston Children's Hospital carry out the whole genome sequence, obviously we were able to then find exactly where the broken, underlying broken kind of genetic mutation was and why that was important was for two reasons: 1) was so that we could actually have a diagnosis and even though it was the worst diagnosis we could have ever asked for, at least there was an answer and for so many years I didn't have an answer and there is nothing worse than seeing your child, you know, having all of these different symptoms and problems and having you know tens, if not hundreds, of different doctors and therapists tell you that they don't know and maybe you're just a little bit over-worked and over-worried about things, and having no answer and no idea what's wrong is like living in this limbo that's just terrible. And so whole genome sequencing allowed for us to have a full diagnosis for Mila, and it also allowed us to use that data since it was truly the precise place where, you know, we could find the precise plan where her gene was broken. It allowed the researchers to then also think about what could be done about it as well, which is the second thing a parent thinks about after they have the kind of relief in some ways, which is a strange word to use but it's true, of knowing what is wrong and then thinking, “What could I do about it now?” And so for me I would say that's how, Ana Lisa, that's how I reacted to that, is there was enormous relief initially, which is just the weirdest word ever to use for that but at least I felt like I wasn't crazy and that there was an actual reason and that it allowed us, allowed me and others to think what kind of action can we take now. Rich: One of the things that often strikes me, I'm a clinical geneticist by background, just like Ana Lisa, is how often particularly several years ago when we were in a different situation, it depended on families and parents pushing and pushing and pushing and asking, that's something I think in the UK we're really lucky that there have been changes in terms of availability of testing. Julia, as you know, we were set up ten years ago initially to run a project, a research project in partnership with the NHS called ‘The 100,000 Genome Project' asking the question about whether whole genome sequencing could be used in a diagnostic setting. Whole genome sequencing had just emerged as a thing that could even be conceived of as affordable in a healthcare system back then, and we worked with the NHS and tens of thousands of families with rare conditions and people with cancer to ask that question and again, we're really proud of what that work and our partnership with the NHS has led to, which is now in the UK. There is the availability nationally of whole genome sequencing to test in certain settings including in rare conditions that are hard to solve in this sort of way and it's one of the things which has really changed the way we can go about this, but we also know that there's still, it's still hard often to identify who should be seen by a specialist who might do a test and so on. But it has really changed things and I think it's hearing from families like yours about how challenging it is and thinking about how we turn, looking across all of the story that you told us of everything you went through, how we can make that be something where we can make it be more systematically available and work for many more people, and I know your phrase from Mila to millions really strikes a chord with me, and I know with the NHS mind-set here in the UK where it's about equity of access and I think that mind-set that you bring is so important. Julia: Yes, Rich, I think it's a really good point you know, because a lot of parents like myself, we're talking about probably millions around the world and tens of thousands just in the UK alone, spend so much time going from one physician to another and to a therapist and it takes an enormous amount of energy and time in a family that's already dealing with pain and confusion and not understanding what's going on, not to mention usually that child, in my case, Mila, is having problems that it's not easy to leave the house and get in the car and go to all these appointments. And the more we can push towards whole genome sequencing as one of the first places to go, if not the first place to go, the more it's going to cut that sort of diagnostic odyssey down to the very bare minimal. And so of course a dream would be is that any child that has, I like to think of it as soon as you kind of have more than one symptom that shouldn't normally go together, that sort of has a little red flag that goes off and in most parts of the world right now no physician wants to scare a parent like me, it's happened a number of times to me where a physician has said, “Well, you know, there is this rare condition but I'm not going to bring that up because it's so rare that the likelihood that your daughter has that, I wouldn't want to scare you.” But the more we can move towards whole genome sequencing right away to help with that answer that could cut months and very often years from that odyssey, and that is where we need to be, we can't have the tapping on the knee and stacking up blocks and running down the hall for months and years just to figure out what's going on. Ana Lisa: And I think Rich also there said a power of having a national healthcare service where patients who are having whole genome sequencing can also decide whether they wish to consent to be part of research and combining that with a national genomic research library and then the ability to work so closely with the NHS and go back to patients if there is a new diagnosis that could benefit them is really powerful I think, and that's definitely one thing that we've also learnt from these big whole genome sequencing efforts is that our knowledge is continuing to develop and some people will get a diagnosis from that immediately and we've got amazing colleagues working on diagnostic discovery looking at whole cohorts of patients now who are having whole genome sequencing and that's also been really informative and allowed a lot of new diagnoses identified also through research and through these efforts to be found. Julia: Absolutely and I think that the UK is incredibly well suited to have such widespread sort of country-wide whole genome sequencing project like what Genomics England has done because you have one system where all of the clinical and genetic data can all come in and kind of be analysed both for like you said diagnostics but also it could be, if families and patients are interested, right, in contributing to the research which then comes full circle and helps the entire system benefit from better treatments you know and better understanding of diseases. Rich: And that point of sort of thinking about how to move things forward, so the NHS has a service based in Exeter which is addressing the question where children are on intensive care, where often intervention is needed really rapidly to make a difference, so that's one of the examples where sort of thinking about making sure that service is available early and rapidly is being set up and that's been really successful and identifying a cause where that really changes the care of that child on intensive care. The other area where we're working really closely with the NHS at the moment, as you know, Julia, and in fact I think this was probably one of the reasons we first came to talk to you was thinking about our newborn genomes programme where if you like, the big question there is saying we know that there are a few hundred conditions that are within that longer list of rare conditions where there is a treatment available routinely if the diagnosis is made, and saying could we use whole genome sequencing alongside existing newborn heel prick testing which in the UK currently looks for nine, shortly to be ten, conditions. So we're just about to launch that programme and that will sequence the genomes of 100,000 babies born at maternity hospitals, not selected for children where there's something, a concern, raised, but any baby at that hospital would be eligible for the family to choose to join that research programme and really to ask that question about whether this is something that we should offer to all babies developing the scientific evidence around it, learning about how you might implement it in practice, and also having conversations about how one might do that, what public attitudes are to it and so forth, developing evidence that can move us forward in that area too. And back to Ana Lisa's point about improving knowledge, we know that today there are a certain number of conditions that one might think are comparable to those nine that are currently looked for in the UK on the heel prick that we could use genetics as a way in. We also know that through the sort of innovation and the new knowledge that you mentioned that was relevant to Mila, that list might grow quite considerably in the coming years, so it's thinking about how we set ourselves up to make sure that we're able to take advantage of that to its full. Julia: Yeah, and I think it's a great, I'm glad you brought this up Rich because the UK really is leading the world in this, there is no-one else that is doing whole genome sequencing at birth, and ultimately, that's where we need to be. You know it's not going to happen overnight and like you said, the purpose of this is really to learn a lot about how and if to roll this out maybe in a larger scale way across the UK. But ultimately, you know, as Mila's mom, I think all the time about you know how incredible what I saw at a very progressed state for Mila with this treatment and the only way to actually really truly help Mila and other Milas is to get to these children early enough so that they're diagnosed before they have symptoms and they're treated before they have symptoms. And the way to move towards that is to at least have efforts like the project, you know, the newborn screening project so that we can get to children, find them before they have symptoms, treat them before that and from what I saw from Mila I feel pretty strongly that if Mila had received Milasen at birth she might never know the effects of Batten Disease, and we as a family might never know what it's like living with a rare condition, and this is a step in that direction to help. Effie Parks: Hi there, I'm Effie Parks, mom to Ford, who lives with a rare neurodevelopmental disorder called CTNNB1 and the host of the Once Upon a Gene podcast. Our show connects families facing rare diseases, offering stories from parents, insights from experts and discussions on everything from navigating grief to exploring genetic advances. It's a space for understanding, connection and empowerment. For support and inspiration on your rare disease journey, subscribe to the Once Upon a Gene podcast on your favourite podcast app and let's navigate this path together. Ana Lisa: Julia, I'm interested to hear what you think the development of individualised medicines like the N1 treatment Mila had what that means for the sort of collaboration that's required across the genomics ecosystem to achieve that. Julia: Yeah, that's a really good question. It's been seven years that I've been thinking about this kind of individualised medicine concept, you know, as Mila kind of became the pioneer in this field and I'm not a scientist, I'm not a physician, but I've learned a lot because I've been fortunate enough to be part of thousands and thousands of conversations, including with all of you and others, Genomics England, and around the world and I think what I learned and what I've learned so far is that when you have a genetic condition most genetic conditions are individually rare and unfortunately that doesn't make them very suited to have anyone go after a treatment for them because really the only way to connect a patient, a child like Mila, to a science or technology is if they're lucky enough, and I hate to use the word ‘lucky' but they're lucky enough to be part of a large kind of cohort of people, and that allows them to be, you know, commercially viable, so a company will be maybe develop if they're lucky, a treatment for that, for those people. The only other option is this sort of like Herculean effort of which myself and Dr Yu and others went through, we had to raise millions of dollars and get hundreds of people to get on board and develop a novel medicine for one person – now how scalable is that? How many times can we do that, right? And so the only people that really have access to medicines today with genetic conditions are those that are fortunate to be part of one of these two groups, but what about everyone else which is 95% of the people? And so I think what the field is learning is that we kind of have the patients and we're finding them, especially thanks to Genomics England and others, we're starting to find them more rapidly earlier, more of them, and we have these technologies to be able to not only find them but to also treat them but we just do not have the infrastructure and the processes to connect them, we have clinical trials and we have these sort of named patient route but we don't have anything else. And so I think the genomics community, especially in the UK because it's so well suited with all the efforts that we've just brought up, is really well suited to kind of try to work together to allow for access kind of no matter how many people could benefit, it's not only one, it could be six or 20, or 200 or 500. Right now there is no access for them. So I think that the UK is really well suited, starting with whole genome sequencing, that's where it begins, it begins by identifying patients early enough and getting the data that's needed in order to diagnose them and also to help with the treatment you know, and so this is how I think the UK is really leading the world right now, including in the recent announcement of the rare therapies launch pad, which Genomics England is part of, I am part of, others are part of, Oxford Harrington Rare Disease Centre, the MHRA, others are all part of really trying to be dedicated to building the infrastructure and resources and processes that are needed to connect the patients to these technologies that exist today. Rich: I've been really inspired by the conversations and the drive that you, Julia, personally have given to those conversations. And I think what's really interesting and I think it's relevant more broadly than just in rare therapies particularly, but I think that challenge of recognising the need for the system to change to be able to respond to evidence and make the response proportionate to the expectations of various people, the patients or the families who are receiving it, the system as a whole, these sorts of therapies and rare conditions as well, are just not the shape that works well with existing paradigms, but I think it's relevant you know, in other settings as well. I'm really interested in some of the conversations that I've had with you before about balancing risk and understanding how to get that right and the fact that that really needs an open discussion in public to also understand the journey and the situation that families find themselves in. I wonder if you could tell us a bit about your perspective on getting that risk balance right? Julia: Thanks for bringing that up, Rich. I think it's really, really important because to me the way we think of risk and benefit and the risk tolerance maybe is a better way to put it is the foundation of the house that we're building. So, you know, the regulatory process and everything behind that are built on top of how we think about risk. And one of the things that I regularly think about is children that have end stage cancer, and that we as a society have accepted an enormous amount of risk for a child at end-stage cancer that has no other options that's going to die no matter what, probably very rapidly and that if they don't respond to kind of some of the main line treatments then to turn to an experimental cancer treatment which carries a very high risk is considered very acceptable by our society and that everyone, the clinicians, the families, the regulators, everyone is willing to take that risk for that child because they're going to die otherwise. And they're willing to spend money and they're willing to take the risk and often perhaps to buy that child maybe three or six months of life. So then if you look at Mila and if I tell you that instead of having a rare condition that she has an end-stage genetic disease, and I use the words from cancer, from oncology, is now suddenly the discussion changes a little bit, so Mila's going to die no matter what, no child has ever lived with her form of Batten Disease and she's going to lose all of her ability, so we know the risk of not treating Mila. The risk of treating Mila in this case was an antisense oligonucleotide, which is a modality that's been around for 30+ years, tested in animals and more frequently in numerous humans across different sort of trials. And the labs that worked on Mila's medicine felt that it was safe enough and hopefully efficacious enough. And at that point why is the hurdle so exponentially higher than what it would be for a child with end-stage cancer? The way that we are thinking about these children with end-stage genetic disease and end-stage cancer, is drastically different, so we need to first, to your point Rich, we need to start realising we've already set that precedent, we don't need to be having this discussion again. We know the risk we're willing to take for a dying child when there's no other therapeutic, no other option and they're going to die no matter what. So the risk of treating Mila, versus the risk of not treating Mila is black and white and we need to do our best and then we need to not only treat Mila but we need to learn from the treatment of Mila. We need to collect those learnings, they must be iterative learnings so that the next child that's treated with an individualised different ASO or different medicine that they don't happen in silos, but that all of this knowledge comes together so that the second and the third and the fourth and the tenth and the twentieth, the process gets better and faster and eventually cheaper so that it's accessible. Rich: Yes, and that's very much back to Ana Lisa's point on the link and for diagnostics too on continuing to learn and creating a system that recognises that that's crucial to offering the best care today but also in the future and being able to make proactive decisions more confidently if you're a policymaker, knowing that you'll continue to learn, you don't have to pretend you know everything today. Julia: It's very meaningful for parents. So when parents, children, are diagnosed whether it's a fatal or life-longing debilitating or difficult disease, if you know that what's being learned from your child both from just the genomics to the potential treatments that that's helping the next child, that helps parents like me be able to continue living. And so you know, research is this kind of generic word, I wish there were a better word for it. Really what it is, is it's learnings and it's what can be learned from my child that can help the next child? Ana Lisa: And then that learning requires a lot of collaboration, which is the super important part I think of your story. Julia: Yes, it does, it requires a lot of people starting with those diagnosing the children with whole genome sequencing all the way through just to the clinicians who are in the NHS, not to mention the researchers who are then looking at the data and bettering their understanding. Ana Lisa: I think there are also, maybe one can extend some of those parallels as well, in that I think currently we sometimes think of an individualised therapy of NF1 as being something that takes a lot of time and benefits an individual, and actually if we can really collaborate we can really set up processes that work across the ecosystem and keep learning, then I'd love to dream that actually this could help many, many different patients, with many, many different types of rare conditions because actually we've learnt how to target a little bit more at source, perhaps a particular type of genetic variant, and so a bit like cancer, we're not thinking about breast cancer, we're thinking about what sub-type, what genetic causes there are and targeting those, and if we can apply that one day more broadly across rare conditions then it might be that actually once you've learnt a certain amount, that you could scale up and treat many, many different conditions, not dependent on their frequency in the population. Julia: Yeah, that's a great dream, I share that dream. Rich, what is your, you've been in this for many years, what's your dream for the next five, ten years? Rich: I guess I have, I think there's two aspects to it. I think there's two, I think there's a lot of distance left to run for us improving on the diagnostics and I think thinking back to your conceptualisation of it Julia, of sort of thinking about how we can bring that earlier, whether that is that for example we're able to sort of more proactively flag when children have you know, more than one visit to a particular type of doctor or something that makes that happen much earlier in the process. So the tooling that we now know works whether it's whole genome sequencing or something more targeted can be used earlier in the process, or whether for example in our newborn genomes programme we get that evidence that we can look for a broader range of conditions in a screening context right at the beginning of life. And I think in five to ten years we should be in a substantially different place, we'll know whether or not we think whole genome sequencing should be there but offered for every baby at birth, and we can be much more proactive also when symptoms arise. I would also hope that on the side of therapies and intervention, we're in a substantially different position and I think, I've been amazed the last five years how my level of hope has increased. I believe we should now be in a position in five to ten years where those with a therapy that is potentially there to benefit them, should at least be able to be aware of it and there will be a clear pathway by which either that is available if it's proven, or there's a pathway that we all understand about how that can be trialled. And I think we're at the beginning of that journey and I now feel it's a responsibility of ours to work through how we can bring the right pieces into place, we can't prejudge the science, but we can set up the system that makes us be able to respond to it. Julia: Yeah, I remember Rich when you and I were speaking a number of months ago and maybe you could share the story because you talked about your hope kind of changing over time as a clinician I thought that was really powerful to me. Rich: Yeah, I remember it's probably now maybe 15 years ago being asked by a family about what my advice would be to them on the likelihood of there being a treatment for their child's particular condition being available and in fact they asked me to do it in a way that I sort of provided a formal written report to them that I spent a lot of time thinking about and agonising over and was very honestly you know saying it was highly unlikely that something would become available. If I had to write that same report today it would be very different. Julia: That's so promising to hear that. I don't know, Ana Lisa, have you had any experiences like that in the past that you feel differently now of how you would approach a family like mine? Ana Lisa: I think it's a real balance between having that hope ourselves, sharing that hope with other people and not giving false hope and it's such a balance when right now more than 95% of rare diseases don't have a treatment and I think that's such a difficult position to be in right now. And everything we've been talking about gives me massive hope for the future and a lot of what we're pouring our energy and efforts into is both the diagnostics so that we're not trying to make a puzzle with missing pieces in the dark and that's mission-critical, and then the real hope that actually this will drive therapies, which is what we really want for everybody who needs a therapy to have a therapy that's effective, whether they've got a common condition, a rare condition and that's our driving ideal. So I think I'm full of hope and optimism and I hope that it will accelerate, that's what I really hope, the momentum will build and we'll get to a certain level of knowledge, we're learning the processes, we're learning the evidence, we're learning the collaborative models that are needed to really suddenly explode our ability to treat rare conditions. Julia: Yeah, you know when Mila was, I guess when I look at newborn screening in the United States and Batten CLN7, which is Mila's kind of sub-type of her condition is not on newborn screening tests because there is no treatment for it, but the whole genome sequencing that was done for Mila was the data that we got from that was what was needed to create a treatment for her and so it's an unusual case where she was sequenced and a child and a baby, a newborn in the UK could be sequenced and not only told that they have a disease, so they have time to kind of understand the disease more but also potentially kind of prepare for a treatment that might be in the pipeline, but that data is also going to help scientists and researchers create new treatments that may not be available when that child is born but that's the data that's needed to create the treatment. Right now you guys are you're really at the forefront of solving both halves of the what I consider like a rare condition, you know, global health crisis with tens and hundreds of millions of people that have you know families like mine, like my story sounds unique, it sounds impossible but there are tens of millions of other people like me, like my story sounds unique, it sounds impossible but there is tens of millions of other people like me and so to have the UK kind of leading this effort to solve both halves of the problem, the diagnostic half, you know, what disease does a child have and find it in time and also kind of the treatments, here's where we're headed, and if we don't solve both of those problems then there is no such as access, you know to a better life, so I'm really grateful for the fact that you've set a precedent for other countries because now finally there are other countries that are looking towards you and kind of really trying to do the same thing that you're doing. Rich: Yeah, well I think we feel we're uniquely placed; the NHS in the UK and for Genomics England our partnership with the NHS, together with a number of other factors and I think the recognition from government as well as the NHS over a long period that the importance and the power of genomics and the importance of for example, making changes to regulation to get it right mean that it's something that I think we feel really privileged to be in the position to even be able to ask these big questions. Julia: yeah, I think the UK is really uniquely suited to have hung their hat on genomics so that the topics you're taking on are very central, they're not kind of on the sideline, they seem whenever I'm in the UK they say that what Genomics England is doing is at the forefront and in the middle of all the discussions with academics and companies and regulators and government. What do both of you think are the, what are the biggest kind of hurdles we have coming a few years in the newborn programme or you know, any of your other initiatives? Rich: I guess all of these are big questions and I think we need, it's back to that sort of point from Ana Lisa sort of balancing the hope and expectation, I think we're uniquely placed to develop the evidence really clearly and one of the things that we again think is so important is having this conversation in the public about it and developing a shared view, almost you know, it drives policy but it's also something which I think the whole of society needs to sort of think about how we address and what we want to do collectively. I wouldn't place it as a barrier but I would highlight it as a strength that we've had and I think we're hopeful that we'll continue is that long-term commitment in terms of government and the NHS and I think that's really powerful in this space to maintain the UK's position as being able to ask these questions and to show that leadership. Ana Lisa: And to bring together, we need to work really closely across the ecosystem. So in my mind one of the challenges is if one part is missing then that person is not going to get the treatment and how we keep joining up these really important dots across the whole ecosystem to make sure that most people will one day be able to get a treatment. Julia: And all those dots honestly, those dots can never even start unless you have a diagnosis and it's in time. And so there are so many people around the world working on each of those dots that connect a child or a patient to a treatment, but if you can't even be diagnosed or if you're diagnosed too late, which is what the reality is in the world of rare conditions right, then you know, then it's a little bit futile to race to a treatment or even think if that's possible. So I think the very, very first thing is: can we find children and patients, like can we find children like Mila in time? And I love hearing the word ‘hope' that's the word that keeps me going and doing what I'm doing because if there isn't any hope it's pretty hard to keep fighting, so I'm really glad, thank you both for having hope. Okay, we'll wrap up here. Thank you to Ana Lisa and to Rich for joining me in this conversation today as we shed some light on the challenges you know that those with rare conditions are facing. We touched on the work being carried out across the Genomics ecosystem in the UK to support those living with rare conditions. If you'd like to hear more of this, please subscribe to the G Word on your favourite podcast app. And thank you so much for listening. I've been your host, Julia Vitarello. This podcast was edited by Mark Kendrick at Ventoux Digital, and produced by Naimah Callachand.  

4 Peaks by 3 Friends for 2 Children in 1 Day Alannah and Adam Foley from Killorglin, Co.Kerry were diagnosed with and undergoing continuous treatment for Neurofibromatosis Type 1 (NF1). What is the 4 Peaks Challenge? The challenge involves scaling the highest peaks in each of Ireland's four provinces: Carrauntoohil (1040m) in Co. Kerry, Mweelrea (841m) in Co. Mayo, Slieve Donard (840m) in Co. Down, and Lugnaquilla (925m) in Co. Wicklow. While typically spread over a few days, three friends aim to conquer it within 24 hours. The hospitality trio, comprising Alannah and Adam's father, Andrew Foley, along with TJ O'Connor, a lecturer at Munster Technological University in Tralee, and Padraig McGillicuddy, Proprietor of Ballygarry Estate Hotel & Spa in Tralee take on this challenge. They share a connection through their work and passion for the hospitality industry and believe in supporting one of their own in times of need. They stand united in solidarity for a meaningful cause. Anyone who wants to donate or get involved in any way can do so at https://www.gofundme.com/f/need-for-neuro-4-peaks-challenge?qid=6ae7e6d93943044569e04bedd434154b

Episode 24 - Wrapping up our last episode with a guest with a bang. In this episode, we get Tim back on the show, this time with a healthy Justin onboard as well. A chat about lifting, food etc, turned into a much deeper conversation when Tim and Justin shared experiences with both their sons having NF1 (Neurofibromatosis type 1) and the mental struggles associated with having a child with this rare condition.  This episode was great ~ a light of humour sprinkled in the episode along with questionable jokes and stereotyping. It captures what we feel podcasting should be - a chat with mates that others can get some wisdom from or just laugh. One love all. Tim's Socials:https://www.instagram.com/naturaformafitness/https://www.instagram.com/zequali/Lonely Drivers Driving Club: Website: https://lonelydriversdriving.club/ Insta: https://www.instagram.com/lonelydriversdriving.club/ Justin's Socials: Insta: https://www.instagram.com/justinarmarego/

ASCO: You're listening to a podcast from Cancer.Net. This cancer information website is produced by the American Society of Clinical Oncology, known as ASCO, the voice of the world's oncology professionals. The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guests' statements on this podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Cancer research discussed in this podcast is ongoing, so data described here may change as research progresses. In this podcast, Dr. Allison Kurian and genetic counselor Kristen Mahoney Shannon talk about what people should know about genetic testing and hereditary breast cancer, including what to expect when meeting with a genetic counselor, ways to reduce your risk of developing cancer, and talking about genetic test results with family.  Dr. Kurian is a Professor of Medicine and of Epidemiology and Population Health at Stanford University School of Medicine, and Director of the Stanford Women's Clinical Cancer Genetics Program. She is also the 2023 Cancer.Net Specialty Editor for Breast Cancer. Ms. Shannon is a senior genetic counselor and Director of the Cancer Center Genetics Program and Director of Genetic Counseling for the Massachusetts General Hospital Department of Medicine. She is also a 2023 Cancer.Net Advisory Panelist. View disclosures for Dr. Kurian and Ms. Shannon at Cancer.Net. Dr. Allison Kurian: I'm Allison Kurian. I am a professor of medicine, oncology, and epidemiology and population health at Stanford University. And I am speaking today with my colleague, Kristen Shannon, who will introduce herself. Kristen Shannon: Hi, it's great to be here. My name is Kristen Shannon. I am a genetic counselor and the director of cancer genetics at Massachusetts General Hospital in Boston. And I have no financial relevant disclosures to report. Dr. Allison Kurian: Thank you, and I have no relevant financial disclosures either. Very good. So today we will be talking about breast cancer and inherited risk and genetic testing. And let me start by providing a definition of a genetic or hereditary condition. So the way we think about this is something that has a high risk for developing a disease, not a certainty, but a high risk, and runs in families, generally because of a genetic finding that we can identify. And that typically is identified through sequencing, testing of blood or saliva samples, and typically allows us to find a change that we know is clearly associated with disease. A good example for breast cancer are the genes BRCA1 and BRCA2, which some may have heard of, and we will talk about further. So that is just an example, and we will get into more of the details of this as we go on. But I think the point is something that runs in families often is seen with the trait, so for BRCA1 or BRCA2, that would be breast cancer or ovarian cancer, affecting people in every generation. And having what we call for these kinds of genes an autosomal dominant inheritance pattern, so inherited from either parent. And taking only 1 copy that is not functioning to give a person higher risk of the condition. So that's sort of a bit of the basics here on genetic or hereditary risk. And just to give a sense of how common hereditary breast cancer is, we think that in general this may account for, I would say, somewhere between 5% to perhaps 10% of cases of breast cancer. And Kristen, please jump in and tell me if you think differently. But that would be my ballpark. And I think probably the majority of those are the BRCA1 and BRCA2 genes that I mentioned, although there are others that we are recognizing are playing more of a role than we thought, and we'll discuss those, too. So let me give you a chance to continue and respond, Kristen. Kristen Shannon: Yeah, no, I totally agree. And I was thinking that maybe I could talk a little bit about some of the features that are suggestive that there could be one of these inherited breast cancers in the family, because recognizing these signs of hereditary breast cancer can be super important for early detection and prevention of breast cancer. So first, multiple cases of breast cancer within the family, especially among close relatives like parents, siblings, children, those can be a sign that the cancer is inherited. Another important sign is early age of onset of disease. So breast cancer diagnosed at a young age, typically before the age of 50, might point towards hereditary risk. And it's not always the case, but it's something to be aware of. Also, if there is a history of ovarian cancer in the family, especially if you see it in conjunction with breast cancer cases, that's a significant sign that there could be something inherited in the family. And while it's rarer, male breast cancer can also be associated with hereditary gene mutations. So if there's a history of male breast cancer in the family, it's definitely something to think about in terms of hereditary risk. Multiple cancer types in the family can also be another clue. It's not always just breast and ovarian cancer. If you see a family history of both breast and ovarian cancer or pancreatic cancer or prostate cancer within the same family, that also might be a sign of an inherited cancer syndrome. For individuals of Ashkenazi Jewish descent, it's worth noting that they have a higher prevalence of certain gene mutations in specific genes, specifically BRCA1 and BRCA2, which Dr. Kurian has mentioned before. So a family of history of breast or ovarian cancer in an Ashkenazi Jewish individual should be noted as a higher sign that this cancer could be due to an inherited gene. And lastly, if someone has had breast cancer in both breasts, that's called bilateral breast cancer, and that might indicate hereditary risk. It's important, though, to remember that it's not just about any single sign in isolation. You really need to take a look at the bigger picture and the bigger context of the family. So if you notice any of these signs in your family, it's a good idea to seek guidance from a health care professional, like a genetic counselor or a medical oncologist, and they can help assess the family's risk and recommend genetic testing if needed. Dr. Kurian, did I forget anything or leave anything off? Dr. Allison Kurian: Perfect as always. I will just add a little bit here in terms of the specific gene names that we think about, because sometimes it helps people to have sort of a list in their minds, not that we expect you to remember the whole alphabet soup of these different genes. And let me just say that I think it's always a bit of a hodgepodge, some of these names. I used to wonder how people come up with these names, and often there's a bit of a history there. But I will just go through a few of them. We now have some practice guidelines, and they are basically put together by a group of experts who review all the evidence frequently and come up with recommendations. And so there is a list in these guidelines of basically which genes we think are appropriate to test for breast cancer in families, because there's enough evidence to suggest that. And so in addition to BRCA1 and BRCA2, the ones that I think of as the most important, and I'll want to hear Kristen's thoughts about this, too, but the ones that we see most often are called ATM. Sounds like a cash machine, unfortunately not, but ATM. CHEK2, C-H-E-K-2, and then one called PALB2, which stands for Partner and Localizer of BRCA2, and is a lot like BRCA2 in its risks. There are some other genes that give breast cancer risks that are less common. One of them, CDH1, is a gene that also causes an increased risk of stomach cancer. There are a few others that we always keep in mind. There's one called PTEN that's very rare that causes a syndrome called Cowden syndrome that I certainly haven't seen much of. Kristen may have seen more, but it's not something we see often and goes with a lot of other features in families. There are 2 genes that I think we recognize more in recent years and like to be sure we test, called RAD51C and RAD51D, and those both give increased risks. And then another one that I always think of as important here is TP53, and that is a gene that causes something called Li-Fraumeni syndrome, which has probably the highest cancer risks of which we know. There's another one, STK11, that gives some risk, NF1. We see these as being less frequent contributors. Those are the ones that I kind of keep in mind. And again, there will not be a quiz on the alphabet soup, but just so you're aware of what kinds of names you might hear. Kristen, please jump in if I've forgotten any or anything else you want to say. Kristen Shannon: No, I think that that's important. I think the only thing that I would add is that some people think when they go in for breast cancer genetic testing, they only are getting the BRCA1 and BRCA2 gene. And it's just important for people to realize that that's not really a complete test at this point, as you mentioned, Dr. Kurian. Dr. Allison Kurian: Totally agree, and thank you. Kristen Shannon: Should we move into how to prepare for a genetic counseling appointment? Dr. Allison Kurian: Please, yes. Kristen Shannon: Sure, okay. So preparing for a genetic counseling appointment for breast cancer risk can be helpful. First and foremost, we suggest that you gather your family health history. So reach out to your relatives and compile as much information as possible about your family's health background. Pay special attention to any instances of breast cancer and ovarian cancer, prostate cancer, pancreatic cancer in the family. And if any family members have had genetic testing, it's really helpful to jot down those test results as well and bring them with you to the appointment. The other thing is to think about your own personal medical history. You know, think about if you've had any past diagnosis, any treatments, surgeries, or medical conditions, especially those related to breast cancer, your genetic counseling appointment will include a discussion of those. The other thing is, you know, if you've had any medical tests related to cancer, it's important to gather those records if they're not already in your hospital's medical record system that you are going to. Another good idea is to just prepare a list of questions that you might want to have answered. So what do you want to know? Are there specific concerns or specific things you're curious about? It's also important to understand what you want to get out of this genetic counseling encounter. Do you want to just clarify your risk of having a gene? Do you want to consider genetic testing? Or do you want to talk about just managing your risk for breast cancer? That's super important to have that in mind before you actually go into your appointment. Lastly, I would consider bringing along a person, a supportive person with you to the appointment. Having someone with you can help provide emotional support because sometimes these visits can get emotionally charged, but it also can help to have someone remember important details that you will discuss with your health care provider. So it's really important to just arm yourself with information, questions, and support so that the appointment is as productive and informative as it can be. Do you have anything else you'd like to add, Dr. Kurian? Dr. Allison Kurian: It's wonderful to have your expert perspective on this. And I guess any thoughts about really what's inside the box? I think sometimes people just sort of wonder what's going to happen when I go in that room. Sometimes we have patients come in and say, “What are you guys going to do to me? Will there be surgery done?” And we reassure them that we are not doing anything that wild. And so maybe just a sense of kind of walking people through what will happen when they go to meet with genetic counselors. Kristen Shannon: Absolutely, thanks for bringing that up. So during the initial meeting, first you'll probably discuss your personal health history, again, any past diagnoses, surgeries, medical conditions. And then typically a genetic counselor or a medical professional will dive right into your family health history. So they'll ask a whole bunch of questions about your close and extended family members to build a really comprehensive picture of your family and the cancer diagnosis in it. They'll want to know if anyone in your family has had cancer, and they'll also want to know what type of cancer that person has had and also the age at which that person was diagnosed. So those are the 3 pieces of information that your health care provider will want to get from you. The genetic counselor will also probably ask you about what you want to get out of this encounter to make sure that you're both on the same page. Again, do you want genetic testing? You know that already. Or do you want to just talk through the process? So the big part of the initial meeting is really education. The genetic counselor will explain what Dr. Kurian described at the very outset of this discussion, what's the genetic basis of hereditary breast cancer, including all the specific genes that Dr. Kurian—the alphabet soup that we talked about. Talk about inheritance patterns and the implications of having a genetic mutation. The genetic counselor will probably also first assess your risk of having a mutation in one of the genes, and then they'll also talk to you often about genetic testing. So if genetic testing is on the table and you and the genetic counselor both agree that it's a good step, they'll walk you through the process of informed consent. And so this ensures that you understand what the testing entails, the potential outcomes, the implications of the test results. And then if you decide to go through with genetic testing, you will provide a blood or a saliva sample. And then it's a waiting game because these test results can take several weeks, usually about 3 to 4 weeks to get the test results back. When the test results come back, you'll typically have a follow-up appointment, either in-person or on the phone with your genetic counselor. And that's when they spend a lot of time interpreting the test results, explain what they mean for you and your health, as well as discussing the appropriate risk management strategies, if necessary. And if a gene mutation is identified, a genetic counselor will guide you on how to manage these risks. But it will depend on the specific mutation that is identified. And then the other thing that the genetic counselor can help with is just the emotional support. Some people have a harder time than others hearing this information. And also to talk about how to tell your family members about this. So in a nutshell, the initial meeting with the genetic counselor is about gathering information, assessing risk, and potentially deciding on whether or not you're going to have genetic testing. And then after that step, it's about interpreting the test results, talking about next steps, and providing emotional support. Dr. Allison Kurian: Thank you, Kristen. That was wonderful and very complete. And as I was listening to you, first of all, I was thinking about my general admiration for genetic counselors, which is huge. They taught me everything I know about this field. But so also kind of highlighting the key things that a meeting with a genetic counselor will do for you, as you so nicely did. And I think it's getting the right test ordered, making sure that the results make sense to you, and going beyond the patient. But I think those are sort of the key aspects that you communicated really well of the things that we want to get done there. Kristen Shannon: Well said, well said. And I couldn't agree more. Dr. Allison Kurian: And what do you think about the family part in terms of how that gets done? Kristen Shannon: Right, so discussing your genetic test results with family members can be hard and challenging, but it's really, really important. In terms of talking to your family members, I think first, determine the way you're going to notify your family members. So are you going to talk to them? Are you going to send them a letter or an email? And how you share the information may be different based on your relationship with that person. So for example, you may sit down over coffee with a close family member to talk about your test results, but you may choose to write a letter to someone that you don't have that much contact with. The next thing that I think is really important is to be prepared. So before you even start to have this conversation, make sure that you have a clear understanding of your genetic test results, the implications to you and to the family member. That's super important before you even start to have the conversation so that you can explain things to people in simple terms without too much medical jargon and make sure you keep it straightforward. It's really helpful to have a copy of your genetic test results and to provide that to your relatives if you're comfortable doing so, because then they can take that information with them to their genetic counseling or genetic testing appointment, which can be incredibly essential in terms of making sure that they get the correct test at the right time and the test results are interpreted correctly. The only other suggestion I have is just to keep in mind that family members are going to react very differently to this information. And some people will be very matter of fact about it. Some people might get a little distracted by this whole thing. So just to be patient with people and keep the conversation open. Allow them to call you if you're willing to do that so that the conversation can develop over time because, you know, really, in the end, the goal is to make sure that everyone in the family is well informed and makes decisions based on their own health and their well-being. Dr. Allison Kurian: Thank you. I couldn't agree more. And we sometimes, as people may have heard, call this “cascade genetic testing.” So a patient is tested. Somebody who's already had cancer maybe is tested. But then we have the opportunity to have this cascade of beneficial genetic testing, where we can get to people before they have cancer and work on prevention and screening, which I'll talk about in a minute. And I will say that, in general, we here in the United States, and certainly other places as well, don't do as well as we would like with cascade testing despite all best efforts of everyone. And so just to emphasize that family notification is super important, genetic counselors are wonderful at helping people to do that. And I think also additional strategies and interventions are underway to try to help make that easier. So if I may, I'll talk just a little bit about kind of what we do when we find something. Is that okay to do? Kristen Shannon: That sounds great. Talk about people, you know, what they can do about their test results. Dr. Allison Kurian: Good. Yeah, so I always think that's important. I'm an oncologist by training. I'm not a geneticist. And again, it's only thanks to the brilliance of genetic counselors like Kristen that I have learned what I have for the last 2 decades working in the field. But so I tend to think in terms of what can we do to treat this person differently if they have cancer to prevent or reduce the risk of a future cancer. And so what I would say is increasingly over the last few years for a person with breast cancer, as well as some additional cancers, it started to matter what these results are in terms of how we treat the person, whether we might give different medications. And that's really exciting because for years in this field, we didn't have that, and now we do. And so the drugs that are increasingly important are called PARP, P-A-R-P, inhibitors. And sometimes, if a person has a BRCA1 or BRCA2 gene mutation, we might even offer those drugs to treat a breast cancer or, in other cases, ovarian, prostate, or pancreatic cancer. So I think the testing can matter like never before in terms of what we might do to take care of people's cancer. Sometimes we might also choose a different surgery. So sometimes a woman who has a diagnosis of breast cancer might choose to do a more extensive breast surgery, she might choose a double mastectomy to reduce her risk of getting a second breast cancer. That's never required. She certainly doesn't have to do so extensive a surgery if she doesn't choose, but it is an option that some people might choose. And there might also be other cancer risks to manage in somebody who had breast cancer. BRCA1 and BRCA2, for example, give a high risk of ovarian cancer. And so we might talk with someone about the possibility of removing ovaries to prevent an ovarian cancer, which often is recommended with BRCA1, BRCA2, and other such gene mutations. I will say that I think for somebody who hasn't had cancer yet, or hopefully ever, particularly as we think about breast cancer, we're often thinking about intensive screening. So starting often earlier than a person would if she didn't have high risk and generally adding magnetic resonance imaging, MRI, to screening with mammogram alone. And that really is, I think, the cornerstone for women at high risk is adding that breast MRI screening. For pretty much all of the genes I mentioned, that would be clinically indicated and covered by insurance and important to do. MRI has no radiation, very effective at finding breast cancer early. So I think to summarize, it's really all about understanding risk based on a particular gene mutation, understanding if a different kind of treatment is needed for the cancer that a person has, understanding if any sort of preventive measure is needed for future cancer risk, and making sure that the screening we have for breast and for other cancers is appropriate to the level of risk. Anything to add there, Kristen? Kristen Shannon: No. No, I think that that's great. Dr. Allison Kurian: Absolutely. Yeah, so I think it's wonderful to have this opportunity to speak about the importance of genetic testing, which is I think more important than it ever has been at this time for the care of patients with breast cancer and their families. And so as we move into breast cancer awareness month, it's great to be able to talk about this. Thanks so much. Kristen Shannon: Thank you so much. I agree. And if you have any questions, I would suggest you reach out to your doctor or look up on the ASCO website for a referral to a genetic counselor. ASCO: Thank you, Dr. Kurian and Ms. Shannon. Learn more about hereditary breast cancer and genetic testing at www.cancer.net/hboc. Cancer.Net Podcasts feature trusted, timely, and compassionate information for people with cancer, survivors, and their families and loved ones. Subscribe wherever you listen to podcasts for expert information and tips on coping with cancer, recaps of the latest research advances, and thoughtful discussions on cancer care. And check out other ASCO Podcasts to hear the latest interviews and insights from thought leaders, innovators, experts, and pioneers in oncology. Cancer.Net is supported by Conquer Cancer, the ASCO Foundation, which funds lifesaving research for every type of cancer, helping people with cancer everywhere. To help fund Cancer.Net and programs like it, donate at CONQUER.ORG/Donate.

Join us on a remarkable journey as we delve into the inspiring life of Amit Ghose, a courageous individual who has faced the challenges of living with neurofibromatosis type 1 (NF1) head-on. In this podcast, Amit shares his experiences, from growing up with this rare condition that only affects 1 in 3000 people, to the hurdles he encountered during his school years, including the painful struggle of not being accepted and the heart-wrenching experiences of bullying. Discover how cricket became his refuge, transforming his life and instilling in him the resilience to face adversity. At just 11 years old, Amit faced a life-altering moment when a tumour led to the removal of his eye. We explore the profound impact this had on his life, the challenges he encountered, and the incredible strength it took to navigate this new reality. But Amit's story takes a heartwarming turn when he opens up about finding love. His journey of acceptance and self-love is nothing short of remarkable and a testament to the power of his human spirit. Today, Amit dedicates his life to spreading awareness about NF1, using his voice to make a difference in others facing similar challenges. Through his story, we learn about the importance of acceptance, building confidence, and the transformative power of love. Join us in this extraordinary conversation as Amit shares his experiences, triumphs, and mission to create a world where awareness and understanding of NF1 shine brightly. What is neurofibromatosis type 1

Go online to PeerView.com/RFJ860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Recent developments targeting the RAS/MAPK signaling pathway have led to the first approved MEK inhibitor for the treatment of pediatric patients with symptomatic, inoperable PNs. To help lay the foundation of personalized NF1 care, this activity—based on a live event at the recent ASPHO meeting—features expert panelists sharing real-world cases to illustrate the collaborative management of NF1 tumors with highly efficacious targeted agents. The case-based conversations cover the diagnostic-treatment arc of NF1-PNs, culminating with tips and tactics arising from the clinical experience with MEK inhibitors—and going beyond to include insights on targeted strategies in other NF1 tumor settings. Watch now to start building your personalized management on a bedrock of solid science! Upon completion of this activity, participants should be better able to: Summarize current evidence and guideline recommendations supporting modern diagnostic strategies and treatment plans incorporating targeted agents, including MEK inhibitors, for the management of pediatric patients with NF1-related PNs and other tumors; Develop evidence-based treatment plans using MEK inhibitors and other targeted therapies for the management of pediatric patients with NF1-related PNs and other tumors based on prognostic information and safety considerations; and Manage practical aspects of patient care when using innovative targeted approaches, including patient/caregiver education, monitoring, and the unique spectrum of adverse events.

Go online to PeerView.com/RFJ860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Recent developments targeting the RAS/MAPK signaling pathway have led to the first approved MEK inhibitor for the treatment of pediatric patients with symptomatic, inoperable PNs. To help lay the foundation of personalized NF1 care, this activity—based on a live event at the recent ASPHO meeting—features expert panelists sharing real-world cases to illustrate the collaborative management of NF1 tumors with highly efficacious targeted agents. The case-based conversations cover the diagnostic-treatment arc of NF1-PNs, culminating with tips and tactics arising from the clinical experience with MEK inhibitors—and going beyond to include insights on targeted strategies in other NF1 tumor settings. Watch now to start building your personalized management on a bedrock of solid science! Upon completion of this activity, participants should be better able to: Summarize current evidence and guideline recommendations supporting modern diagnostic strategies and treatment plans incorporating targeted agents, including MEK inhibitors, for the management of pediatric patients with NF1-related PNs and other tumors; Develop evidence-based treatment plans using MEK inhibitors and other targeted therapies for the management of pediatric patients with NF1-related PNs and other tumors based on prognostic information and safety considerations; and Manage practical aspects of patient care when using innovative targeted approaches, including patient/caregiver education, monitoring, and the unique spectrum of adverse events.

Go online to PeerView.com/RFJ860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Recent developments targeting the RAS/MAPK signaling pathway have led to the first approved MEK inhibitor for the treatment of pediatric patients with symptomatic, inoperable PNs. To help lay the foundation of personalized NF1 care, this activity—based on a live event at the recent ASPHO meeting—features expert panelists sharing real-world cases to illustrate the collaborative management of NF1 tumors with highly efficacious targeted agents. The case-based conversations cover the diagnostic-treatment arc of NF1-PNs, culminating with tips and tactics arising from the clinical experience with MEK inhibitors—and going beyond to include insights on targeted strategies in other NF1 tumor settings. Watch now to start building your personalized management on a bedrock of solid science! Upon completion of this activity, participants should be better able to: Summarize current evidence and guideline recommendations supporting modern diagnostic strategies and treatment plans incorporating targeted agents, including MEK inhibitors, for the management of pediatric patients with NF1-related PNs and other tumors; Develop evidence-based treatment plans using MEK inhibitors and other targeted therapies for the management of pediatric patients with NF1-related PNs and other tumors based on prognostic information and safety considerations; and Manage practical aspects of patient care when using innovative targeted approaches, including patient/caregiver education, monitoring, and the unique spectrum of adverse events.

Go online to PeerView.com/RFJ860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Recent developments targeting the RAS/MAPK signaling pathway have led to the first approved MEK inhibitor for the treatment of pediatric patients with symptomatic, inoperable PNs. To help lay the foundation of personalized NF1 care, this activity—based on a live event at the recent ASPHO meeting—features expert panelists sharing real-world cases to illustrate the collaborative management of NF1 tumors with highly efficacious targeted agents. The case-based conversations cover the diagnostic-treatment arc of NF1-PNs, culminating with tips and tactics arising from the clinical experience with MEK inhibitors—and going beyond to include insights on targeted strategies in other NF1 tumor settings. Watch now to start building your personalized management on a bedrock of solid science! Upon completion of this activity, participants should be better able to: Summarize current evidence and guideline recommendations supporting modern diagnostic strategies and treatment plans incorporating targeted agents, including MEK inhibitors, for the management of pediatric patients with NF1-related PNs and other tumors; Develop evidence-based treatment plans using MEK inhibitors and other targeted therapies for the management of pediatric patients with NF1-related PNs and other tumors based on prognostic information and safety considerations; and Manage practical aspects of patient care when using innovative targeted approaches, including patient/caregiver education, monitoring, and the unique spectrum of adverse events.

MLB – Major League Baseball Yesterday St. Louis Cardinals 12, Detroit Tigers 6 Miami Marlins 5, Chicago Cubs 4 – 14 Innings Chicago White Sox 17, Cincinnati Reds 4 Cardinals 12, Tigers 6 – Goldschmidt 3 HRs, Cards end 8-game skid, beat Tigers 12-6 Paul Goldschmidt homered three times, Brendan Donovan hit a three-run drive and the St. Louis Cardinals stopped an eight-game losing streak with a 12-6 win over the Detroit Tigers. Goldschmidt, had four hits and four RBIs. Lars Nootbaar added a two-run single to cap off a seven-run sixth inning for the Cardinals, who had been on their longest skid in 16 years. Jake Rogers hit a grand slam for the Tigers, whose five-game winning steak was stopped. Marlins 5, Cubs 4 – F/14 – Marlins stop 5-game slide with 14-inning win over Cubs Garrett Hampson scored on Adbert Alzolay’s balk in the 14th inning, and the Miami Marlins stopped a five-game slide by outlasting the Chicago Cubs for a wild 5-4 victory. Hampson opened the inning on second as the automatic runner. He advanced on Luis Arraez’s groundout and trotted home when Alzolay was called for a balk with a 2-2 count on Jesús Sánchez. Steven Okert got three outs for the win, and Andrew Nardi pitched the 14th for his first career save. White Sox 17, Reds 4 – White Sox score 11 in 2nd, beat Reds 17-4 Hanser Alberto had four hits, a career-high four RBIs and Chicago scored 11 runs in the second inning to rout the Cincinnati Reds 17-4 on Sunday. The 11 runs are the most for the team in one inning in 16 years and third-most ever for the franchise. The White Sox had 11 runs in the fifth at Kansas City on Sept. 17, 2007. Chicago, which came in batting .176 with runners in scoring position, delivered plenty of big hits against Graham Ashcraft (2-1) in the second, sending 14 batters to the plate. Michael Kopech (1-3) allowed four solo homers by pitched six innings to earn his first victory of the season. Tonight Detroit (Wentz 0-3) at Cleveland (Bibee 1-0), 6:10 p.m.   News/Talk/Sports 94.9 WSJM 7:50 Chicago White Sox (Cease 2-1) at Kansas City (Greinke 1-4), 7:40 p.m. St. Louis (Mikolas 1-1) at Chicago Cubs (Stroman 2-2), 7:40 p.m. NHL – National Hockey League – 2023 Stanley Cup Playoffs – Round 2 (Best of 7) Last Night New Jersey Devils 8, Carolina Hurricanes 4                             (CAR leads 2-1) Florida Panthers 3, Toronto Maple Leafs 2 – OT                        (FLA leads 3-0) Seattle Kraken 7, Dallas Stars 2                                           (SEA leads 2-1) Devils 8, Hurricanes 4 – Devils answer in Game 3, rout Canes 8-4, deficit now 2-1 Jack Hughes scored two goals, set up two more and had a near fight as the New Jersey Devils began the task of digging out of another hole with a 8-4 win over the Carolina Hurricanes in Game 3 of the Eastern Conference semifinals Sunday. Timo Meier, Nico Hischier and Damon Severson added their first goals of playoffs and Vitek Vanecek returned to the net and made 26 saves in helping New Jersey cut its deficit in the best-of-seven series to 2-1. Panthers 3, Leafs 2 – OT – Reinhart the hero, as Panthers top Leafs in OT for 3-0 lead Sam Reinhart scored 3:02 into overtime and the Florida Panthers beat the Toronto Maple Leafs 3-2 to take a commanding 3-0 lead in their Eastern Conference semifinal series. Reinhart dumped the puck off the boards behind the net to set up his game-winner, taking a pass back from Anton Lundell and scoring to give Florida its first 3-0 series lead in 27 years. Anthony Duclair and Carter Verhaeghe scored for Florida. Sam Lafferty and Erik Gustafsson scored for Toronto. Kraken 7, Stars 2 – Kraken ride 2nd period outburst, thump Stars 7-2 in Game 3 Jordan Eberle sparked a five-goal outburst in the second period with his fourth goal of the playoffs, Philipp Grubauer made 24 saves and the Seattle Kraken beat the Dallas Stars 7-2 to take a 2-1 series lead in their Western Conference semifinal. Eberle’s goal was just the start for Seattle. Alex Wennberg doubled the lead 1:26 after Eberle’s goal; Carson Soucy became Seattle’s 16th different goal scorer this postseason, beating Oettinger five-hole at 6:30; and Matty Beniers made it 4-0 at 8:22. Tonight Vegas Golden Knights at Edmonton Oilers, 8:30 p.m.                 (Series tied 1-1) NBA – National Basketball Association Playoffs – Round 2 (Best of 7) Last Night Philadelphia 76ers 116, Boston Celtics 115 – OT                      (Series tied 2-2) Phoenix Suns 129, Denver Nuggets 124                                  (Series tied 2-2) Sixers 116, Celtics 115 – OT – Harden makes winning 3 in OT, 76ers tie series with Celtics James Harden hit the go-ahead 3-pointer with 18 seconds left in overtime and scored 42 points to help the Philadelphia 76ers stave off a wild Boston Celtics comeback in a 116-115 victory on Sunday that evened their playoff series at 2-2. Marcus Smart’s potential winner was a tick too late and the Celtics now head home for Tuesday’s Game 5. Joel Embiid had 34 points and 13 rebounds. Harden added nine assists and eight rebounds. Jayson Tatum struggled to score early but finished with 24 points, 18 rebounds, six assists and four blocks. Suns 129, Nuggets 124 – Booker, Durant both score 36, Suns even series with Nuggets Devin Booker had 36 points and 12 assists, Kevin Durant also had 36 points and the Phoenix Suns beat the Denver Nuggets 129-124 to even their Western Conference semifinal playoff series at two games apiece. Backup guard Landry Shamet made four crucial 3-pointers in the fourth quarter to keep the Suns ahead. Denver lost despite a huge game from MVP runner-up Nikola Jokic, who poured in 53 points. The Suns took a 98-92 lead into the fourth quarter after a scoring flurry from Booker, who had 17 points in the third. Phoenix wouldn’t trail in the fourth. The series returns to Denver for Game 5 on Tuesday. Tonight New York Knicks at Miami Heat, 7:30 p.m.                                (MIA leads 2-1) Golden State Warriors at Los Angeles Lakers, 10:00 p.m.          (LAL leads 2-1) NBA – 76ers’ Harden visits with Michigan State shooting victim James Harden met with Michigan State shooting victim John Hao before a playoff game. Then he signed his sneakers and gave them to Hao after scoring 42 points and making the winning shot in overtime. The 20-year-old Hao was paralyzed from the chest down in a February shooting on the East Lansing campus that killed three students and injured five others. Harden learned Hao was a fan of his and the two struck up a friendship over FaceTime. Harden also donated sneakers and money toward Hao’s recovery. Hao recently left a Chicago rehabilitation facility and said he may move with his family back to China. NBA – Nick Gilbert, son of Cavaliers owner, dies at 26 Nicolas “Nick” Gilbert, the son of Cleveland Cavaliers owner Dan Gilbert who became the team’s good luck charm at NBA draft lotteries, has died. He was 26. A funeral announcement posted by the Ira Kaufman Chapel said Gilbert died Saturday “peacefully at home surrounded by family.” Gilbert was diagnosed as a child with neurofibromatosis (NF1), a genetic condition that causes tumors to grow in the brain, spinal cord and skin. Wearing a signature bow tie and dark-rimmed glasses, Gilbert became a sensation at the 2011 draft lottery. NBA – Analysis: Wemby’s farewell tour will be a French celebration Victor Wembanyama’s first basket on Sunday night looked so easy. He deflected a pass, ran it down, dribbled twice and dunked the ball with his left hand. And 15,000 people roared. He’s called a generational talent, though really, there’s never been one in France quite like Wembanyama. The 7-foot-3, 19-year-old, soon-to-be No. 1 pick in the NBA draft is on his farewell tour of his homeland, playing his final pro games there before he comes to North America and accepts the challenge of trying to truly become the game’s next superstar. Golf – PGA – Clark holds off Schauffele for first PGA win at Wells Fargo Wyndham Clark shot 68 on Sunday for a four-shot victory over Xander Schauffele at the Wells Fargo Championship to earn his first career win on the PGA Tour. Clark finished the tournament at 19-under 265, the second-lowest score in relation to par in tournament history behind only three-time champion Rory McIlroy’s 21-under 267 in 2015 when par for the course was 72. Clark struggled to hold back tears as he sank a bogey putt on the 18th hole to seal the win. Schauffele has accuracy issues with his driver on Sunday and shot 70, finishing at 15 under. Tyrrell Hatton and Harry English finished tied for third at 12 under, one shot better than Tommy Fleetwood and Adam Scott. Defending champion Max Homa shot 70 on Sunday and finished tied for ninth at 9-under 275. MWL – Midwest League Baseball Yesterday Lansing Lugnuts 4, Dayton Dragons 3 Great Lakes Loons 9, Quad Cities River Bandits 6 Cedar Rapids Kernels 6, South Bend Cubs 1 West Michigan Whitecaps 7, Beloit Sky Carp 2 Today No games tonight MHSAA – High School Sports Today Girls Soccer St. Joseph at Lakeshore, 6:30 p.m. Our Lady of the Lake at Saugatuck, 5:00 p.m. Battle Creek Central at Mattawan, 6:30 p.m. Portage Central at Battle Creek Lakeview, 6:30 p.m. Gull Lake at Kalamazoo Central, 6:30 p.m. Portage Northern at Kalamazoo Loy Norrix, 6:30 p.m. Paw Paw at Edwardsburg, 5:30 p.m. Vicksburg at Niles, 6:30 p.m. Otsego at Sturgis, 6:00 p.m. Plainwell at Three Rivers, 6:00 p.m. Watervliet at South Haven, 6:30 p.m. Holland Black River at Coloma, 6:00 p.m. Fennville at Bridgman, 5:00 p.m. Berrien Springs at Covert, 5:00 p.m. Buchanan at New Buffalo, 6:00 p.m. Allegan at Schoolcraft, 5:00 p.m. Comstock at Marcellus, 5:30 p.m. Delton-Kellogg at Kalamazoo Hackett, 5:00 p.m. Kalamazoo Christian at Lawton, 6:00 p.m. Constantine at Parchment, 6:00 p.m. Baseball Michigan Lutheran at Brandywine, 4:00 p.m. Fennville at Bridgman, 4:30 p.m. Loy Norrix at River Valley, 4:15 p.m. Lawrence at Cassopolis, 4:30 p.m. Bangor at Centreville, 4:30 p.m. Hartford at Comstock, 4:30 p.m. Bloomingdale at Marcellus, 4:30 p.m. Decatur at Mendon, 4:30 p.m. Portage Central at Otsego, 4:00 p.m. Plainwell at Kalamazoo Central, 4:00 p.m. Kalamazoo Hackett at Portage Northern, 4:00 p.m. Otsego at Gull Lake, 4:00 p.m. Martin at Saugatuck, 4:30 p.m. Softball St. Joseph at Zeeland West, 5:00 p.m. Michigan Lutheran at Brandywine, 4:15 p.m. Howardsville Chr. at River Valley, 4:15 p.m. Fennville at Bridgman, 4:30 p.m. Bronson at Buchanan, 4:15 p.m. Lawrence at Cassopolis, 4:30 p.m. Bangor at Centreville, 4:30 p.m. Hartford at Comstock, 4:30 p.m. Bloomingdale at Marcellus, 4:30 p.m. Decatur at Mendon, 4:30 p.m. Three Rivers at Kalamazoo Central, 4:00 p.m. Kalamazoo Christian at Portage Central, 4:00 p.m. Otsego at Gull Lake, 4:00 p.m. Lawton at Paw Paw, 4:30 p.m. Wyoming at Delton-Kellogg, 4:30 p.m. Constantine at Parchment, 4:30 p.m. Boys Golf Battle Creek Lakeview Invitational, 9:00 p.m. St. Joseph, Lakeshore, Battle Creek Lakeview, Loy Norrix, Portage Central, Parchment, Kalamazoo Central, Harper Creek, Pennfield, Coldwater, Marshall, Mattawan, Gull Lake, Vicksburg, Niles, Girls Tennis Lakeshore at Portage Northern, 4:00 p.m. Track and Field St. Joseph, Lakeshore, at Mattawan, 4:00 p.m.See omnystudio.com/listener for privacy information.

MLB – Major League Baseball Yesterday St. Louis Cardinals 12, Detroit Tigers 6 Miami Marlins 5, Chicago Cubs 4 – 14 Innings Chicago White Sox 17, Cincinnati Reds 4 Cardinals 12, Tigers 6 – Goldschmidt 3 HRs, Cards end 8-game skid, beat Tigers 12-6 Paul Goldschmidt homered three times, Brendan Donovan hit a three-run drive and the St. Louis Cardinals stopped an eight-game losing streak with a 12-6 win over the Detroit Tigers. Goldschmidt, had four hits and four RBIs. Lars Nootbaar added a two-run single to cap off a seven-run sixth inning for the Cardinals, who had been on their longest skid in 16 years. Jake Rogers hit a grand slam for the Tigers, whose five-game winning steak was stopped. Marlins 5, Cubs 4 – F/14 – Marlins stop 5-game slide with 14-inning win over Cubs Garrett Hampson scored on Adbert Alzolay’s balk in the 14th inning, and the Miami Marlins stopped a five-game slide by outlasting the Chicago Cubs for a wild 5-4 victory. Hampson opened the inning on second as the automatic runner. He advanced on Luis Arraez’s groundout and trotted home when Alzolay was called for a balk with a 2-2 count on Jesús Sánchez. Steven Okert got three outs for the win, and Andrew Nardi pitched the 14th for his first career save. White Sox 17, Reds 4 – White Sox score 11 in 2nd, beat Reds 17-4 Hanser Alberto had four hits, a career-high four RBIs and Chicago scored 11 runs in the second inning to rout the Cincinnati Reds 17-4 on Sunday. The 11 runs are the most for the team in one inning in 16 years and third-most ever for the franchise. The White Sox had 11 runs in the fifth at Kansas City on Sept. 17, 2007. Chicago, which came in batting .176 with runners in scoring position, delivered plenty of big hits against Graham Ashcraft (2-1) in the second, sending 14 batters to the plate. Michael Kopech (1-3) allowed four solo homers by pitched six innings to earn his first victory of the season. Tonight Detroit (Wentz 0-3) at Cleveland (Bibee 1-0), 6:10 p.m.   News/Talk/Sports 94.9 WSJM 7:50 Chicago White Sox (Cease 2-1) at Kansas City (Greinke 1-4), 7:40 p.m. St. Louis (Mikolas 1-1) at Chicago Cubs (Stroman 2-2), 7:40 p.m. NHL – National Hockey League – 2023 Stanley Cup Playoffs – Round 2 (Best of 7) Last Night New Jersey Devils 8, Carolina Hurricanes 4                             (CAR leads 2-1) Florida Panthers 3, Toronto Maple Leafs 2 – OT                        (FLA leads 3-0) Seattle Kraken 7, Dallas Stars 2                                           (SEA leads 2-1) Devils 8, Hurricanes 4 – Devils answer in Game 3, rout Canes 8-4, deficit now 2-1 Jack Hughes scored two goals, set up two more and had a near fight as the New Jersey Devils began the task of digging out of another hole with a 8-4 win over the Carolina Hurricanes in Game 3 of the Eastern Conference semifinals Sunday. Timo Meier, Nico Hischier and Damon Severson added their first goals of playoffs and Vitek Vanecek returned to the net and made 26 saves in helping New Jersey cut its deficit in the best-of-seven series to 2-1. Panthers 3, Leafs 2 – OT – Reinhart the hero, as Panthers top Leafs in OT for 3-0 lead Sam Reinhart scored 3:02 into overtime and the Florida Panthers beat the Toronto Maple Leafs 3-2 to take a commanding 3-0 lead in their Eastern Conference semifinal series. Reinhart dumped the puck off the boards behind the net to set up his game-winner, taking a pass back from Anton Lundell and scoring to give Florida its first 3-0 series lead in 27 years. Anthony Duclair and Carter Verhaeghe scored for Florida. Sam Lafferty and Erik Gustafsson scored for Toronto. Kraken 7, Stars 2 – Kraken ride 2nd period outburst, thump Stars 7-2 in Game 3 Jordan Eberle sparked a five-goal outburst in the second period with his fourth goal of the playoffs, Philipp Grubauer made 24 saves and the Seattle Kraken beat the Dallas Stars 7-2 to take a 2-1 series lead in their Western Conference semifinal. Eberle’s goal was just the start for Seattle. Alex Wennberg doubled the lead 1:26 after Eberle’s goal; Carson Soucy became Seattle’s 16th different goal scorer this postseason, beating Oettinger five-hole at 6:30; and Matty Beniers made it 4-0 at 8:22. Tonight Vegas Golden Knights at Edmonton Oilers, 8:30 p.m.                 (Series tied 1-1) NBA – National Basketball Association Playoffs – Round 2 (Best of 7) Last Night Philadelphia 76ers 116, Boston Celtics 115 – OT                      (Series tied 2-2) Phoenix Suns 129, Denver Nuggets 124                                  (Series tied 2-2) Sixers 116, Celtics 115 – OT – Harden makes winning 3 in OT, 76ers tie series with Celtics James Harden hit the go-ahead 3-pointer with 18 seconds left in overtime and scored 42 points to help the Philadelphia 76ers stave off a wild Boston Celtics comeback in a 116-115 victory on Sunday that evened their playoff series at 2-2. Marcus Smart’s potential winner was a tick too late and the Celtics now head home for Tuesday’s Game 5. Joel Embiid had 34 points and 13 rebounds. Harden added nine assists and eight rebounds. Jayson Tatum struggled to score early but finished with 24 points, 18 rebounds, six assists and four blocks. Suns 129, Nuggets 124 – Booker, Durant both score 36, Suns even series with Nuggets Devin Booker had 36 points and 12 assists, Kevin Durant also had 36 points and the Phoenix Suns beat the Denver Nuggets 129-124 to even their Western Conference semifinal playoff series at two games apiece. Backup guard Landry Shamet made four crucial 3-pointers in the fourth quarter to keep the Suns ahead. Denver lost despite a huge game from MVP runner-up Nikola Jokic, who poured in 53 points. The Suns took a 98-92 lead into the fourth quarter after a scoring flurry from Booker, who had 17 points in the third. Phoenix wouldn’t trail in the fourth. The series returns to Denver for Game 5 on Tuesday. Tonight New York Knicks at Miami Heat, 7:30 p.m.                                (MIA leads 2-1) Golden State Warriors at Los Angeles Lakers, 10:00 p.m.          (LAL leads 2-1) NBA – 76ers’ Harden visits with Michigan State shooting victim James Harden met with Michigan State shooting victim John Hao before a playoff game. Then he signed his sneakers and gave them to Hao after scoring 42 points and making the winning shot in overtime. The 20-year-old Hao was paralyzed from the chest down in a February shooting on the East Lansing campus that killed three students and injured five others. Harden learned Hao was a fan of his and the two struck up a friendship over FaceTime. Harden also donated sneakers and money toward Hao’s recovery. Hao recently left a Chicago rehabilitation facility and said he may move with his family back to China. NBA – Nick Gilbert, son of Cavaliers owner, dies at 26 Nicolas “Nick” Gilbert, the son of Cleveland Cavaliers owner Dan Gilbert who became the team’s good luck charm at NBA draft lotteries, has died. He was 26. A funeral announcement posted by the Ira Kaufman Chapel said Gilbert died Saturday “peacefully at home surrounded by family.” Gilbert was diagnosed as a child with neurofibromatosis (NF1), a genetic condition that causes tumors to grow in the brain, spinal cord and skin. Wearing a signature bow tie and dark-rimmed glasses, Gilbert became a sensation at the 2011 draft lottery. NBA – Analysis: Wemby’s farewell tour will be a French celebration Victor Wembanyama’s first basket on Sunday night looked so easy. He deflected a pass, ran it down, dribbled twice and dunked the ball with his left hand. And 15,000 people roared. He’s called a generational talent, though really, there’s never been one in France quite like Wembanyama. The 7-foot-3, 19-year-old, soon-to-be No. 1 pick in the NBA draft is on his farewell tour of his homeland, playing his final pro games there before he comes to North America and accepts the challenge of trying to truly become the game’s next superstar. Golf – PGA – Clark holds off Schauffele for first PGA win at Wells Fargo Wyndham Clark shot 68 on Sunday for a four-shot victory over Xander Schauffele at the Wells Fargo Championship to earn his first career win on the PGA Tour. Clark finished the tournament at 19-under 265, the second-lowest score in relation to par in tournament history behind only three-time champion Rory McIlroy’s 21-under 267 in 2015 when par for the course was 72. Clark struggled to hold back tears as he sank a bogey putt on the 18th hole to seal the win. Schauffele has accuracy issues with his driver on Sunday and shot 70, finishing at 15 under. Tyrrell Hatton and Harry English finished tied for third at 12 under, one shot better than Tommy Fleetwood and Adam Scott. Defending champion Max Homa shot 70 on Sunday and finished tied for ninth at 9-under 275. MWL – Midwest League Baseball Yesterday Lansing Lugnuts 4, Dayton Dragons 3 Great Lakes Loons 9, Quad Cities River Bandits 6 Cedar Rapids Kernels 6, South Bend Cubs 1 West Michigan Whitecaps 7, Beloit Sky Carp 2 Today No games tonight MHSAA – High School Sports Today Girls Soccer St. Joseph at Lakeshore, 6:30 p.m. Our Lady of the Lake at Saugatuck, 5:00 p.m. Battle Creek Central at Mattawan, 6:30 p.m. Portage Central at Battle Creek Lakeview, 6:30 p.m. Gull Lake at Kalamazoo Central, 6:30 p.m. Portage Northern at Kalamazoo Loy Norrix, 6:30 p.m. Paw Paw at Edwardsburg, 5:30 p.m. Vicksburg at Niles, 6:30 p.m. Otsego at Sturgis, 6:00 p.m. Plainwell at Three Rivers, 6:00 p.m. Watervliet at South Haven, 6:30 p.m. Holland Black River at Coloma, 6:00 p.m. Fennville at Bridgman, 5:00 p.m. Berrien Springs at Covert, 5:00 p.m. Buchanan at New Buffalo, 6:00 p.m. Allegan at Schoolcraft, 5:00 p.m. Comstock at Marcellus, 5:30 p.m. Delton-Kellogg at Kalamazoo Hackett, 5:00 p.m. Kalamazoo Christian at Lawton, 6:00 p.m. Constantine at Parchment, 6:00 p.m. Baseball Michigan Lutheran at Brandywine, 4:00 p.m. Fennville at Bridgman, 4:30 p.m. Loy Norrix at River Valley, 4:15 p.m. Lawrence at Cassopolis, 4:30 p.m. Bangor at Centreville, 4:30 p.m. Hartford at Comstock, 4:30 p.m. Bloomingdale at Marcellus, 4:30 p.m. Decatur at Mendon, 4:30 p.m. Portage Central at Otsego, 4:00 p.m. Plainwell at Kalamazoo Central, 4:00 p.m. Kalamazoo Hackett at Portage Northern, 4:00 p.m. Otsego at Gull Lake, 4:00 p.m. Martin at Saugatuck, 4:30 p.m. Softball St. Joseph at Zeeland West, 5:00 p.m. Michigan Lutheran at Brandywine, 4:15 p.m. Howardsville Chr. at River Valley, 4:15 p.m. Fennville at Bridgman, 4:30 p.m. Bronson at Buchanan, 4:15 p.m. Lawrence at Cassopolis, 4:30 p.m. Bangor at Centreville, 4:30 p.m. Hartford at Comstock, 4:30 p.m. Bloomingdale at Marcellus, 4:30 p.m. Decatur at Mendon, 4:30 p.m. Three Rivers at Kalamazoo Central, 4:00 p.m. Kalamazoo Christian at Portage Central, 4:00 p.m. Otsego at Gull Lake, 4:00 p.m. Lawton at Paw Paw, 4:30 p.m. Wyoming at Delton-Kellogg, 4:30 p.m. Constantine at Parchment, 4:30 p.m. Boys Golf Battle Creek Lakeview Invitational, 9:00 p.m. St. Joseph, Lakeshore, Battle Creek Lakeview, Loy Norrix, Portage Central, Parchment, Kalamazoo Central, Harper Creek, Pennfield, Coldwater, Marshall, Mattawan, Gull Lake, Vicksburg, Niles, Girls Tennis Lakeshore at Portage Northern, 4:00 p.m. Track and Field St. Joseph, Lakeshore, at Mattawan, 4:00 p.m.See omnystudio.com/listener for privacy information.

MLB – Major League Baseball Yesterday St. Louis Cardinals 12, Detroit Tigers 6 Miami Marlins 5, Chicago Cubs 4 – 14 Innings Chicago White Sox 17, Cincinnati Reds 4 Cardinals 12, Tigers 6 – Goldschmidt 3 HRs, Cards end 8-game skid, beat Tigers 12-6 Paul Goldschmidt homered three times, Brendan Donovan hit a three-run drive and the St. Louis Cardinals stopped an eight-game losing streak with a 12-6 win over the Detroit Tigers. Goldschmidt, had four hits and four RBIs. Lars Nootbaar added a two-run single to cap off a seven-run sixth inning for the Cardinals, who had been on their longest skid in 16 years. Jake Rogers hit a grand slam for the Tigers, whose five-game winning steak was stopped. Marlins 5, Cubs 4 – F/14 – Marlins stop 5-game slide with 14-inning win over Cubs Garrett Hampson scored on Adbert Alzolay’s balk in the 14th inning, and the Miami Marlins stopped a five-game slide by outlasting the Chicago Cubs for a wild 5-4 victory. Hampson opened the inning on second as the automatic runner. He advanced on Luis Arraez’s groundout and trotted home when Alzolay was called for a balk with a 2-2 count on Jesús Sánchez. Steven Okert got three outs for the win, and Andrew Nardi pitched the 14th for his first career save. White Sox 17, Reds 4 – White Sox score 11 in 2nd, beat Reds 17-4 Hanser Alberto had four hits, a career-high four RBIs and Chicago scored 11 runs in the second inning to rout the Cincinnati Reds 17-4 on Sunday. The 11 runs are the most for the team in one inning in 16 years and third-most ever for the franchise. The White Sox had 11 runs in the fifth at Kansas City on Sept. 17, 2007. Chicago, which came in batting .176 with runners in scoring position, delivered plenty of big hits against Graham Ashcraft (2-1) in the second, sending 14 batters to the plate. Michael Kopech (1-3) allowed four solo homers by pitched six innings to earn his first victory of the season. Tonight Detroit (Wentz 0-3) at Cleveland (Bibee 1-0), 6:10 p.m.   News/Talk/Sports 94.9 WSJM 7:50 Chicago White Sox (Cease 2-1) at Kansas City (Greinke 1-4), 7:40 p.m. St. Louis (Mikolas 1-1) at Chicago Cubs (Stroman 2-2), 7:40 p.m. NHL – National Hockey League – 2023 Stanley Cup Playoffs – Round 2 (Best of 7) Last Night New Jersey Devils 8, Carolina Hurricanes 4                             (CAR leads 2-1) Florida Panthers 3, Toronto Maple Leafs 2 – OT                        (FLA leads 3-0) Seattle Kraken 7, Dallas Stars 2                                           (SEA leads 2-1) Devils 8, Hurricanes 4 – Devils answer in Game 3, rout Canes 8-4, deficit now 2-1 Jack Hughes scored two goals, set up two more and had a near fight as the New Jersey Devils began the task of digging out of another hole with a 8-4 win over the Carolina Hurricanes in Game 3 of the Eastern Conference semifinals Sunday. Timo Meier, Nico Hischier and Damon Severson added their first goals of playoffs and Vitek Vanecek returned to the net and made 26 saves in helping New Jersey cut its deficit in the best-of-seven series to 2-1. Panthers 3, Leafs 2 – OT – Reinhart the hero, as Panthers top Leafs in OT for 3-0 lead Sam Reinhart scored 3:02 into overtime and the Florida Panthers beat the Toronto Maple Leafs 3-2 to take a commanding 3-0 lead in their Eastern Conference semifinal series. Reinhart dumped the puck off the boards behind the net to set up his game-winner, taking a pass back from Anton Lundell and scoring to give Florida its first 3-0 series lead in 27 years. Anthony Duclair and Carter Verhaeghe scored for Florida. Sam Lafferty and Erik Gustafsson scored for Toronto. Kraken 7, Stars 2 – Kraken ride 2nd period outburst, thump Stars 7-2 in Game 3 Jordan Eberle sparked a five-goal outburst in the second period with his fourth goal of the playoffs, Philipp Grubauer made 24 saves and the Seattle Kraken beat the Dallas Stars 7-2 to take a 2-1 series lead in their Western Conference semifinal. Eberle’s goal was just the start for Seattle. Alex Wennberg doubled the lead 1:26 after Eberle’s goal; Carson Soucy became Seattle’s 16th different goal scorer this postseason, beating Oettinger five-hole at 6:30; and Matty Beniers made it 4-0 at 8:22. Tonight Vegas Golden Knights at Edmonton Oilers, 8:30 p.m.                 (Series tied 1-1) NBA – National Basketball Association Playoffs – Round 2 (Best of 7) Last Night Philadelphia 76ers 116, Boston Celtics 115 – OT                      (Series tied 2-2) Phoenix Suns 129, Denver Nuggets 124                                  (Series tied 2-2) Sixers 116, Celtics 115 – OT – Harden makes winning 3 in OT, 76ers tie series with Celtics James Harden hit the go-ahead 3-pointer with 18 seconds left in overtime and scored 42 points to help the Philadelphia 76ers stave off a wild Boston Celtics comeback in a 116-115 victory on Sunday that evened their playoff series at 2-2. Marcus Smart’s potential winner was a tick too late and the Celtics now head home for Tuesday’s Game 5. Joel Embiid had 34 points and 13 rebounds. Harden added nine assists and eight rebounds. Jayson Tatum struggled to score early but finished with 24 points, 18 rebounds, six assists and four blocks. Suns 129, Nuggets 124 – Booker, Durant both score 36, Suns even series with Nuggets Devin Booker had 36 points and 12 assists, Kevin Durant also had 36 points and the Phoenix Suns beat the Denver Nuggets 129-124 to even their Western Conference semifinal playoff series at two games apiece. Backup guard Landry Shamet made four crucial 3-pointers in the fourth quarter to keep the Suns ahead. Denver lost despite a huge game from MVP runner-up Nikola Jokic, who poured in 53 points. The Suns took a 98-92 lead into the fourth quarter after a scoring flurry from Booker, who had 17 points in the third. Phoenix wouldn’t trail in the fourth. The series returns to Denver for Game 5 on Tuesday. Tonight New York Knicks at Miami Heat, 7:30 p.m.                                (MIA leads 2-1) Golden State Warriors at Los Angeles Lakers, 10:00 p.m.          (LAL leads 2-1) NBA – 76ers’ Harden visits with Michigan State shooting victim James Harden met with Michigan State shooting victim John Hao before a playoff game. Then he signed his sneakers and gave them to Hao after scoring 42 points and making the winning shot in overtime. The 20-year-old Hao was paralyzed from the chest down in a February shooting on the East Lansing campus that killed three students and injured five others. Harden learned Hao was a fan of his and the two struck up a friendship over FaceTime. Harden also donated sneakers and money toward Hao’s recovery. Hao recently left a Chicago rehabilitation facility and said he may move with his family back to China. NBA – Nick Gilbert, son of Cavaliers owner, dies at 26 Nicolas “Nick” Gilbert, the son of Cleveland Cavaliers owner Dan Gilbert who became the team’s good luck charm at NBA draft lotteries, has died. He was 26. A funeral announcement posted by the Ira Kaufman Chapel said Gilbert died Saturday “peacefully at home surrounded by family.” Gilbert was diagnosed as a child with neurofibromatosis (NF1), a genetic condition that causes tumors to grow in the brain, spinal cord and skin. Wearing a signature bow tie and dark-rimmed glasses, Gilbert became a sensation at the 2011 draft lottery. NBA – Analysis: Wemby’s farewell tour will be a French celebration Victor Wembanyama’s first basket on Sunday night looked so easy. He deflected a pass, ran it down, dribbled twice and dunked the ball with his left hand. And 15,000 people roared. He’s called a generational talent, though really, there’s never been one in France quite like Wembanyama. The 7-foot-3, 19-year-old, soon-to-be No. 1 pick in the NBA draft is on his farewell tour of his homeland, playing his final pro games there before he comes to North America and accepts the challenge of trying to truly become the game’s next superstar. Golf – PGA – Clark holds off Schauffele for first PGA win at Wells Fargo Wyndham Clark shot 68 on Sunday for a four-shot victory over Xander Schauffele at the Wells Fargo Championship to earn his first career win on the PGA Tour. Clark finished the tournament at 19-under 265, the second-lowest score in relation to par in tournament history behind only three-time champion Rory McIlroy’s 21-under 267 in 2015 when par for the course was 72. Clark struggled to hold back tears as he sank a bogey putt on the 18th hole to seal the win. Schauffele has accuracy issues with his driver on Sunday and shot 70, finishing at 15 under. Tyrrell Hatton and Harry English finished tied for third at 12 under, one shot better than Tommy Fleetwood and Adam Scott. Defending champion Max Homa shot 70 on Sunday and finished tied for ninth at 9-under 275. MWL – Midwest League Baseball Yesterday Lansing Lugnuts 4, Dayton Dragons 3 Great Lakes Loons 9, Quad Cities River Bandits 6 Cedar Rapids Kernels 6, South Bend Cubs 1 West Michigan Whitecaps 7, Beloit Sky Carp 2 Today No games tonight MHSAA – High School Sports Today Girls Soccer St. Joseph at Lakeshore, 6:30 p.m. Our Lady of the Lake at Saugatuck, 5:00 p.m. Battle Creek Central at Mattawan, 6:30 p.m. Portage Central at Battle Creek Lakeview, 6:30 p.m. Gull Lake at Kalamazoo Central, 6:30 p.m. Portage Northern at Kalamazoo Loy Norrix, 6:30 p.m. Paw Paw at Edwardsburg, 5:30 p.m. Vicksburg at Niles, 6:30 p.m. Otsego at Sturgis, 6:00 p.m. Plainwell at Three Rivers, 6:00 p.m. Watervliet at South Haven, 6:30 p.m. Holland Black River at Coloma, 6:00 p.m. Fennville at Bridgman, 5:00 p.m. Berrien Springs at Covert, 5:00 p.m. Buchanan at New Buffalo, 6:00 p.m. Allegan at Schoolcraft, 5:00 p.m. Comstock at Marcellus, 5:30 p.m. Delton-Kellogg at Kalamazoo Hackett, 5:00 p.m. Kalamazoo Christian at Lawton, 6:00 p.m. Constantine at Parchment, 6:00 p.m. Baseball Michigan Lutheran at Brandywine, 4:00 p.m. Fennville at Bridgman, 4:30 p.m. Loy Norrix at River Valley, 4:15 p.m. Lawrence at Cassopolis, 4:30 p.m. Bangor at Centreville, 4:30 p.m. Hartford at Comstock, 4:30 p.m. Bloomingdale at Marcellus, 4:30 p.m. Decatur at Mendon, 4:30 p.m. Portage Central at Otsego, 4:00 p.m. Plainwell at Kalamazoo Central, 4:00 p.m. Kalamazoo Hackett at Portage Northern, 4:00 p.m. Otsego at Gull Lake, 4:00 p.m. Martin at Saugatuck, 4:30 p.m. Softball St. Joseph at Zeeland West, 5:00 p.m. Michigan Lutheran at Brandywine, 4:15 p.m. Howardsville Chr. at River Valley, 4:15 p.m. Fennville at Bridgman, 4:30 p.m. Bronson at Buchanan, 4:15 p.m. Lawrence at Cassopolis, 4:30 p.m. Bangor at Centreville, 4:30 p.m. Hartford at Comstock, 4:30 p.m. Bloomingdale at Marcellus, 4:30 p.m. Decatur at Mendon, 4:30 p.m. Three Rivers at Kalamazoo Central, 4:00 p.m. Kalamazoo Christian at Portage Central, 4:00 p.m. Otsego at Gull Lake, 4:00 p.m. Lawton at Paw Paw, 4:30 p.m. Wyoming at Delton-Kellogg, 4:30 p.m. Constantine at Parchment, 4:30 p.m. Boys Golf Battle Creek Lakeview Invitational, 9:00 p.m. St. Joseph, Lakeshore, Battle Creek Lakeview, Loy Norrix, Portage Central, Parchment, Kalamazoo Central, Harper Creek, Pennfield, Coldwater, Marshall, Mattawan, Gull Lake, Vicksburg, Niles, Girls Tennis Lakeshore at Portage Northern, 4:00 p.m. Track and Field St. Joseph, Lakeshore, at Mattawan, 4:00 p.m.See omnystudio.com/listener for privacy information.

MLB – Major League Baseball Yesterday St. Louis Cardinals 12, Detroit Tigers 6 Miami Marlins 5, Chicago Cubs 4 – 14 Innings Chicago White Sox 17, Cincinnati Reds 4 Cardinals 12, Tigers 6 – Goldschmidt 3 HRs, Cards end 8-game skid, beat Tigers 12-6 Paul Goldschmidt homered three times, Brendan Donovan hit a three-run drive and the St. Louis Cardinals stopped an eight-game losing streak with a 12-6 win over the Detroit Tigers. Goldschmidt, had four hits and four RBIs. Lars Nootbaar added a two-run single to cap off a seven-run sixth inning for the Cardinals, who had been on their longest skid in 16 years. Jake Rogers hit a grand slam for the Tigers, whose five-game winning steak was stopped. Marlins 5, Cubs 4 – F/14 – Marlins stop 5-game slide with 14-inning win over Cubs Garrett Hampson scored on Adbert Alzolay’s balk in the 14th inning, and the Miami Marlins stopped a five-game slide by outlasting the Chicago Cubs for a wild 5-4 victory. Hampson opened the inning on second as the automatic runner. He advanced on Luis Arraez’s groundout and trotted home when Alzolay was called for a balk with a 2-2 count on Jesús Sánchez. Steven Okert got three outs for the win, and Andrew Nardi pitched the 14th for his first career save. White Sox 17, Reds 4 – White Sox score 11 in 2nd, beat Reds 17-4 Hanser Alberto had four hits, a career-high four RBIs and Chicago scored 11 runs in the second inning to rout the Cincinnati Reds 17-4 on Sunday. The 11 runs are the most for the team in one inning in 16 years and third-most ever for the franchise. The White Sox had 11 runs in the fifth at Kansas City on Sept. 17, 2007. Chicago, which came in batting .176 with runners in scoring position, delivered plenty of big hits against Graham Ashcraft (2-1) in the second, sending 14 batters to the plate. Michael Kopech (1-3) allowed four solo homers by pitched six innings to earn his first victory of the season. Tonight Detroit (Wentz 0-3) at Cleveland (Bibee 1-0), 6:10 p.m.   News/Talk/Sports 94.9 WSJM 7:50 Chicago White Sox (Cease 2-1) at Kansas City (Greinke 1-4), 7:40 p.m. St. Louis (Mikolas 1-1) at Chicago Cubs (Stroman 2-2), 7:40 p.m. NHL – National Hockey League – 2023 Stanley Cup Playoffs – Round 2 (Best of 7) Last Night New Jersey Devils 8, Carolina Hurricanes 4                             (CAR leads 2-1) Florida Panthers 3, Toronto Maple Leafs 2 – OT                        (FLA leads 3-0) Seattle Kraken 7, Dallas Stars 2                                           (SEA leads 2-1) Devils 8, Hurricanes 4 – Devils answer in Game 3, rout Canes 8-4, deficit now 2-1 Jack Hughes scored two goals, set up two more and had a near fight as the New Jersey Devils began the task of digging out of another hole with a 8-4 win over the Carolina Hurricanes in Game 3 of the Eastern Conference semifinals Sunday. Timo Meier, Nico Hischier and Damon Severson added their first goals of playoffs and Vitek Vanecek returned to the net and made 26 saves in helping New Jersey cut its deficit in the best-of-seven series to 2-1. Panthers 3, Leafs 2 – OT – Reinhart the hero, as Panthers top Leafs in OT for 3-0 lead Sam Reinhart scored 3:02 into overtime and the Florida Panthers beat the Toronto Maple Leafs 3-2 to take a commanding 3-0 lead in their Eastern Conference semifinal series. Reinhart dumped the puck off the boards behind the net to set up his game-winner, taking a pass back from Anton Lundell and scoring to give Florida its first 3-0 series lead in 27 years. Anthony Duclair and Carter Verhaeghe scored for Florida. Sam Lafferty and Erik Gustafsson scored for Toronto. Kraken 7, Stars 2 – Kraken ride 2nd period outburst, thump Stars 7-2 in Game 3 Jordan Eberle sparked a five-goal outburst in the second period with his fourth goal of the playoffs, Philipp Grubauer made 24 saves and the Seattle Kraken beat the Dallas Stars 7-2 to take a 2-1 series lead in their Western Conference semifinal. Eberle’s goal was just the start for Seattle. Alex Wennberg doubled the lead 1:26 after Eberle’s goal; Carson Soucy became Seattle’s 16th different goal scorer this postseason, beating Oettinger five-hole at 6:30; and Matty Beniers made it 4-0 at 8:22. Tonight Vegas Golden Knights at Edmonton Oilers, 8:30 p.m.                 (Series tied 1-1) NBA – National Basketball Association Playoffs – Round 2 (Best of 7) Last Night Philadelphia 76ers 116, Boston Celtics 115 – OT                      (Series tied 2-2) Phoenix Suns 129, Denver Nuggets 124                                  (Series tied 2-2) Sixers 116, Celtics 115 – OT – Harden makes winning 3 in OT, 76ers tie series with Celtics James Harden hit the go-ahead 3-pointer with 18 seconds left in overtime and scored 42 points to help the Philadelphia 76ers stave off a wild Boston Celtics comeback in a 116-115 victory on Sunday that evened their playoff series at 2-2. Marcus Smart’s potential winner was a tick too late and the Celtics now head home for Tuesday’s Game 5. Joel Embiid had 34 points and 13 rebounds. Harden added nine assists and eight rebounds. Jayson Tatum struggled to score early but finished with 24 points, 18 rebounds, six assists and four blocks. Suns 129, Nuggets 124 – Booker, Durant both score 36, Suns even series with Nuggets Devin Booker had 36 points and 12 assists, Kevin Durant also had 36 points and the Phoenix Suns beat the Denver Nuggets 129-124 to even their Western Conference semifinal playoff series at two games apiece. Backup guard Landry Shamet made four crucial 3-pointers in the fourth quarter to keep the Suns ahead. Denver lost despite a huge game from MVP runner-up Nikola Jokic, who poured in 53 points. The Suns took a 98-92 lead into the fourth quarter after a scoring flurry from Booker, who had 17 points in the third. Phoenix wouldn’t trail in the fourth. The series returns to Denver for Game 5 on Tuesday. Tonight New York Knicks at Miami Heat, 7:30 p.m.                                (MIA leads 2-1) Golden State Warriors at Los Angeles Lakers, 10:00 p.m.          (LAL leads 2-1) NBA – 76ers’ Harden visits with Michigan State shooting victim James Harden met with Michigan State shooting victim John Hao before a playoff game. Then he signed his sneakers and gave them to Hao after scoring 42 points and making the winning shot in overtime. The 20-year-old Hao was paralyzed from the chest down in a February shooting on the East Lansing campus that killed three students and injured five others. Harden learned Hao was a fan of his and the two struck up a friendship over FaceTime. Harden also donated sneakers and money toward Hao’s recovery. Hao recently left a Chicago rehabilitation facility and said he may move with his family back to China. NBA – Nick Gilbert, son of Cavaliers owner, dies at 26 Nicolas “Nick” Gilbert, the son of Cleveland Cavaliers owner Dan Gilbert who became the team’s good luck charm at NBA draft lotteries, has died. He was 26. A funeral announcement posted by the Ira Kaufman Chapel said Gilbert died Saturday “peacefully at home surrounded by family.” Gilbert was diagnosed as a child with neurofibromatosis (NF1), a genetic condition that causes tumors to grow in the brain, spinal cord and skin. Wearing a signature bow tie and dark-rimmed glasses, Gilbert became a sensation at the 2011 draft lottery. NBA – Analysis: Wemby’s farewell tour will be a French celebration Victor Wembanyama’s first basket on Sunday night looked so easy. He deflected a pass, ran it down, dribbled twice and dunked the ball with his left hand. And 15,000 people roared. He’s called a generational talent, though really, there’s never been one in France quite like Wembanyama. The 7-foot-3, 19-year-old, soon-to-be No. 1 pick in the NBA draft is on his farewell tour of his homeland, playing his final pro games there before he comes to North America and accepts the challenge of trying to truly become the game’s next superstar. Golf – PGA – Clark holds off Schauffele for first PGA win at Wells Fargo Wyndham Clark shot 68 on Sunday for a four-shot victory over Xander Schauffele at the Wells Fargo Championship to earn his first career win on the PGA Tour. Clark finished the tournament at 19-under 265, the second-lowest score in relation to par in tournament history behind only three-time champion Rory McIlroy’s 21-under 267 in 2015 when par for the course was 72. Clark struggled to hold back tears as he sank a bogey putt on the 18th hole to seal the win. Schauffele has accuracy issues with his driver on Sunday and shot 70, finishing at 15 under. Tyrrell Hatton and Harry English finished tied for third at 12 under, one shot better than Tommy Fleetwood and Adam Scott. Defending champion Max Homa shot 70 on Sunday and finished tied for ninth at 9-under 275. MWL – Midwest League Baseball Yesterday Lansing Lugnuts 4, Dayton Dragons 3 Great Lakes Loons 9, Quad Cities River Bandits 6 Cedar Rapids Kernels 6, South Bend Cubs 1 West Michigan Whitecaps 7, Beloit Sky Carp 2 Today No games tonight MHSAA – High School Sports Today Girls Soccer St. Joseph at Lakeshore, 6:30 p.m. Our Lady of the Lake at Saugatuck, 5:00 p.m. Battle Creek Central at Mattawan, 6:30 p.m. Portage Central at Battle Creek Lakeview, 6:30 p.m. Gull Lake at Kalamazoo Central, 6:30 p.m. Portage Northern at Kalamazoo Loy Norrix, 6:30 p.m. Paw Paw at Edwardsburg, 5:30 p.m. Vicksburg at Niles, 6:30 p.m. Otsego at Sturgis, 6:00 p.m. Plainwell at Three Rivers, 6:00 p.m. Watervliet at South Haven, 6:30 p.m. Holland Black River at Coloma, 6:00 p.m. Fennville at Bridgman, 5:00 p.m. Berrien Springs at Covert, 5:00 p.m. Buchanan at New Buffalo, 6:00 p.m. Allegan at Schoolcraft, 5:00 p.m. Comstock at Marcellus, 5:30 p.m. Delton-Kellogg at Kalamazoo Hackett, 5:00 p.m. Kalamazoo Christian at Lawton, 6:00 p.m. Constantine at Parchment, 6:00 p.m. Baseball Michigan Lutheran at Brandywine, 4:00 p.m. Fennville at Bridgman, 4:30 p.m. Loy Norrix at River Valley, 4:15 p.m. Lawrence at Cassopolis, 4:30 p.m. Bangor at Centreville, 4:30 p.m. Hartford at Comstock, 4:30 p.m. Bloomingdale at Marcellus, 4:30 p.m. Decatur at Mendon, 4:30 p.m. Portage Central at Otsego, 4:00 p.m. Plainwell at Kalamazoo Central, 4:00 p.m. Kalamazoo Hackett at Portage Northern, 4:00 p.m. Otsego at Gull Lake, 4:00 p.m. Martin at Saugatuck, 4:30 p.m. Softball St. Joseph at Zeeland West, 5:00 p.m. Michigan Lutheran at Brandywine, 4:15 p.m. Howardsville Chr. at River Valley, 4:15 p.m. Fennville at Bridgman, 4:30 p.m. Bronson at Buchanan, 4:15 p.m. Lawrence at Cassopolis, 4:30 p.m. Bangor at Centreville, 4:30 p.m. Hartford at Comstock, 4:30 p.m. Bloomingdale at Marcellus, 4:30 p.m. Decatur at Mendon, 4:30 p.m. Three Rivers at Kalamazoo Central, 4:00 p.m. Kalamazoo Christian at Portage Central, 4:00 p.m. Otsego at Gull Lake, 4:00 p.m. Lawton at Paw Paw, 4:30 p.m. Wyoming at Delton-Kellogg, 4:30 p.m. Constantine at Parchment, 4:30 p.m. Boys Golf Battle Creek Lakeview Invitational, 9:00 p.m. St. Joseph, Lakeshore, Battle Creek Lakeview, Loy Norrix, Portage Central, Parchment, Kalamazoo Central, Harper Creek, Pennfield, Coldwater, Marshall, Mattawan, Gull Lake, Vicksburg, Niles, Girls Tennis Lakeshore at Portage Northern, 4:00 p.m. Track and Field St. Joseph, Lakeshore, at Mattawan, 4:00 p.m.See omnystudio.com/listener for privacy information.

MLB – Major League Baseball Yesterday St. Louis Cardinals 12, Detroit Tigers 6 Miami Marlins 5, Chicago Cubs 4 – 14 Innings Chicago White Sox 17, Cincinnati Reds 4 Cardinals 12, Tigers 6 – Goldschmidt 3 HRs, Cards end 8-game skid, beat Tigers 12-6 Paul Goldschmidt homered three times, Brendan Donovan hit a three-run drive and the St. Louis Cardinals stopped an eight-game losing streak with a 12-6 win over the Detroit Tigers. Goldschmidt, had four hits and four RBIs. Lars Nootbaar added a two-run single to cap off a seven-run sixth inning for the Cardinals, who had been on their longest skid in 16 years. Jake Rogers hit a grand slam for the Tigers, whose five-game winning steak was stopped. Marlins 5, Cubs 4 – F/14 – Marlins stop 5-game slide with 14-inning win over Cubs Garrett Hampson scored on Adbert Alzolay’s balk in the 14th inning, and the Miami Marlins stopped a five-game slide by outlasting the Chicago Cubs for a wild 5-4 victory. Hampson opened the inning on second as the automatic runner. He advanced on Luis Arraez’s groundout and trotted home when Alzolay was called for a balk with a 2-2 count on Jesús Sánchez. Steven Okert got three outs for the win, and Andrew Nardi pitched the 14th for his first career save. White Sox 17, Reds 4 – White Sox score 11 in 2nd, beat Reds 17-4 Hanser Alberto had four hits, a career-high four RBIs and Chicago scored 11 runs in the second inning to rout the Cincinnati Reds 17-4 on Sunday. The 11 runs are the most for the team in one inning in 16 years and third-most ever for the franchise. The White Sox had 11 runs in the fifth at Kansas City on Sept. 17, 2007. Chicago, which came in batting .176 with runners in scoring position, delivered plenty of big hits against Graham Ashcraft (2-1) in the second, sending 14 batters to the plate. Michael Kopech (1-3) allowed four solo homers by pitched six innings to earn his first victory of the season. Tonight Detroit (Wentz 0-3) at Cleveland (Bibee 1-0), 6:10 p.m.   News/Talk/Sports 94.9 WSJM 7:50 Chicago White Sox (Cease 2-1) at Kansas City (Greinke 1-4), 7:40 p.m. St. Louis (Mikolas 1-1) at Chicago Cubs (Stroman 2-2), 7:40 p.m. NHL – National Hockey League – 2023 Stanley Cup Playoffs – Round 2 (Best of 7) Last Night New Jersey Devils 8, Carolina Hurricanes 4                             (CAR leads 2-1) Florida Panthers 3, Toronto Maple Leafs 2 – OT                        (FLA leads 3-0) Seattle Kraken 7, Dallas Stars 2                                           (SEA leads 2-1) Devils 8, Hurricanes 4 – Devils answer in Game 3, rout Canes 8-4, deficit now 2-1 Jack Hughes scored two goals, set up two more and had a near fight as the New Jersey Devils began the task of digging out of another hole with a 8-4 win over the Carolina Hurricanes in Game 3 of the Eastern Conference semifinals Sunday. Timo Meier, Nico Hischier and Damon Severson added their first goals of playoffs and Vitek Vanecek returned to the net and made 26 saves in helping New Jersey cut its deficit in the best-of-seven series to 2-1. Panthers 3, Leafs 2 – OT – Reinhart the hero, as Panthers top Leafs in OT for 3-0 lead Sam Reinhart scored 3:02 into overtime and the Florida Panthers beat the Toronto Maple Leafs 3-2 to take a commanding 3-0 lead in their Eastern Conference semifinal series. Reinhart dumped the puck off the boards behind the net to set up his game-winner, taking a pass back from Anton Lundell and scoring to give Florida its first 3-0 series lead in 27 years. Anthony Duclair and Carter Verhaeghe scored for Florida. Sam Lafferty and Erik Gustafsson scored for Toronto. Kraken 7, Stars 2 – Kraken ride 2nd period outburst, thump Stars 7-2 in Game 3 Jordan Eberle sparked a five-goal outburst in the second period with his fourth goal of the playoffs, Philipp Grubauer made 24 saves and the Seattle Kraken beat the Dallas Stars 7-2 to take a 2-1 series lead in their Western Conference semifinal. Eberle’s goal was just the start for Seattle. Alex Wennberg doubled the lead 1:26 after Eberle’s goal; Carson Soucy became Seattle’s 16th different goal scorer this postseason, beating Oettinger five-hole at 6:30; and Matty Beniers made it 4-0 at 8:22. Tonight Vegas Golden Knights at Edmonton Oilers, 8:30 p.m.                 (Series tied 1-1) NBA – National Basketball Association Playoffs – Round 2 (Best of 7) Last Night Philadelphia 76ers 116, Boston Celtics 115 – OT                      (Series tied 2-2) Phoenix Suns 129, Denver Nuggets 124                                  (Series tied 2-2) Sixers 116, Celtics 115 – OT – Harden makes winning 3 in OT, 76ers tie series with Celtics James Harden hit the go-ahead 3-pointer with 18 seconds left in overtime and scored 42 points to help the Philadelphia 76ers stave off a wild Boston Celtics comeback in a 116-115 victory on Sunday that evened their playoff series at 2-2. Marcus Smart’s potential winner was a tick too late and the Celtics now head home for Tuesday’s Game 5. Joel Embiid had 34 points and 13 rebounds. Harden added nine assists and eight rebounds. Jayson Tatum struggled to score early but finished with 24 points, 18 rebounds, six assists and four blocks. Suns 129, Nuggets 124 – Booker, Durant both score 36, Suns even series with Nuggets Devin Booker had 36 points and 12 assists, Kevin Durant also had 36 points and the Phoenix Suns beat the Denver Nuggets 129-124 to even their Western Conference semifinal playoff series at two games apiece. Backup guard Landry Shamet made four crucial 3-pointers in the fourth quarter to keep the Suns ahead. Denver lost despite a huge game from MVP runner-up Nikola Jokic, who poured in 53 points. The Suns took a 98-92 lead into the fourth quarter after a scoring flurry from Booker, who had 17 points in the third. Phoenix wouldn’t trail in the fourth. The series returns to Denver for Game 5 on Tuesday. Tonight New York Knicks at Miami Heat, 7:30 p.m.                                (MIA leads 2-1) Golden State Warriors at Los Angeles Lakers, 10:00 p.m.          (LAL leads 2-1) NBA – 76ers’ Harden visits with Michigan State shooting victim James Harden met with Michigan State shooting victim John Hao before a playoff game. Then he signed his sneakers and gave them to Hao after scoring 42 points and making the winning shot in overtime. The 20-year-old Hao was paralyzed from the chest down in a February shooting on the East Lansing campus that killed three students and injured five others. Harden learned Hao was a fan of his and the two struck up a friendship over FaceTime. Harden also donated sneakers and money toward Hao’s recovery. Hao recently left a Chicago rehabilitation facility and said he may move with his family back to China. NBA – Nick Gilbert, son of Cavaliers owner, dies at 26 Nicolas “Nick” Gilbert, the son of Cleveland Cavaliers owner Dan Gilbert who became the team’s good luck charm at NBA draft lotteries, has died. He was 26. A funeral announcement posted by the Ira Kaufman Chapel said Gilbert died Saturday “peacefully at home surrounded by family.” Gilbert was diagnosed as a child with neurofibromatosis (NF1), a genetic condition that causes tumors to grow in the brain, spinal cord and skin. Wearing a signature bow tie and dark-rimmed glasses, Gilbert became a sensation at the 2011 draft lottery. NBA – Analysis: Wemby’s farewell tour will be a French celebration Victor Wembanyama’s first basket on Sunday night looked so easy. He deflected a pass, ran it down, dribbled twice and dunked the ball with his left hand. And 15,000 people roared. He’s called a generational talent, though really, there’s never been one in France quite like Wembanyama. The 7-foot-3, 19-year-old, soon-to-be No. 1 pick in the NBA draft is on his farewell tour of his homeland, playing his final pro games there before he comes to North America and accepts the challenge of trying to truly become the game’s next superstar. Golf – PGA – Clark holds off Schauffele for first PGA win at Wells Fargo Wyndham Clark shot 68 on Sunday for a four-shot victory over Xander Schauffele at the Wells Fargo Championship to earn his first career win on the PGA Tour. Clark finished the tournament at 19-under 265, the second-lowest score in relation to par in tournament history behind only three-time champion Rory McIlroy’s 21-under 267 in 2015 when par for the course was 72. Clark struggled to hold back tears as he sank a bogey putt on the 18th hole to seal the win. Schauffele has accuracy issues with his driver on Sunday and shot 70, finishing at 15 under. Tyrrell Hatton and Harry English finished tied for third at 12 under, one shot better than Tommy Fleetwood and Adam Scott. Defending champion Max Homa shot 70 on Sunday and finished tied for ninth at 9-under 275. MWL – Midwest League Baseball Yesterday Lansing Lugnuts 4, Dayton Dragons 3 Great Lakes Loons 9, Quad Cities River Bandits 6 Cedar Rapids Kernels 6, South Bend Cubs 1 West Michigan Whitecaps 7, Beloit Sky Carp 2 Today No games tonight MHSAA – High School Sports Today Girls Soccer St. Joseph at Lakeshore, 6:30 p.m. Our Lady of the Lake at Saugatuck, 5:00 p.m. Battle Creek Central at Mattawan, 6:30 p.m. Portage Central at Battle Creek Lakeview, 6:30 p.m. Gull Lake at Kalamazoo Central, 6:30 p.m. Portage Northern at Kalamazoo Loy Norrix, 6:30 p.m. Paw Paw at Edwardsburg, 5:30 p.m. Vicksburg at Niles, 6:30 p.m. Otsego at Sturgis, 6:00 p.m. Plainwell at Three Rivers, 6:00 p.m. Watervliet at South Haven, 6:30 p.m. Holland Black River at Coloma, 6:00 p.m. Fennville at Bridgman, 5:00 p.m. Berrien Springs at Covert, 5:00 p.m. Buchanan at New Buffalo, 6:00 p.m. Allegan at Schoolcraft, 5:00 p.m. Comstock at Marcellus, 5:30 p.m. Delton-Kellogg at Kalamazoo Hackett, 5:00 p.m. Kalamazoo Christian at Lawton, 6:00 p.m. Constantine at Parchment, 6:00 p.m. Baseball Michigan Lutheran at Brandywine, 4:00 p.m. Fennville at Bridgman, 4:30 p.m. Loy Norrix at River Valley, 4:15 p.m. Lawrence at Cassopolis, 4:30 p.m. Bangor at Centreville, 4:30 p.m. Hartford at Comstock, 4:30 p.m. Bloomingdale at Marcellus, 4:30 p.m. Decatur at Mendon, 4:30 p.m. Portage Central at Otsego, 4:00 p.m. Plainwell at Kalamazoo Central, 4:00 p.m. Kalamazoo Hackett at Portage Northern, 4:00 p.m. Otsego at Gull Lake, 4:00 p.m. Martin at Saugatuck, 4:30 p.m. Softball St. Joseph at Zeeland West, 5:00 p.m. Michigan Lutheran at Brandywine, 4:15 p.m. Howardsville Chr. at River Valley, 4:15 p.m. Fennville at Bridgman, 4:30 p.m. Bronson at Buchanan, 4:15 p.m. Lawrence at Cassopolis, 4:30 p.m. Bangor at Centreville, 4:30 p.m. Hartford at Comstock, 4:30 p.m. Bloomingdale at Marcellus, 4:30 p.m. Decatur at Mendon, 4:30 p.m. Three Rivers at Kalamazoo Central, 4:00 p.m. Kalamazoo Christian at Portage Central, 4:00 p.m. Otsego at Gull Lake, 4:00 p.m. Lawton at Paw Paw, 4:30 p.m. Wyoming at Delton-Kellogg, 4:30 p.m. Constantine at Parchment, 4:30 p.m. Boys Golf Battle Creek Lakeview Invitational, 9:00 p.m. St. Joseph, Lakeshore, Battle Creek Lakeview, Loy Norrix, Portage Central, Parchment, Kalamazoo Central, Harper Creek, Pennfield, Coldwater, Marshall, Mattawan, Gull Lake, Vicksburg, Niles, Girls Tennis Lakeshore at Portage Northern, 4:00 p.m. Track and Field St. Joseph, Lakeshore, at Mattawan, 4:00 p.m.See omnystudio.com/listener for privacy information.

Listen to Nora's song, "Stay Strong (by Nora, a 9 year-old NF1 patient)"Want to learn more about Hear Your Song? Visit our website!Support Hear Your Song by making a tax-exempt donation to keep our programs free of charge for the kids and families we serve! You can donate here or on Venmo (@HearYourSong)!Want to register your child or teen to write a song with us? Looking to volunteer? Excited to partner? Reach out by contacting Hear Your Song here!Follow/subscribe to Hear Your Song onInstagramYouTubeFacebookTwitterSpotifyTikTokHosted by Hear Your Song's Executive Director and Co-Founder Dan Rubins, Co-Music Director Sofía Campoamor, and Programs Fellow Jack Softcheck Produced by Jacob MillerHear Your Song is a 501(c)(3) nonprofit empowering children and teens with serious illnesses and complex health needs to make their voices heard through collaborative songwriting. Season One of The Hear Your Song Podcast is made possible through the generous support of the Colburn-Keenan Foundation.

Mina Lobbous, MD, MSPH, discusses the long-term management needs of patients who progress into adulthood with NF1.

Featuring perspectives from Drs Courtney DiNardo and Mark Levis, including the following topics: Introduction (0:00) Case: A man in his early 80s with newly diagnosed acute myeloid leukemia (AML) with significant comorbidities receives decitabine/venetoclax — Rebecca L Olin, MD, MSCE (7:36) Cases: A man in his mid 50s after 7 + 3 and allogeneic stem cell transplantation (SCT) presents with myeloid sarcoma; a man in his late 70s after 7 + 3 and allogeneic SCT presents with myeloid sarcoma — Spencer H Bachow, MD and Ranju Gupta, MD (12:16) Case: A man in his late 30s with core binding factor AML after induction CLAG-M with gemtuzumab ozogamicin followed by high-dose cytarabine x 4 — Anna Halpern, MD (18:10) Case: A woman in her mid 60s with newly diagnosed del(5q) AML with monocytic differentiation and multiple mutations (GATA2, BCOR, NF1 and RUNX1) receives azacitidine and venetoclax — Bhavana (Tina) Bhatnagar, DO (31:05) Selection of Therapy for Patients with AML (35:20) Cases: A man in his early 50s with therapy-related AML with an MLL mutation who receives CPX-351; a man in his early 70s with secondary AML with an IDH mutation — Amany R Keruakous, MD, MS and Priya Rudolph, MD, PhD (41:42) Case: A man in his early 70s with recurrent AML with an IDH2 mutation receives enasidenib and develops differentiation syndrome/disease progression — Dr Halpern (50:00) CME information and select publications

This CPS Podcast will discuss Neurofibromatosis Type 1 or NF1, a congenital neuro-oculocutaneous disease and its possible neurologic, ophthalmic, and cutaneous manifestations. The podcast was created by Miles Jaques, a fourth-year medical student at the University of British Columbia with the support of Dr. Jennifer Ling, an ophthalmology resident at the University of British Columbia, and Dr. Gardiner, a pediatric ophthalmologist at the University of British Columbia in Vancouver, BC.

With guest show host Dustin Chandler, talking with the Moss family about their diagnosis of NF1 in the household.See omnystudio.com/listener for privacy information.

Five-and-a-half year old Alannah Foley was nominated by TJ O’Connor of MTU. In 2019, Alannah was diagnosed with a condition which causes tumours to grow on nerve tissues – neurofibromatosis type 1 (NF1) - this has led to extensive surgery, chemotherapy and caused hydrocephalus. Alannah’s good humour, grace and fight to keep her sight has inspired the county. Jerry speaks to Alannah, her parents Andrew and Geraldine, and to TJ.

While birthdays, anniversaries, and the holidays are typically calls for celebration – when you've lost someone important in your life – those days can be extremely painful and serve as giant reminders that your loved one is no longer here.  We want to make getting through those times easier.We've brought back the incomparable Jaime Breeze who is a Spiritual Medium, Psychic and Animal Communicator. Jaime offers practical ways to help manage the grief and loss that you may be feeling at this time of year. She offers ways to to incorporate signs and memories of your deceased loved ones into potentially new and meaningful holiday memories with them. She also shares messages of hope from her experiences working with the other side.In this episode, Jaime also does a live reading right here on Seeking Center! Jaime has no idea who will be calling in.Karen and I had the honor and privilege of inviting our friend Kate Doerge to be the guest for the reading. Tragically, Kate lost her daughter Penny this year from Neurofibromatosis (NF). Karen and I know that there's divine timing with everything – so the fact that this opportunity became available right before the holidays – it's definitely not a coincidence.Jaime was able to connect with specific messages from Penny that assured Kate that Penny is not only safe, but still very present in their lives. We think you'll appreciate the power in the reading as well.To hear this inspirational session, listen to this week's podcast. Please consider donating to Penny's Flight (https://pennysflight.org/). The foundation was created in Penny Doerge's memory to advance medical research in NF1 and its related disorders, as well as to inspire others to live with positivity and humor and find beauty and joy in everything. As Kate says in Penny's honor, spread your wings and shine your light.To book a session with Jaime or take one of her courses, visit jaimebreeze.com.  You can also follow her at @jaimebreeze on Instagram.For more from Robyn + Karen, and to sign up for Weekly Inspo visit seekingcenter.appYou can also follow Seeking Center on Instagram at @seekingcenterrobyn

Meet Nathanael! He was a baby when he was diagnosed with a rare genetic condition called NF1. He spends so much time with his medical team and could use a little escape to Disney!

Karun V. Sharma, M.D., Ph.D., is the Director of Interventional Radiology at Children's National Hospital, and an Associate Professor of Pediatrics and Radiology at the George Washington University School of Medicine and Health Sciences. His clinical practice and translational research focuses on minimally invasive image-guided therapies for musculoskeletal and oncology conditions. Dr. Sharma leads the Image-Guided Non-Invasive Therapeutic Energy (IGNITE) program, a collaboration of the Sheikh Zayed Institute and the departments of Radiology, Oncology, Surgery, and Anesthesiology at Children's National Hospital. The IGNITE program aims to improve the quality of life and outcomes for pediatric patients through the development and clinical translation of novel minimally invasive and noninvasive surgery technologies and combination therapy approaches, with the ultimate goal of making pediatric surgery more precise, less invasive and pain-free. In the recent years, Dr. Sharma and the IGNITE team have developed Magnetic Resonance Imaging –guided High Intensity Focused Ultrasound (MR-HIFU) applications for pediatric patients and lead clinical trials for osteoid osteoma and other tumors. AeRang Kim, M.D., Ph.D., is a member of the solid tumor faculty at Children's National Hospital and an Associate Professor of Pediatrics. Dr. Kim's specializes in sarcomas and developmental therapeutics. Her research focuses on development of novel therapeutics for pediatric cancer including pre-clinical testing of novel agents, pharmacokinetic analysis, developing innovative methods for toxicity monitoring and clinical trial design. She serves as the principal investigator of multiple early phase trials in pediatric oncology, sarcomas and NF1 associated tumors. --- What We Do at MIB Agents: PROGRAMS: ✨ End-of-Life MISSIONS ✨ Gamer Agents ✨ Agent Writers ✨ Prayer Agents ✨ Healing Hearts - Bereaved Parent Support ✨ Ambassador Agents - Peer Support ✨ Warrior Mail ✨ Young Adult Survivorship Support Group ✨ EDUCATION for physicians, researchers and families: ✨ OsteoBites, weekly webinar & podcast with thought leaders and innovators in Osteosarcoma ✨ MIB Book: Osteosarcoma: From our Families to Yours ✨ RESEARCH: Annual MIB FACTOR Research Conference ✨ Funding $100,000 annually for OS research ✨ MIB Testing & Research Directory ✨ The Osteosarcoma Project partner with Broad Institute of MIT and Harvard ... Kids are still dying with 40+ year old treatments. Help us MakeItBetter.

Matt Hay was a sophomore in college when he began to have problems with his hearing. He soon learned his hearing loss was caused by tumors on his nerves and was diagnosed with the rare condition neurofibromatosis. As a result of the condition, which can cause tumors to grow on nerves throughout the body, Hay has had to undergo 20 surgeries, including one to remove a tumor that blocked 80 percent of his spinal fluid and caused him to lose the ability to walk for a time. His diagnosis started him on not only a personal journey to fight his condition, but on a professional one as well as he became a patient advocate. We spoke to Hay, U.S. Director of advocacy for NF1 at Alexion, about his own journey as someone living with a rare disease, neurofibromatosis, and how his experience led him to become a patient advocate within the biopharmaceutical industry.

In episode 36 of the Summits Podcast, co-hosts Vince Todd, Jr. and Daniel Abdallah are joined by Dr. Steve Angus from the Indiana University School of Medicine's Department of Pediatrics. Tune in as Dr. Angus shares the pediatric oncology treatment advances initiated by funding from the Heroes Foundation's Team JOEY program. Dr. Angus also details his personal leukemia journey that further fueled his fight against cancer. Subscribe to the audio version of the Summits Podcast https://summitspodcast.fireside.fm Find out more about the Heroes Foundation https://www.heroesfoundation.org Find out more about The Brookfield Group https://thebrookfieldgroup.com Discover Platform 24 co-working https://www.platform24.co What's your cancer story? Hosted by cancer survivor and philanthropist Vince Todd, Jr., Chairman and Co-Founder of the Heroes Foundation, and Heroes Foundation Board Member Daniel Abdallah, the Summits Podcast is a place for people to share their stories. Everyone has a cancer story. From battling a deadly disease to caring for a loved one, when we rise up and face life's greatest challenges, we see with a new vision, feel with a greater passion, and think with a deeper perspective. Along the way, paths cross, journeys intersect, and missions converge. For Vince Todd, it was his own cancer diagnosis that led him and his wife, Cindy, to launch the Heroes Foundation to provide meaningful support to cancer patients, education to promote cancer prevention, and resources to advance research for a cure. What started with friends and family grew into a community. The Summits Podcast is an extension of that community. Our stories are what bring us together. Artists, athletes, doctors, business people - we're all family members, community leaders, and activists. Everyone has a story. Anyone can inspire. No one battles alone. Join the conversation. Let's climb the summit together.

They say a picture is worth a thousand words, but some pictures move from the eyes, straight to the heart, without any need for words.  Erin Borzellino is a photographer who captures such images, waiting patiently to catch unpolished moments of raw joy that might otherwise pass unnoticed. Erin is a storyteller, whose photo projects, Unstoppable , Below the Water Line, and Women Who Rock each evoke and celebrate the best of the human spirit.  After college, Erin's passion for photography took a backseat to a more “practical” career in financial services.  She moved to London, where she met her husband.  Shortly after having their first child, Giorgio, in the UK, Giorgio was diagnosed with a rare genetic mutation of the NF1 gene, which is responsible for suppressing tumor growth. Erin and her husband had to quickly adapt to the daily uncertainty of Giorgio's condition and learned how to care for him moment to moment.  Along the way, they also learned to enjoy each day, to focus on the present, not worry too much about the future, and to be grateful for all that they have.  Erin says that in many ways, having a child with special needs changed her life positively in unexpected ways.  A high achiever destined to be a "Type A" mom, once she started raising her three kids, Erin was surprised to find that she was actually much more of a "Type Z" mom.  Having a child with special needs changed her perspective on a lot of things: career, success, and what really matters.  She's less inclined to hound any of her children about piano practice and soccer lessons, instead maintaining her focus on their happiness and teaching them to be kind to others. Episode Resources:Erin Borzellino Photography:  https://erinborzellino.com/Erin's Instagram: @erinborzellinoThe Giorgio Foundation:  https://endnf1.org/Support the podcast by subscribing and reviewing!Music is considered “royalty-free” and discovered on Audio Blocks.Technical Podcast Support by: Jon Keur at Wayfare Recording Co.© 2022 Silver Linings Media LLC. All Rights Reserved

Go online to PeerView.com/YBF860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Neurofibromatosis type 1 (NF1) is an incurable and progressive genetic disorder caused by a partial or complete loss of function of the NF1 tumor suppressor gene, resulting in elevated RAS-mitogen-activated protein kinase (RAS/MAPK) pathway signaling and the potential development of subsequent NF1-associated tumors. Given current breakthroughs, including the emergence of MEK inhibitors, the ongoing challenge is how to effectively employ modern therapeutics in the management of patients with NF1 tumors, particularly pediatric patients. This case-based video discussion, based on a PeerView live “Seminars & Practicum” CME event, will offer an expert-guided review of the challenges inherent to the management of NF1-associated tumors and provide practical guidance on state-of-the-art solutions and the role that MEK-targeting agents can play in patient management. Upon completion of this activity, participants should be better able to: Summarize the genetic etiology, diverse clinical symptomatology, and diagnostic criteria of neurofibromatosis type 1 (NF1), Cite the current evidence from pivotal clinical trials on MEK inhibitors and other targeted therapies for the treatment of NF1-related PNs and other tumors in pediatric populations, Select personalized treatment plans using MEK inhibitors and other targeted therapies in pediatric populations with NF1-related plexiform neurofibromas (PNs) and other tumors based on prognostic information, safety considerations, and the latest evidence and guideline recommendations, Develop a management plan for the unique spectrum of adverse events associated with novel therapeutics including MEK inhibitors in pediatric patients with NF1-associated tumors.

Go online to PeerView.com/YBF860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Neurofibromatosis type 1 (NF1) is an incurable and progressive genetic disorder caused by a partial or complete loss of function of the NF1 tumor suppressor gene, resulting in elevated RAS-mitogen-activated protein kinase (RAS/MAPK) pathway signaling and the potential development of subsequent NF1-associated tumors. Given current breakthroughs, including the emergence of MEK inhibitors, the ongoing challenge is how to effectively employ modern therapeutics in the management of patients with NF1 tumors, particularly pediatric patients. This case-based video discussion, based on a PeerView live “Seminars & Practicum” CME event, will offer an expert-guided review of the challenges inherent to the management of NF1-associated tumors and provide practical guidance on state-of-the-art solutions and the role that MEK-targeting agents can play in patient management. Upon completion of this activity, participants should be better able to: Summarize the genetic etiology, diverse clinical symptomatology, and diagnostic criteria of neurofibromatosis type 1 (NF1), Cite the current evidence from pivotal clinical trials on MEK inhibitors and other targeted therapies for the treatment of NF1-related PNs and other tumors in pediatric populations, Select personalized treatment plans using MEK inhibitors and other targeted therapies in pediatric populations with NF1-related plexiform neurofibromas (PNs) and other tumors based on prognostic information, safety considerations, and the latest evidence and guideline recommendations, Develop a management plan for the unique spectrum of adverse events associated with novel therapeutics including MEK inhibitors in pediatric patients with NF1-associated tumors.

Go online to PeerView.com/YBF860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Neurofibromatosis type 1 (NF1) is an incurable and progressive genetic disorder caused by a partial or complete loss of function of the NF1 tumor suppressor gene, resulting in elevated RAS-mitogen-activated protein kinase (RAS/MAPK) pathway signaling and the potential development of subsequent NF1-associated tumors. Given current breakthroughs, including the emergence of MEK inhibitors, the ongoing challenge is how to effectively employ modern therapeutics in the management of patients with NF1 tumors, particularly pediatric patients. This case-based video discussion, based on a PeerView live “Seminars & Practicum” CME event, will offer an expert-guided review of the challenges inherent to the management of NF1-associated tumors and provide practical guidance on state-of-the-art solutions and the role that MEK-targeting agents can play in patient management. Upon completion of this activity, participants should be better able to: Summarize the genetic etiology, diverse clinical symptomatology, and diagnostic criteria of neurofibromatosis type 1 (NF1), Cite the current evidence from pivotal clinical trials on MEK inhibitors and other targeted therapies for the treatment of NF1-related PNs and other tumors in pediatric populations, Select personalized treatment plans using MEK inhibitors and other targeted therapies in pediatric populations with NF1-related plexiform neurofibromas (PNs) and other tumors based on prognostic information, safety considerations, and the latest evidence and guideline recommendations, Develop a management plan for the unique spectrum of adverse events associated with novel therapeutics including MEK inhibitors in pediatric patients with NF1-associated tumors.

Go online to PeerView.com/YBF860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Neurofibromatosis type 1 (NF1) is an incurable and progressive genetic disorder caused by a partial or complete loss of function of the NF1 tumor suppressor gene, resulting in elevated RAS-mitogen-activated protein kinase (RAS/MAPK) pathway signaling and the potential development of subsequent NF1-associated tumors. Given current breakthroughs, including the emergence of MEK inhibitors, the ongoing challenge is how to effectively employ modern therapeutics in the management of patients with NF1 tumors, particularly pediatric patients. This case-based video discussion, based on a PeerView live “Seminars & Practicum” CME event, will offer an expert-guided review of the challenges inherent to the management of NF1-associated tumors and provide practical guidance on state-of-the-art solutions and the role that MEK-targeting agents can play in patient management. Upon completion of this activity, participants should be better able to: Summarize the genetic etiology, diverse clinical symptomatology, and diagnostic criteria of neurofibromatosis type 1 (NF1), Cite the current evidence from pivotal clinical trials on MEK inhibitors and other targeted therapies for the treatment of NF1-related PNs and other tumors in pediatric populations, Select personalized treatment plans using MEK inhibitors and other targeted therapies in pediatric populations with NF1-related plexiform neurofibromas (PNs) and other tumors based on prognostic information, safety considerations, and the latest evidence and guideline recommendations, Develop a management plan for the unique spectrum of adverse events associated with novel therapeutics including MEK inhibitors in pediatric patients with NF1-associated tumors.

May is NF Awareness Month, and in doing my part to “Shine a Light on NF,” I want to bring you a conversation I shared on the podcast this time last year with my sweet friend Christa Castanon. Christa and I both have children with Neurofibromatosis Type 1 or NF1. In this episode, we chat about:The importance of finding a community and the ability to create your own.Supporting other moms with children of special needs.The fear, the struggles, and the beauty of parenting children with special needs.Finding self-care in times when your child and family are demanding your utmost attention.This episode is not just for mamas with children of NF. It's an episode for ALL mamas because even if you don't have a special-needs child, chances are good you know someone who does. As I am re-releasing this episode, Christa and her daughter Cataleya (Cat) are going through a very challenging, scary, and unknown time. Cat's midbrain tumor has grown, and she recently went through a brain biopsy procedure. Their family needs all of our support and consideration at this time. I only ask that you help by educating yourself for a few moments on this rare disease. Children's Tumor Foundation Website: https://www.ctf.org/ ------------Check the brand-new blog: www.mominprocess.com/blogJoin the Mom: In-Process Community:Facebook InstagramWebsite Don't forget to check out the latest swag!Get your Mom: In-Process merch today www.mominprocess.com/shop