Podcasts about fusions

Alex and Richard of the Anime Egotists have created their own YuGiOh Fusion monsters! Sure Fusions have been pretty cool over the years, but the boys have their own ideas on which to make! Some monsters are just cool enough to work together! The boys make their own Fusion monsters! Whether cool, funny, or just interesting, these are the monsters that could be cool if fused together! Let us know what monsters you'd like to fuse! Thanks to Kaori for the thumbnail! https://x.com/TKaori90

In this episode, CJ Peterson, CEO of Nature's Fusions, shares a deeply personal journey that led his family into the world of essential oils. Growing up in a large family with limited resources, CJ recounts how his sister's battle with thyroid cancer prompted his parents to explore alternative medicines, despite skepticism and misinformation within the industry. Motivated to uncover the truth, CJ and his family dove into scientific research, revealing the real benefits and risks of essential oils. He discusses the challenges of misinformation in multi-level marketing, the complexities of the essential oil supply chain, and the unique extraction processes for different oils. CJ also highlights Nature's Fusions' success on Amazon and the shifting wellness trends, emphasizing education, science, and transparency as the foundation of their brand.      

What are lumbar fusions and how common is it among younger patients? Lester Kiewit speaks to Toni-Lynne Monger, physiotherapist and clinical director of The Balance Group about the condition and how physiotherapy can be used to treat it.See omnystudio.com/listener for privacy information.

Dragon Ball Daima Episode 4 is out and we already have mentions of Fusion so of course we had to discuss it right here on Ki Moments Episode 59!

We're diving into the fascinating connections between hip hop and its diverse cultural influences. We explore how these genres have helped shape hip hop's evolution, pointing out the back-and-forth nature of the genre and its ties to dancehall & West Indian music. There's also a focus on the powerful impact of jazz and funk on hip hop, with legends like James Brown playing a major role. Plus, we touch on the rising influence of Desi hip hop and the longstanding collaborations between rap and rock, showing just how much these blended sounds have defined today's music. There is also a strong relationship between rock and hip hop, the evolution of different music styles, and how Afrobeat is shaping UK hip hop. We also get into the significance of mosh pits in hip hop culture as well as talk about artists like J Hus, and look ahead to the future of Afrobeat in the music scene. Songs played this episodeCaribbean (Neil) Bad Boyz (feat. Barrington Levy) - ShyneIndia (Kiran)Big Dawgs - Hanumankind & KalmiJazz/Funk (Sam)Funky Drummer (Bonus Beat Reprise) - James BrownRap-Rock (Sean)Empty Vessels (Official Video) (feat. Roots Manuva) - The MaccabeesAfrobeats (Theo)Bouff Daddy - J HusKey TopicsHip hop has deep roots in Caribbean culture, particularly reggae and dancehall.The iterative nature of hip hop allows it to evolve and incorporate various influences over time.Grime music has significant connections to dancehall, often drawing inspiration from its rhythms and styles.Caribbean music has had a lasting impact on pop culture, often influencing mainstream music trends.Indian music and culture are increasingly influencing hip hop, with a growing number of artists emerging from the Desi scene.Jazz and funk have played a crucial role in shaping the sound and style of hip hop.James Brown is one of the most sampled artists in hip hop, showcasing the genre's reliance on funk and soul.The collaboration between rap and rock has a rich history, with many iconic moments in music history.Artists like MIA and Jay Sean have successfully blended their cultural backgrounds with hip hop.The cyclical nature of music means that influences from the past continue to resurface in contemporary sounds. The crossover between rock and hip hop has a rich history.Iconic collaborations like Jay-Z and Linkin Park set a precedent.Mosh pits have become a significant part of hip hop culture.Afrobeat is increasingly influencing UK hip hop artists.J Hus is seen as a pioneer in bringing African sounds to UK rap.The music scene is evolving with new artists emerging.There is a nostalgic appreciation for past collaborations.The impact of live instruments is returning to hip hop.The conversation reflects on the changing nature of music consumption.Future collaborations may redefine genre boundaries.

This week Aloka, Negoo, Kaval are running things, with second to none company, Maiden, Debba, Beatrice M & Naemi, Beats & Fusions abound with enough Bass and Word to tear the roof off. A Sonic Sedition, generating Culture, celebrating change, this is Dub Intervention presented by Ed2000For more info and tracklisting, visit: https://thefaceradio.com/dub-intervention/Tune into new broadcasts of Dub Intervention, Saturdays from 8 - 10 PM EST / 1 - 3 AM GMT (Sunday).//Dig this show? Please consider supporting The Face Radio: http://support.thefaceradio.com Support The Face Radio with PatreonSupport this show http://supporter.acast.com/thefaceradio. Join the family at https://plus.acast.com/s/thefaceradio. Hosted on Acast. See acast.com/privacy for more information.

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Edwina Bassil est la cinquième invitée de Pinkies. Elle incarne la réussite par le “faire”. Elle est la professionnelle des fusions acquisitions qui a certainement analysé le plus de dossiers de rachat de société sur la place de Paris. Elle sait mener ses projets au bon endroit avec efficacité et discrétion. Edwina a quitté le Liban à 18 ans pour poursuivre des études brillantes à Dauphine. Une fois son diplôme en poche, elle intègre les institutions financières les plus prestigieuses : Accenture puis Rothschild et Cambon Partners, entre autres. En 2019, elle rejoint Vincent Klingbeil pour créer European Digital Group, un groupe d'experts dont l'objectif est de concurrencer les géants du digital. Son équipe est aujourd'hui constituée de jeunes femmes ambitieuses qui changent les codes de la finance. Edwina nous inspire par son efficacité sobre et élégante qui ne manquera pas de vous surprendre. Découvrez dès maintenant son histoire inspirante et son parcours exceptionnel sur toutes vos plateformes d'écoute préférées. Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.

Turn up the heat, it's the daily podcast with Mike and Vernetta!See omnystudio.com/listener for privacy information.

Lured Up Podcast 307   Apologies on how late the audio version of this episode is! We had some major tech issues that we finally have worked through! Hopefully the quality is ok!   Niantic dropped a news bomb just in time to close out the Season of Wonders. We run through a huge list of items and bring in Chris and Jamal from Wayspotters to help make sense of the latest Wayfarer Challenge!   Flock Together - https://bit.ly/LU306Flock  Catching Wonders - https://bit.ly/LU306CatchingWonders  Wayfarer Challenge - https://bit.ly/LU307Wayfarer  GO Hub Wayfarer - https://bit.ly/LU307GOHubWayfarer  Wayfarer Criteria - https://bit.ly/LU307Criteria  GO Fest - https://bit.ly/LU307GOFest GO Fest Sendai - https://bit.ly/LU307Sendai  Lapras Café - https://bit.ly/LU307Lapras  Necrozma - https://bit.ly/LU307Necrozma  Pokémon Fusions - https://bit.ly/LU307Fusion  Ultra Space Wonders - https://bit.ly/LU307UltraSpace  No Comment - https://bit.ly/LU307NoComment    LuredUp@PokemonProfessor.com     Voicemail and SMS: 732-835-8639    Use code FULLHEAL at https://tgacards.com/ for 10% off your order!   Support the show by bookmarking and shopping at TCGPlayer.com using this link - https://bit.ly/TCGPlayerAffiliate    Connect with us on multiple platforms! https://linktr.ee/PokemonProfessorNetwork    Hosts Ken Pescatore Adam Tuttle   Writer and Producer Ken Pescatore   Executive Producer  Paul Bhatt   Show music provided by GameChops and licensed through Creative Commons   ▾ FOLLOW GAMECHOPS ▾ http://instagram.com/GameChops http://twitter.com/GameChops http://soundcloud.com/GameChops http://facebook.com/GameChops http://youtube.com/GameChops http://www.gamechops.com   Intro Music Lake Verity (Drum & Bass Remix)  Tetracase GameChops - Ultraball http://gamechops.com/ultraball/ https://soundcloud.com/tetracase  https://soundcloud.com/MegaFlare0   Break Music National Park Mikel & GameChops GameChops - Poké & Chill http://smarturl.it/pokechill https://twitter.com/mikel_beats   Outro Music Vast Poni Canyon CG5 & GlitchxCity (Future Bass Remix) GameChops - Ultraball http://gamechops.com/ultraball/  http://soundcloud.com/cg5-beats https://soundcloud.com/glitchxcity Pokémon And All Respective Names are Trademark and © of Nintendo 1996-2024 Pokémon GO is Trademark and © of Niantic, Inc. Lured Up and the Pokémon Professor Network are not affiliated with Niantic Inc., The Pokémon Company, Game Freak or Nintendo.   #pokemon #pokemongo #podcast  

JCO PO author Dr. Jun Gong shares insights into his JCO PO articles, “Phase II Study of Erdafitinib in Patients with Tumors with FGFR Amplifications: Results from the NCI-MATCH ECOG-ACRIN Trial (EAY131) Sub-protocol K1" and “Phase II Study of Erdafitinib in Patients with Tumors with FGFR Mutations or Fusions: Results from the NCI-MATCH ECOG-ACRIN Trial (EAY131) Sub-protocol K2”. Host Dr. Rafeh Naqash and Dr. Gong discuss the limited activity of FGFR inhibition in solid tumors with FGFR amplifications and mutations or fusions in this NCI-MATCH phase II trial. TRANSCRIPT  Dr. Rafeh Naqash: Hello and welcome to JCO Precision Oncology Conversations, where we bring you engaging conversations of clinically relevant and highly significant JCO PO articles. I'm your host, Dr. Rafeh Naqash, Social Media Editor for JCO Precision Oncology and Assistant Professor at the Stevenson Cancer Center at the University of Oklahoma.  Today, we are excited to be joined by Dr. Jun Gong, Associate Professor in the Division of Medical Oncology at Cedars-Sinai Medical Center and lead author of the JCO Precision Oncology article entitled "Phase II Study of Erdafitinib in Patients with Tumors Harboring FGFR Amplifications: Results from the NCI-MATCH ECOG-ACRIN Trial EAY131 Subprotocol K1" and "Phase II Study of Erdafitinib in Patients with Tumors with FGFR Mutations or Fusions: Results from the NCI-MATCH ECOG-ACRIN Trial EAY131 Subprotocol K2."   Our guest's disclosures will be linked in the transcript.   Dr. Gong, welcome to our podcast and thank you for joining us.  Dr. Jun Gong: Thank you, Dr. Naqash and JCO Precision Oncology for having me. Dr. Rafeh Naqash: We are excited to be discussing some interesting aspects that you have led and published on from the NCI-MATCH trial. We were trying to understand from a background perspective, since this master protocol has been going on for quite some time, could you give us a little bit of background for the sake of our listeners on what the NCI-MATCH is and what were the specific objectives for these two subprotocols?  Dr. Jun Gong: Yes, of course, Dr. Naqash. So, as you may all know, the importance of targeted therapies in the current era of precision oncology. And on that backdrop, the NCI-MATCH was a national multicenter study designed essentially to look for signals of efficacy across various solid tumor and hematologic malignancy types, with a focus on specific mutations. The master protocol is unique in that there are several arms to the trial, each targeting a specific potential targetable alteration using available agents in cancer today. Dr. Rafeh Naqash: Excellent. Thank you for that background. I know this master protocol has been going on for quite some time with different subprotocols. I believe some of them are immunotherapy-based. Also, you've led two important subprotocols, which are the FGFR amplification and the FGFR mutation or fusion. There are some differences, from what I gather, in responses for the fusions versus the amplifications or mutations versus the amplifications. Could you first delve into the first paper of the fusions, and describe what were the tumor types? As you mentioned in the paper, some tumors were excluded. What was the reason for the exclusion of some of those tumor types? Why did you want to study the fusions and mutations versus the amplifications separately? What was the background for that? Could you highlight some of those points for us? Dr. Jun Gong: Firstly, as a kind of a more background, FGFR has been a recognizable target for a couple of tumor types. And if you look at the broad landscape of FGFR alterations, they occur in about 5%-10% of cancers, with the majority being FGFR amplifications actually, and mutations and rearrangements following second and third respectively in most commonly identified alterations. With that being said, FGFR mutations and rearrangements have already been established in a couple of tumor types. Actually, the first FDA approval for an oral FGFR inhibitor was erdafitinib, which was the agent used in both of these back-to-back trials. However, erdafitinib was first approved in urothelial carcinoma, and since then, there has been an explosion in oral FGFR inhibitors targeting fusions and mutations in other cancer types, such as cholangiocarcinoma.   More recently, there was even an FDA approval in a myeloid malignancy as well. So, we used erdafitinib, being that it was the first FDA-approved, orally available agent to target this alteration. We conducted the two back-to-back studies in recognition that although rearrangements and mutations have already been established in certain tumor types, we were more interested in looking at the more common FGFR alteration, that being amplifications. However, the efficacy in that was a little unknown, and so these two separate subprotocols were developed: K2, which was to look at FGFR mutations and fusions in tumor types, excluding urothelial carcinoma, to look if there was a signal of efficacy beyond currently FDA-approved indications, and amplification as a separate cohort. Dr. Rafeh Naqash: That's a very good explanation of why you concentrated on the tumor types in these protocols.  Now, going back to subprotocol K1, could you tell us what were some of the tumor types that you did include, and what was the sample size, and what was the hypothesis for the sample size as a meaningful level of activity that you wanted to see and would have potentially led to a bigger, broader trial? Dr. Jun Gong: So, subprotocol K1 was the arm investigating erdafitinib in those with FGFR amplifications, and these were predefined on the NCI-MATCH protocol, looking at FGFR 1, 2, 3, and 4 amplifications essentially. These were allowed to have local testing through a local CLIA-certified assay, but then they needed to be confirmed on a central assay, which is the NCI-MATCH Oncomine assay. These statistics are uniform for the NCI-MATCH trials, and the goal was at least 31 patients, with the hypothesis that if the response rate was 16% or more, this was considered a signal of activity. However, there was an additional protocol specific requirement in that if the sample size was fewer than 31 patients, then the primary efficacy population would be assessed against a null hypothesis overall response rate of 5%. Meaning that if there were less than 31 subjects, an overall response rate of greater than 5% would be defined as positive. Again, the NCI-MATCH was uniform. Secondary objectives included progression-free survival, overall survival, and safety and toxicity. With that being said, K1 originally began accrual. The NCI-MATCH actually launched in 2015, but in the subprotocol K1, 35 patients were initially enrolled in the study. If you go down the eligibility criteria, however, a lot of these patients dropped out due to a lack of central tumor confirmation and various reasons. Ultimately, 18 patients were included in the pre-specified primary efficacy cohort. Dr. Rafeh Naqash: Thank you. I did see for subprotocol K1, you mostly had stable disease in a couple of patients, no responses, and I think one individual with breast cancer had a prolonged stable disease.   Now, from an FGFR amplification standpoint, did you or were you able to correlate - again, this is not objective responses, it's not a partial response or a complete response - was there any correlation from the level of amplification to the duration of stable disease?  Dr. Jun Gong: That's actually the core of our discussion about why K1, despite a variety basket of solid tumor types, somewhere, preclinical data had suggested FGFR amplifications could be targeted, that K1 was ultimately a negative trial with a 0% response rate. We dive in that although we included as an eligibility criteria a copy number variation of seven as the threshold for amplification, we realized that if you look at some of the literature out there, that even in the FGFR 1 and 2 amplification cohorts, where these are the more common cohorts of amplified tumor types that have been targeted, you really needed a high level of amplification, more than 99% of tumor cells being amplified in the previous studies, to actually generate a response.  The thought was that we assumed that FGFR amplification would lead to protein expression and dependence on FGFR signaling, providing sensitivity to FGFR inhibition. However, we realized that there is a certain degree where a high level of amplification needs to happen, and it may not be for all FGFR amplifications. We looked into the literature that FGFR 1 and 2 were the more commonly studied FGFR amplifications. FGFR 1, if you actually look at the amplicon structure, it tends to amplify a lot of other genes because it's such a huge amplicon structure. But FGFR 2 is shorter and centered on just FGFR 2 with a few other genes co-amplified. So, actually in the literature, they've already been seeing that maybe FGFR 2 amplification tumors are more readily targetable based on the robustness of evidence, rather than FGFR 1. But across all of these, the higher the level of amplification, seems the more targetable. Dr. Rafeh Naqash: Those are interesting discussions around protein expression on the tumor that could imply therapeutic vulnerability. So I've always thought about it, whether trials like NCI-MATCH trials or ASCO TAPUR, for example, would be perhaps more informative if, on a secondary analysis standpoint, proteomics is something that could be done on the tumor tissue, because similar to NCI-MATCH, ASCO TAPUR has other sub protocols where some of these mutations or amplifications don't necessarily result in antitumor responses. But I think from a biology standpoint, as you mentioned, a certain amplification might correspond to RNA expression and that might correspond to protein expression, which is downstream. So looking at that would be something interesting. Have you planned for something like that on these tumor specimens? If you have biobanked any of those specimens. Dr. Jun Gong: I think that's a great future direction. And I know you, Dr. Naqash, being involved in so many cooperative trials, I think it is possible, but it really depends on good trial planning from the onset. When designing such massive trials like this, I think the more important thing is if your trials are negative, but they are informative for the field to go back and have these postdoc available biobanks that you said. And I think having it integrated firstly, is way more efficient than to have kind of an amendment kind of going through halfway or when the trial is started. That could be a little bit more logistically difficult.  Dr. Rafeh Naqash: I completely agree. And you mentioned corporate groups, I think we've been discussing, and I'm pretty sure you have also, there's a lot to be learned from clinical trials that are negative. We often, in the academic or non-academic setting, end up not publishing some of those negative results, pharma or corporate group based studies. And I think the resources, the specimens, and the negative results could correlate to some other novel findings if some of those exploratory analyses are done in the appropriate manner.   Now, going to the drug itself or the erdafitinib here, it's a pan-FGFR inhibitor. Is that something that you think is a limitation in the drug development space? I do early phase trials, and I'm pretty sure you do a lot of these basket early phase trials. Is that something that you feel is a limitation when you have a drug that targets different mutations or different protein changes of the same gene or different amplifications? Could that be a reason why something like this doesn't necessarily work because it doesn't have as much specificity against the isoform as one might need to inhibit the downstream kinase activation?  Dr. Jun Gong: That is also a great point. The NCI-MATCH sub protocol K1 and K2 used erdafitinib, which was the first FDA-approved FGFR inhibitor. But as many of the listeners and yourself may know, there have been newer iterations in next-generation development of the FGFR inhibitors. And it's very fascinating, the tyrosine kinase inhibitors, with each iteration, you seem to have a little more potency and the ability to bypass some of the resistance mutations, almost paralleling the lung cancer space, where we kind of follow that, and they've been kind of the pioneers in that space. And to your point, yes, we consider– the NCI-MATCH was developed nearly a decade ago, and the available agents at that time, would it have changed the findings if we used a kind of a newer generation or more potent FGFR inhibitor? It's possible, I think, especially in the K1 cohort with the amplifications. We even suggested in the discussion of the paper future directions, is that one way to kind of bypass the amplification issue is to use more potent and specific FGFR inhibitors. And so I think it's very possible that you highlight this point.  Dr. Rafeh Naqash: And for the sake of our listeners, Jun, especially trainees, could you highlight what are currently some of the FDA-approved FGFR inhibitors, and what tumor types are they currently approved in?  Dr. Jun Gong: The first one, as we have hinted, was in treatment of refractory, essentially urothelial carcinoma with FGFR mutations and rearrangements, mainly 2 and 3. And this is where oral erdafitinib was approved. And it's interesting, I kind of teach my fellows and our health staff that erdafitinib is interesting in that its FDA label insert requires a starting dose of about 8 milligrams daily, and it's a 28-day cycle. But during the first 14 days, we're really looking at the serum phosphate levels. If they are within a certain level, if they are within 5.5 to 7, for example, you continue the current dose. But if they are less than 5.5, the FDA label actually mandates that you increase it to 9 milligrams oral daily, continuously. This is biologically logical to me. FGFR is located to the renal tubules, and so this is a major phosphate kind of metabolism pathway here. And so you're using that as a surrogate, essentially, if the right dosing is achieved. And so that's unique.  And then the subsequent kind of FGFR inhibitors that came about, you had a couple in cholangiocarcinoma, where, unlike urothelial carcinoma, where it's about 30% of the time, you'll find the FGFR alterations of target. It's about half of that 15% in cholangiocarcinoma, and it's mainly intrahepatic cholangiocarcinoma in that sense. And here you have pemigatinib, which is one of the FGFR inhibitors approved for cholangiocarcinoma. And then you also had infragatinib, which is approved. But however, infigratinib eventually had their FDA label culled. It was withdrawn by the company, I think it was in 2022. And then more recently, you had even a more potent FGFR inhibitor in cholangio approved and futibatinib. It's interesting that with these more later generations of FGFR inhibitors, they do show a correlation with phosphate levels, but they don't have that specific kind of dosing early on in the first cycle, like erdafitinib. And so it's interesting to see that with the later generations, you're seeing more potency as well. Dr. Rafeh Naqash: Thank you for that overview, which I'm sure most of the trainees appreciate since this is an up and coming field in the space of precision medicine, especially FGFR. From a side-effect profile standpoint, you mentioned phosphate issues. Do you think that is a drug class effect here, or is that an FGFR receptor subtype effect, depending on which FGFR receptor, 1 or 2 or 3, that is being targeted?  Dr. Jun Gong: I do think this is a class effect that you'll see across a lot of the trials where phosphorus elevations or decreases are going to be probably your most common treatment-related adverse event. And I actually emphasize this is probably one of the most trickier side effects of this class, where we're almost having to have to monitor the phosphorus levels pretty routinely, pretty closely. And you also have other class effects on the nails. There's some rare retinal ocular toxicities that's unique to the FGFR class as well. And so it's a very exciting class of compounds, but it does require some close monitoring of some unique class effects as you've hinted. Dr. Rafeh Naqash: Based on the results from your K1 sub protocol, are FGFR inhibitors still the approach within, let's say, within cholangio or urothelial with FGFR amplifications? Is that still something that has been established and seen from a clinical response standpoint? Dr. Jun Gong: The FDA approvals are really for mutations and fusions. So this K1 sub protocol, essentially, I think provides one answer that we've been all wondering about for the longest time, “Hey, could amplifications be targeted as well?” Unfortunately, we didn't include urothelial carcinomas in this study because of the FDA approval. But from a kind of a basket solid tumor perspective, I think this really dampens the enthusiasm. As of right now, it really is fusions and mutations that are targetable. Amplifications need further investigation before becoming established in solid tumors. Dr. Rafeh Naqash: Going to the discussion with the second K2 protocol, which is mutations and fusions, can you highlight again which tumor types there where you saw some clinical outcomes that you saw and any unique insights on certain mutations or protein changes that were a little more relevant than some others?  Dr. Jun Gong: Sure. So this is the parallel study to K1, in that now we are looking at fusions and mutations of FGFR1, 2, 3, and 4. And essentially, we, again, excluded those with urothelial carcinoma, given the FDA approval for erdafitinib in this trial. The trial actually opened then the FDA approvals for the FGFR inhibitors for cholangiocarcinoma happened. So this trial didn't really exclude those with FGFR mutated or rearranged cholangiocarcinoma as well. If you look at the breakdown of the cohort in K2, you saw a good mix of breast cancers or a couple of gynecologic malignancies. There were a couple of head and neck cancers. There were several brain tumors as well. There was one lung cancer. There were four noted intrahepatic cholangiocarcinomas. Again, we could not exclude those due to the fact that the trial had opened and was accruing when the FGFR inhibitors approved for cholangiocarcinoma happened. Similar design, with a phase II, single-arm, open-label of erdafitinib, and again, the same statistical design was implemented in that if it's higher than 31 patients, 16% overall response rate was a primary endpoint goal. If it was less than that, it was against the 5% overall response rate.   And here in K2, 35 patients were enrolled and 25 patients were ultimately included in the primary efficacy analysis. So because it was fewer than 31 in the primary efficacy cohort, it followed the NCI-MATCH to be specified with a primary endpoint goal of 5% or higher. And here, in a heavily pre-treated cohort of more than 50% of subjects who have received prior than 3 or higher lines of therapy, overall response rate essentially confirmed was 16% with the p value of 0.034, which met the positivity cutoff of 5%. However, an additional seven patients experienced stable disease as best confirmed response. And it's important to note that four of these were grade IV glioblastomas with prolonged progression-free survival. So ultimately, this trial was positive in reading the endpoint that outside of urothelial carcinoma, could FGFR inhibition be pursued in other tumor types that had FGFR rearrangements or fusions? Dr. Rafeh Naqash: You mentioned glioblastoma, which is an area of huge unmet need. Do you think a trial like this as an upfront approach in glioblastoma, perhaps maybe after Temodar, could be a more meaningful way using the strongest, more precise therapy earlier on when there are certain mechanisms that inhibition of which would result in anti-tumor responses? Do you think doing this earlier on rather than second, third, fourth line would be more intriguing in some ways?  Dr. Jun Gong: I think you've hit upon several key points there. Firstly, just a high unmet need in glioblastomas, in general. And then to us, although it was a stable disease it was quite noticeable that four of these occurred in IDH1 and 2 wild-type brain tumors. We kind of discussed that in the discussion as well. And of these, we actually realized that in the pre-clinical and other published literatures space that for some reason, IDH1 and wild-type tended to have more FGFR alterations, while 0% were found in IDH1 and 2 mutant high grade gliomas. So I think there is something hypothesis generating coming out of this study as well even though there were stable disease. And that you may be selecting for– We may be able to have future studies to select for a specific niche of glioblastomas. And as to your point, Dr. Naqash, I think  if we can have a design trial looking for these specific molecular subsets, I think it's wide open for trials of this nature in the first line, second line, or refractory space. Even piggybacking into cholangiocarcinoma, you see, they're now looking at these in the neoadjuvant and adjuvant space as well. So I think we can identify the subset - it's wide open out there. Dr. Rafeh Naqash: I completely agree. I remember my program director a few years back when immunotherapy was in the metastatic setting, it was very exciting. He gave a talk in which he said "Early, earlier, earliest," and the more early, the better it seems. So I'm guessing that it's probably something similar for precision medicine-based approaches like targeting FGFR perhaps earlier.   So what is next for some of these two studies, or these ideas that have come out of these two studies? Are you trying to develop something subsequently, or is NCI-MATCH looking at it from a certain perspective? Or what would you want to do as a next step, ideally if you had the funding and the pharma support? Dr. Jun Gong: That's the million dollar question. So just from the broad strokes, I think what these two back to back papers and studies comment is that amplifications may not be the more targetable of FGFR subset, but there is avenue for improvement there and further investigation. FGFR fusions and mutations however seem to go along with what we know in some of the FDA approved types now. Now the next step is in the area of precision oncology is could we expand the label indications now to other subtypes with FGFR fusions and mutations. And this is I think following precedent. You and the audience may know that there are a lot of different tumor agnostic approvals now for both immunotherapy and other targeted therapy types. So I think the goal of this study was to provide momentum for, perhaps, advancements into a tumor agnostic indication for FGFR inhibitors.  And we do cite in the K2 manuscript the results of a phase II study that was also published around the time we were writing the study up. It was the phase II RAGNAR study. And that enrolled patients, again, with FGFR fusions and mutations. And that trial was positive, too. That one was a larger study of 217 subjects. We highlight some differences in study populations as to why maybe the difference in responders were detected. Both were positive studies. It was reassuring that the overall survival impulse studies were about the same. And again, I think they don't compete. I rather think they complement each other in providing this body of evidence that  may meet- at one point, the FDA should be approached with this evidence for a tumor agnostic mutation so that more patients with this subset could be benefitting.  Dr. Rafeh Naqash: Excellent. Thank you so much, Jun.  Now, could you tell us briefly what your background is, where you've trained, and your interests, and how you balance clinical research with some of your personal interests?  Dr. Jun Gong: Sure. Thank you for that interest. I did my training in medical school in New York. I went to New York Medical College. And then I did my residency at Cedars-Sinai for medicine. And I went to City of Hope for fellowship where I was trained in GU by Dr. Monty Powell who maybe you folks are familiar with. And my GI training was with Dr. Fakih at City of Hope. And since then I returned back to Cedars-Sinai where I serve as a dual GI/GU focused medical oncologist. I do clinical trials in both and translational science, really focused on targeting tumor metabolism in both as well. My advice to the listeners and trainees and I tell my own fellows this, I think it's very rare now unless you're in phase I to do a dual focus. So I actually emphasized to my trainees that the more focused you can be, the better. Unless you are going into phase I, for example. With that, you can hone in, develop your craft. But then again, I have known several mentors who do multiple tumor types. But I think the more traditional mechanism is to focus as much as you can is my advice for the listeners.  Dr. Rafeh Naqash: Thank you again, Jun, for all those interesting scientific and personal insights. We appreciate you and working with JCO Precision Oncology for both of your manuscripts. This is the first time we have ever invited a lead author for two manuscripts at the same time. It's always good to be the first in something, and I learned a lot and hopefully, our audience would have learned a lot. Dr. Jun Gong: Thank you, Dr. Naqash, for having me. It was a pleasure speaking with you and the crew. Dr. Rafeh Naqash: Thank you.   Thank you for listening to JCO Precision Oncology Conversations. Don't forget to give us a rating or review, and be sure to subscribe so you never miss an episode. You can find all ASCO shows at asco.org/podcasts. 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, experiences, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.  

This week its all good news, thanks to DJ Stingray 313, DJ Polo, Breaka, Swordman, Skiahari, Czn, Robin Wylie, The Crane, Nicoba and a whole lot more. Beats across the tempo spectrum, touching bass on an A to Z of influences, Fusions abound, what's that sound. A new edition of Sonic Sedition,This is Dub Intervention.For more info and tracklisting, visit: https://thefaceradio.com/dub-intervention/Tune into new broadcasts of Dub Intervention, Saturdays from 8 - 10 PM EST / 1 - 3 AM GMT (Sunday).//Dig this show? Please consider supporting The Face Radio: http://support.thefaceradio.com Support The Face Radio with PatreonSupport this show http://supporter.acast.com/thefaceradio. Join the family at https://plus.acast.com/s/thefaceradio. Hosted on Acast. See acast.com/privacy for more information.

La plupart des champs magnétiques stellaires, y compris celui du Soleil, sont produits par une dynamo générée dans des couches intérieures soumises à une convection. Les étoiles massives (huit masses solaires ou plus) n'ont pas d'intérieur convectif, on ne sait donc pas pourquoi environ 7 % d'entre elles ont tout de même un champ magnétique. Une équipe d'astrophysiciens à découvert que dans un système binaire d'étoiles massives, l'une des deux est magnétique mais pas l'autre, et elles semblent n'avoir pas le même âge non plus, ce qui les mène sur une bonne piste d'explication... L'étude est publiée dans Science.https://www.ca-se-passe-la-haut.fr/2024/04/des-fusions-stellaires-lorigine-du.html Source A magnetic massive star has experienced a stellar mergerA. J. Frost et al.Science Vol 384, Issue 6692 (11 Apr 2024)https://doi.org/10.1126/science.adg7700

Chaque mois, le coach Didier Acouetey, président d'AfricSearch, conseille un jeune entrepreneur sur ses difficultés. En deuxième partie, débat avec des patrons de PME du continent. Dans cet épisode : la rentabilité des entreprises. Partie 1 : conseils à un jeune entrepreneur- Didier Acouetey, président du cabinet AfricSearch- Abdourahmane Diallo, fondateur et dirigeant du groupe Cas'ART qui produit et distribue "emanay" le riz local de Casamance, Ziguinchor, SénégalPour aller plus loin, Riz sénégalais: le pays est toujours loin de son objectif d'autosuffisance une chronique des matières première de RFI Partie 2 : Fusions, diversification, association, rachats, comment les PME peuvent grandir par la croissance externe?Didier Acouetey, président du cabinet AfricSearch, conseille un jeune entrepreneur et dialogue avec des patrons de PME du continent africain. Ils évoquent leur parcours, le contexte économique dans leur secteur et approfondissent une thématique. Cette semaine : La croissance externe- Jean-Louis Billon, actionnaire et dirigeant de SIFCA, premier groupe privé ivoirien, géant de l'agroalimentaire et poids lourd de l'économie ouest-africaine et premier employeur privé du pays. Ancien ministre du Commerce de l'artisanat et de la promotion des PME- Serigne Barro, directeur général de P_I Group qui regroupe trois entreprises spécialisées dans la digitalisation : People input (fournisseur d'innovation), Voice Africa (agence de communication) et Dentsu (agence média)- Didier Acouetey, président du cabinet AfricSearch. Programmation musicale : ► Boucantier - Lil Jay Bingerack► Fonike - Guinea Our Paradise

Chaque mois, le coach Didier Acouetey, président d'AfricSearch, conseille un jeune entrepreneur sur ses difficultés. En deuxième partie, débat avec des patrons de PME du continent. Dans cet épisode : la rentabilité des entreprises. Partie 1 : conseils à un jeune entrepreneur- Didier Acouetey, président du cabinet AfricSearch- Abdourahmane Diallo, fondateur et dirigeant du groupe Cas'ART qui produit et distribue "emanay" le riz local de Casamance, Ziguinchor, SénégalPour aller plus loin, Riz sénégalais: le pays est toujours loin de son objectif d'autosuffisance une chronique des matières première de RFI Partie 2 : Fusions, diversification, association, rachats, comment les PME peuvent grandir par la croissance externe?Didier Acouetey, président du cabinet AfricSearch, conseille un jeune entrepreneur et dialogue avec des patrons de PME du continent africain. Ils évoquent leur parcours, le contexte économique dans leur secteur et approfondissent une thématique. Cette semaine : La croissance externe- Jean-Louis Billon, actionnaire et dirigeant de SIFCA, premier groupe privé ivoirien, géant de l'agroalimentaire et poids lourd de l'économie ouest-africaine et premier employeur privé du pays. Ancien ministre du Commerce de l'artisanat et de la promotion des PME- Serigne Barro, directeur général de P_I Group qui regroupe trois entreprises spécialisées dans la digitalisation : People input (fournisseur d'innovation), Voice Africa (agence de communication) et Dentsu (agence média)- Didier Acouetey, président du cabinet AfricSearch. Programmation musicale : ► Boucantier - Lil Jay Bingerack► Fonike - Guinea Our Paradise

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Grammy-nominated percussionist, recording artist and educator Michael Spiro joins Rebecca to speak about his apprenticeship in Matanzas with masters of Afro-Cuban folkloric drumming, differences in drumming styles between Havana and Matanzas, and his innovative recordings, which fuse batá drumming with other Afro-diasporic traditions, such as Brazilian samba, Candomblé, and Zimbabwean mbira music. Songs played:Inspiración a Santiago, Los Muñequitos de MatanzasPara Clave y Guaguancó, Clave y GuaguancóOsain, Michael Spiro & guestsButsu Mutandari/Iyesa, Michael Spiro & guestsMaracambique, Michael Spiro, Joe Galvin & guestsStardust (El Encanto), Michael Spiro,Wayne Wallace & guestsSupport the showIf you like this podcast, please subscribe and give us a 5-star rating on Apple PodcastsFollow The Clave Chronicles on Twitter, Instagram, and Facebook @clavechronicleshttps://theclavechronicles.buzzsprout.comIntro and outro music: "Bengo Latino," Jimmy Fontanez/Media Right Productions

Les fusions d'étoiles à neutrons sont complexes à comprendre. Une petite pièce du puzzle vient peut-être d'être résolue par une équipe d'astrophysiciens grâce à une simulation super chiadée qui permet d'expliquer comment des courts sursauts gamma peuvent être lancés par un magnétar grâce au champ magnétique de type dynamo qui est produit au moment de la collision/fusion. L'étude est publiée dans Nature Astronomy.https://www.ca-se-passe-la-haut.fr/2024/02/un-champ-magnetique-de-type-dynamo.html Source A large-scale magnetic field produced by a solar-like dynamo in binary neutron star mergersKenta Kiuchi et al.Nature Astronomy (15 february 2024)https://doi.org/10.1038/s41550-024-02194-y Illustrations Champs magnétiques produits dans un magnétar résiduel d'une fusion d'étoiles à neutrons (Kiuchi et al.) signaux électromagnétiques du magnétar obtenus dans la simulation (Kiuchi et al.) Kenta Kiuchi

This week, on the Fitness + Technology podcast, host Bryan O'Rourke welcomes Erika Levy to the show. Erika is the founder of The Barre Fusions Method that teaches fitness instructors how to create classes that fuse ballet barre with other formats and streamline class design. She is certified in numerous yoga and active aging certifications and currently teaches Barre Fusions at Gold's Gym in Camas, Washington and West Coast Fitness in Portland, Oregon. Today, Erika joins Bryan to talk about her business and trends in group fitness programming.  One Powerful Quote: 19:38: “I think there's a lot of opportunity to monetize your content and to create online experiences that are an extension of the in-person experience.” 4-10 Bullet Points (w/ timestamps) - Highlighting key topics discussed: 2:38: Bryan opens the show by asking Erika about her background in the fitness space.  4:20: Erika talks about launching her Barre Fusions concept.  8:16: Erika explains how Barre Fusions aligns with distributing group fitness programming. 12:45: Erika shares her thoughts on technology trends in group fitness.  15:51: Erika extrapolates on the common themes around member management and technology for club automation.  19:16: Bryan wraps up the show by asking Erika to impart her final advice to the listeners.  Bullet List of Resources: https://barrefusions.com/ https://erikalevy.com/ Guest Contact Information: https://erikalevy.com/ https://www.linkedin.com/in/erikalevy/ https://www.bryankorourke.com/ https://www.linkedin.com/in/bryankorourke/ http://www.fittechcouncil.org/ https://www.youtube.com/user/bko61163

We have one of our favorite Spiritual Teachers + practitioners back on the podcast today! Ginette Biro is a powerful Spiritual medium who is clairaudient, clairvoyant, clairsentient and claircognizant. She can hear, see, feel and know information from spirit and other dimensions.Since Ginette was a child, she has been channeling beings from the 4th to 12th dimensions, connecting people to the other side and bringing messages to inspire and inform our world.Ginette has many spirit guides, ascended masters and beings who are guiding her to support our planet. In addition to these remarkable gifts, she has spent soul time on the other side through a near death experience which we've discussed on a prior Seeking Center episode. This allowed her to see and understand how our life blueprint and soul's journey actually works.Prior to a career using her spiritual gifts, Ginette pursued science, receiving a Bachelor of Kinesiology and a Diploma of Sports Medicine, and practiced as a kinesiologist. Ginette helps to translate guidance from beyond in a way that we can understand.Karen and I are frequent listeners to her weekly and monthly messages…and we wanted to share what she's been receiving for this month and for 2024 overall. We're talking manifesting, alignment, flow and more. You don't want to miss this enlightening conversation!MORE FROM GINETTE BIROVisit Avalon Spirit to find more about Ginette's readings, experiences, courses, products and her book, Avalon to Aurora: Lessons from The Other Side To Guide Your Life On Earth.Listen to Ginette's podcast "The Ginette Biro Podcast" on YouTube and wherever you listen to your podcasts.Get Ginette's weekly and monthly updates on YouTube: @ginettebiromediumFollow Ginette on SocialIG: @ginettebiro.medium FB: @GinetteBiroMediumGinette on Seeking Center A Near Death Experience, Spirit Guides, Mediumship and MoreDeath Walkers, Walk-Ins, Fusions and Parallel TimelinesVisit theseekingcenter.com for more from Robyn + Karen, plus mega inspo -- and the best wellness + spiritual practitioners, products and experiences on the planet! You can also follow Seeking Center on Instagram @theseekingcenter

Tu peux aussi retrouver cet épisode ici : www.axel.pmHello à tous et bienvenue dans ce nouvel épisode de Product CaféCette semaine on reçoit Vinvent Pavero, le co-fondateur de HomericTu peux trouver Vincent ici : https://www.linkedin.com/in/vincentpavero/Au programme de cet épisode00:05:38 Fraude de 25 millions de dollars, encore un coup des deepfakes.00:07:33 Comment ne pas se faire avoir par les deepfakes00:12:43 Enjeu cybersécurité : secteurs chauds et vulnérabilités.00:15:55 Frameworks au travail, constat de désincarnation.00:17:22 Changement de culture managériale dans les entreprises tech.00:25:56 Fusions-acquisitions et produit : comment gérer tech & peopleL'outil IA de la semaine, c'est HeyGenhttps://heygen.com/Allez, tu peux débaucher, ton "digital twin" prend la relève.À la semaine prochaineAxel, Victor et Anna

There's nothing like a good break-up to set life on a new path, and that's exactly what led Jennifer Blair to a glass shop in Toronto. It wasn't long before she was “secretly” learning the art of glass fusion and has since launched her successful business of turning glass “blobs” into beautiful masterpieces. Learn about the process of glass fusion, how Jen's family made a major life change during covid and how remining in a place that feels content is the secret to happiness. This market mastermind has loads of great life and business tips!  Us on the web: www.mikeandkristen.ca Instagram: www.instagram.com/mike_and_kristen/ Facebook: https://www.facebook.com/mikeandkristencreative Shoot us a message! Say hello, tell us who you think we should have on the podcast, and your deepest and darkest secrets: mikeandkristencreative@gmail.com  Review our book "You and Me" on Amazon (it helps a lot!!): https://amzn.to/3qqNCMo Intro song: "The Walk" Outro song: "The Jam" both by Mike's band The Town Heroes - www.thetownheroes.com Mike's site: www.michaelsryan.com Kristen's site: www.kristenherringtonart.com M & K Fundraiser: https://mikeandkristen.ca/fundraiser Urban Fusions' website: http://www.urbanfusions.ca/ Urban Fusions' Instagram: https://www.instagram.com/urbanfusions/

We're back this week, and we put YOU in charge of the show! We asked you for your Metroid Fusion questions, and you delivered big time! We're touching on subjects like; how could the B.S.L. blow up SR388 just by crashing into it? What's our favorite sound effect from the game? How would we want a remake to handle the SA-X? What's our alternate ideas for how Adams AI could have developed consciousness? Could the intro on SR388 become a playable prologue? If we could change one thing about Fusions story, what would it be? How would we have designed the Varia Suit to avoid the puke colors? All this, and so much more! All this, PLUS we set the stage for next weeks MASSIVE SHOWDOWN between the Zelda Cast and Omega Metroid Podcast's crews as we celebrate our 300th episode! We have a special Jeopardy game planned, so make sure you come and join us on Twitch to watch!   Visit OmegaMetroid.com!   Subscribe! Podbean x iTunes x Spotify x YouTube Support us on Patreon! Omega Metroid Patreon Buy Omega Metroid Merch! Check out our Etsy merch shop! Download the Omega Metroid Theme Song! Get the Single for Free on Bandcamp! Follow us on Twitter! @OmegaMetroidPod x @Spiteri316 x @dakcity_ x @DoominalCross Chat with us in Discord! Omega Metroid Discord Advertise on the Omega Metroid Podcast!

Veritas returns in 2024 to explain fusion and splits with analogies. She also spent some time comparing the differences between fusion and integration. Note: I am not a mental health professional. Everything we say in this podcast is based on what works for us and the other people we know. If you are in a crisis, call your local helpline for qualified assistance. Please take good care of yourself while you listen to this podcast. Image credits: The Current MSU. Com The DIDebunk Community server is available now! Join via this permalink: https://discord.com/invite/TngqmDPpge Looking forward to seeing you there!

Today on our episode #373 of All in the Industry®, Shari Bayer has a special "On the Road" episode from Food on the Edge, a two-day Food Symposium, which took place from October 16-17, 2023 in Dublin, Ireland. Food on the Edge featured approximately 50 speakers who were chosen for their innovation, passion, and influence on today's food culture, and was founded by Symposium Director JP McMahon of Aniar in Galway, Ireland. Shari led a panel on her new book, CHEFWISE – Life Lessons from Leading Chefs Around the World (Phaidon, Spring 2023, #chefwisebook), with CHEFWISE chef contributors Andoni Luis Aduriz of Mugaritz, Donostia-San Sebastian, Spain; Elena Reygadas of Rosetta, Mexico City, Mexico; Tala Bashmi of Fusions by Tala, Manama, Bahrain; and JP McMahon. Shari also signed copies of her book, and took part in two days of excursions around the Dublin area as a part of the speaker program, which was extremely special. This show features several conversations that Shari had while in Dublin with following FOTE speakers: Alessandro Cozzolino, Executive Chef of La Lugia at Villa San Michel, a Belmont hotel, Florence, Italy; Endo Kazutoshi, Chef of Endo at the Rotunda in London, England; Rich Shih, Co-author of Koji Alchemy; Tom Jenkins, Managing Editor of finedininglovers.com and San Pellegrino Young Chef Academy; Arlene Stein, Founder/Executive Director of the Terroir Symposium in Canada; Andrea Petrini, Incontinent Writer/Food Curator/Oblique Strategist, Road Manager of THE GELINAZ!, and more; Jason Bangerter, Executive Chef of the Langdon Hall Country House Hotel and Spa in Canada, and JP McMahon. Thank you and congratulations to all! Shari loved meeting everyone and being a part of this fantastic symposium. And special thanks to JP, Abigail Colleran, Julieann Faherty, and the entire #FOTE2023 team! Today's show also features Shari's PR tip to tell a good story, speed round with JP, and Solo Dining experience at Fish Shop in Dublin, plus mentions of other restaurants and bars that Shari visited on her first trip to Ireland. ** Check out Shari's new book, Chefwise: Life Lessons from Leading Chefs Around the World (Phaidon), available at Phaidon.com, Amazon.com and wherever books are sold! **Photo Courtesy of Shari Bayer.Listen at Heritage Radio Network; subscribe/rate/review our show at iTunes, Stitcher or Spotify. Follow us @allindustry. Thanks for being a part of All in the Industry®. Heritage Radio Network is a listener supported nonprofit podcast network. Support All in the Industry by becoming a member!All in the Industry is Powered by Simplecast.

Today's episode took place during the 1st ever Neurodynamics World Congress. It was also our first time attempting a true integration conversation with two different schools of thought. This episode features Dr. Michael Leahy from Active Release Techniques (ART) and Michael Shacklock from Neurodynamic Solutions. We discuss where these two systems fit together and the synergies between them. Let us know what you think of this new format and enjoy the episode. Show Notes ⁠Upcoming Courses⁠⁠⁠⁠ ⁠⁠⁠⁠Human Locomotion.com | Code 'GESTALTEDUCATION10'⁠⁠⁠⁠ ⁠⁠⁠⁠Core360 Belt | Code 'GESTALT'⁠⁠⁠⁠ ⁠⁠⁠⁠Dynamic Disc Designs | Code 'GESTALT' --- Support this podcast: https://podcasters.spotify.com/pod/show/gestalt-education/support

Timeless Diamonds and Incoming Pearls from David Holmes, Jaydee, Bobby Kondors, Raven Flowers. Drops, fills, voice bits, lickshots & effects bringing the personalised touch & original flava flex, edits and extended versions pushing the do more vibe. Creating new Fusions, Birthing new Genres, Dj Culture dedicated. This Is Dub Intervention. Tune into new broadcasts of Dub Intervention, Saturday from 8 - 10 PM EST / 1 - 3 AM GMT (Sunday).For more info visit: https://thefaceradio.com/dub-intervention///Dig this show? Please consider supporting The Face Radio: http://support.thefaceradio.com Support The Face Radio with PatreonSupport this show http://supporter.acast.com/thefaceradio. Join the family at https://plus.acast.com/s/thefaceradio. Hosted on Acast. See acast.com/privacy for more information.

Today's episode took place during the 1st ever Neurodynamics World Congress. It was also our first time attempting a true integration conversation with two different schools of thought. This episode features Dr. Antonio Stecco from Fascial Manipulation and Michael Shacklock from Neurodynamic Solutions. We discuss where these two systems fit together and Michael Shacklock asks a clarifying question following Dr. Stecco's lecture. Let us know what you think of this new format and enjoy the episode. Show Notes Upcoming Courses⁠⁠⁠ ⁠⁠⁠Human Locomotion.com | Code 'GESTALTEDUCATION10'⁠⁠⁠ ⁠⁠⁠Core360 Belt | Code 'GESTALT'⁠⁠⁠ ⁠⁠⁠Dynamic Disc Designs | Code 'GESTALT' --- Support this podcast: https://podcasters.spotify.com/pod/show/gestalt-education/support

OCT 18TH Rewind featuring the below matches. Matt Cardona (with Saint Laurent) vs. 1 Called Manders Bomaye Fight Club vs. The Mane Event Ichiban vs. Love, Doug 2 title changes! Big returns! Shocking debuts! Slaughterhouse forever changed MLW. What's next? Find out on Fusion! MLW has TRIPLED its security tonight following a wild Slaughterhouse post match brawl between World Titan Federation Superstars® and the Bomaye Fight Club... as well as a second dust-up after the show with Mance Warner and these self-proclaimed “Superstars.” With security maxed out, the World Titan Federation's “Crown Jewel” Matt Cardona steps in the ring in the main event as he looks to put World Champion Alex Kane on notice and keep the eyes of the league on him. But is Cardona alwayz ready for one of the toughest brawlers in MLW? He'll have to be as Cardona battles the 1 Called Manders. Meanwhile, Mance Warner has put it out on social media he has been doing some drinking and thinking and he has plans to confront Cardona, following their after show dust-up as well tonight! Is there enough security to keep MLW fighters from the Superstars® of the World Titan Federation tonight?! For the first time in 2 years “Filthy” Tom Lawlor is back on FUSION… and he has a shocking change in store for his filthy fans. What is it? Watch to find out. Journey to the Atlanta fight camp of World Heavyweight Champion Alex Kane. The fight captain speaks out on the World Titan Federation and the Slaughterhouse brawl. Following the extraordinary events at Slaughterhouse, Salina de la Renta promises BIG NEWS on Fusion! What's next for the “Empresaria of Lucha” as her conquest of MLW continues? Tony Deppen and TJ Crawford's continuous smear campaign against the injury sidelined Kevin Blackwood forces the league to take further action against the dangerous duo. Will security be able to keep the World Titan Federation Superstars® and Bomaye Fight Club apart? They'll be tested as Mr. Thomas tags up with The Bomaye Fight Club's newest middleweight recruit J Boujii as they fight The Mane Event! In a middleweight eliminator, Ichiban represents the NumberOneDojo against wrestling's cupid: Love, Doug. Oct 26th REWIND Featuring the below, Salina de la Renta, who serves as special executive producer of this week's FUSION, has issued the following preview: The Empresaria of Lucha Libre shares her divine vision of Major League Wrestling in a must-see broadcast unlike you'll see with any of these pendejo billionaire promoters (and trust me they are watching this episode and taking notes!). For the first time in broadcasting history, MLW cameras take you neckbeard gringos to the most famous arena in all of lucha: the “Cathedral of Lucha” Arena Mexico! Promociones Dorado's Rocky Romero fights Volador Jr. for the CMLL World Historic Welterweight Title. See 18,000 glorious Mexican fans watch a super lucha clásico! But wait: there's more. Since I have matchmaking powerI will have a biiiiig announcement for FIGHTLAND on FITE+. What could I ever do with such power? For the first-time you'll be enlightened by the words of your new World Featherweight Champion Janai Kai as she makes her first statement as champion… and trust me, the “Kick Demon” is a voice of wrestling that demands you listen! I've also personally invited the World Heavyweight Champion Alex Kane be in attendance. Does he have anything else in his vocabulary beyond “bumblebeeyee”? I highly doubt it. But let's find out! Oh, and that little rat Ichiban has been pestering me for a title fight against my new World Middleweight Champion. Should I stick him in a match or call pest control? PLUS: The greatest voice in lucha libre, Jesus Rodriguez, will serve as master of ceremonies for the evening! So, now that you know tonight's FUSION, do yourself a favor: Tap your phone and set a reminder with those sweaty gordito digits for 8pm tonight. You won't regret it!! Bwahaahahaha Check the LINK TREE BELOW for more content and Merch https://linktr.ee/StraightTalkWrestling​  

CJ has 8 siblings and his family is the most important thing in his life. He's a serial entrepreneur and one of the founders of Nature's Fusions, a full-service manufacturing company that services the essential oil, cosmetic, and supplement space. He also sits on the Board of Directors for the Rollins School of Entrepreneurship at BYU and assists students as they launch their own companies. His passion, however, lies in the tangible bits of history. A book collector for his entire adult life, CJ now owns a bookstore and art gallery (Artifacts of History and the Artifacts Gallery) at the Provo Towne Centre Mall.

The number of spinal fusions performed in Australia has skyrocketed over the past few decades, with the number of privately funded procedures far outstripping those done in the public system. Spinal fusions, which help stabilise the spine by surgically joining two or more vertebrae together, can be used following traumatic injury, or to help correct scoliosis in children. But the most common use for spinal fusions is in degenerative conditions of the spine. This episode of The Medical Republic Podcast explores when this procedure should be considered, and why we are seeing such a large increase in the number of these procedures being performed. Dr Ashish Diwan, director of the Spine Service at St George Hospital in New South Wales, says there are several considerations to be weighed before undertaking a spinal fusion, including the duration, intensity and frequency of back pain; whether other treatment options have been tried; and what the patient wants. Dr Diwan has sympathy for GPs with patients who are considering undergoing a spinal fusion, which is far from a straightforward decision: “It's like trying to get married. If you're in doubt, don't do it.” The decision not to do surgery can be equally challenging, according to Dr Diwan. “There is also an incredible lack of evidence as to what you do for a person who continues to suffer. The alternatives [drugs, spinal cord stimulators or radiofrequency ablations] are not very clear … none of them stack up when you start dealing with people who have pain of a chronic nature.” There are many reasons for the spike in the number of spinal fusions being performed, according to Professor Ian Harris, an orthopaedic surgeon and researcher from the University of NSW. “There is an aging of the population, but [now] there are more so called ‘indications' for spine surgery,” he tells the podcast. “The techniques of doing them have developed in a way that there's now lots of different ways you can do spine fusions.” Several reasons also exist for why more privately, rather than publicly, funded procedures are being done. But Professor Harris feels the inclusion of MRI scans on the MBS is glaringly obvious one. This presents a fine line to walk between using imaging to rule out potential pathologies and jumping at shadows and operating unnecessarily on age-related changes. This reinforces the need for clear discussions with patients about any imaging findings. “Just having a scan doesn't hurt anyone. It's what you do with the results that can harm people.” Hosted on Acast. See acast.com/privacy for more information.

Geoff, Gavin, and Andrew talk about poop game, shit shades, pink eye, juice lab, sleep spaghetti v2, the Panton collection, mystery injuries, gems of war achievements, mouth tape food poisoning, flammable farts, Andrew's realization of seasons, Geoff's morbid American history, and the new flavors taste test. Sponsored by Hello Fresh http://hellofresh.com/50face code 50face , Shady Rays http://shadyrays.com code FACE , Better Help http://betterhelp.com/face Learn more about your ad choices. Visit megaphone.fm/adchoices

Join Ivy and Daria as they watch and talk about Cry for Help and cover such topics as Daria's opinion of Sardonyx, how fusion works between a Fusion and a single Gem, Amethyst and Steven's role in the episode, the issue with Sugilite, Sardonyx's awareness of the fourth wall, the Crying Breakfast Friends parallels, the danger of Peridot, Pearl's rationalisation of her awful betrayal, Garnet failing to see Pearl's motivation with her Future Vision, and Amethyst's first solo. Probing Question: Do you think there's any rhyme or reason to how many eyes and limbs Fusions get? Today's recipe: None. Today's merchandise: Crying Breakfast Friends shirt, Steven Universe Plush Keychain (Series 1), and Night Lion. Follow us on Facebook: https://www.facebook.com/notsogiantwomen Follow us on Twitter: https://twitter.com/NotSoGiantWomen Watch the video version: https://www.youtube.com/watch?v=cQx98oKtCZo

​ @mlw  has a new landscape after #neversaynever with a new Heavyweight ad Tag team champions, as wellas the opera cup starting, corwning a new #1 contender and more we disccus last weeks and this #mlw fusion as we bring you a rewind first....#thedoubleshot MLW July 13th Matches * John Hennigan vs. Willie Mack vs Lio Rush - #1 Contenders Challenger * Delmi Exo vs. Taya Valkyrie - World Featherweight Championship Rematch * Ken Broadway vs. TJ Crawford  MLW July 20th Matches * Davey Boy Smith Jr vs Calvin Tankman - Opera Cup Stage One * B3CCA vs Billie Starkz * Plus MORE! Check the LINK TREE BELOW for more content and Merch https://linktr.ee/StraightTalkWrestling​  

JCO PO authors Dr. Michael J. Kelley and Dr. Katherine I. Zhou share insights into their JCO PO article, “Real-world Experience With Neurotrophic Tyrosine Receptor Kinase Fusion–positive Tumors and Tropomyosin Receptor Kinase Inhibitors in Veterans.” Host Dr. Rafeh Naqash, Dr. Kelley, and Dr. Zhou discuss the robust Veterans Affairs (VA) National Precision Oncology Program (NPOP), accurate identification of gene fusions, and toxicities landscape of TRK inhibitors. Click here to read the article! TRANSCRIPT Dr. Rafeh Naqash: Hello and welcome to JCO Precision Oncology Conversations, where we bring you engaging conversations with authors of clinically relevant and highly significant JCO PO articles. I'm your host, Dr. Rafeh Naqash, Social Media Editor for JCO Precision Oncology, and assistant professor at the OU Stephenson Cancer Center in the Division of Medical Oncology.   Today, I'm thrilled to be joined by Dr. Michael J. Kelley. Dr. Kelley is the executive director of Oncology for the Department of Veterans Affairs. He's also the chief of Hematology-Oncology at the Durham VA Medical Center, and also a Professor of Medicine at the Duke University School of Medicine. And he's also a member of the Duke Cancer Institute. We are also joined by Dr. Katherine I. Zhou who is a Hematology-Oncology fellow at the Duke University. Dr. Zhou also spent time at the Duke Medical Center as part of her fellowship training, which I believe is how this project that was led by her came to fruition.  So thank you both for joining today. This is going to be, hopefully, of very high interest to our listeners and I look forward to chatting with you both. Dr. Michael Kelley: Great, thanks for having us. Dr. Katherine Zhou: Thank you for having us. Dr. Rafeh Naqash: Thank you so much for joining. So I was very intrigued with this paper, and this paper follows a recent podcast that we had with Dr. Alexander Drilon, who's led some of the NTRK tropomyosin receptor kinase inhibitor studies that have been published in the last several years. And we had a very interesting discussion a couple of weeks back and I felt this was going to be a very interesting subsequent discussion into what was also an interesting discussion with Dr. Drilon. So what caught my attention is obviously the fact that you guys in this report, which is a real-world report, did not exactly see what we generally expect from clinical trials as far as response to target therapies in NTRK fusions.  So before I ask you questions related to this project, one of the very interesting things at least I found was the fact is that the Veterans Health Administration is the largest integrated health system. Studies, whether conducted in the UK, for that matter European countries, or in Canada, they have integrated health systems which we do not. But we do have this advantage of the VA trying to do things in a very unique, centralized manner. So I wanted to ask Dr. Kelley first, how is it that you have implemented this National Precision Oncology Program, the NPOP as you call it, into the VA precision medicine workflow and how does it help in conducting research studies like the one that you published in the JCO Precision Oncology? Dr. Michael Kelley: Yeah, thanks for that question, Dr. Naqash. The NPOP started in 2016 as a national program and right from the beginning it grew out of an effort that was a joint collaboration between both clinical operations in the VA and the Research Office or the Office of Research and Development. It was designed from the very beginning to support discovery, new knowledge generation, and identifying patients for clinical trials in addition to bringing them best-in-class molecular testing and a consultation service.  So it was initially funded out of the Cancer Moonshot 1 in 2016 when President Biden was then Vice President. The VA endorsed the model going forward in 2019 and now it's continued on and grown even bigger, it's expanded both in terms of scope and the complexity of the testing that's been done. So it was offered as services to facilities. They didn't have to do this, but I think they all saw the value of using NPOP to provide this group of services and that's what led to the generation of the robust underlying dataset that Dr. Zhou has used for this paper. Dr. Rafeh Naqash: Definitely. Thank you so much for that explanation. I did not know, and was not well aware, of how robust this program is. So I think it's a great learning opportunity for our listeners to know that a program like this exists. As we all know, there are different platforms, sequencing platforms, that each institution uses, whether it's commercial or whether it's in-house based. But the fact is, until and unless we have big pool datasets like the ones that you have generated or have access to, it's not easy to answer real-world questions.  So first of all, I'd like to congratulate you and the rest of the VA administration to set up a program like this that hopefully is helping in matching the right patients to the right therapies and in clinical trial approvals. Now, before we take a deeper dive into the study that Dr. Zhou led, I did want to ask you, you have access to this amazing centralized platform, what are the kind of sequencing strategies or platforms that you use as part of this program? And is there an incorporation of molecular tumor boards to help understand some of these sequencing results that sometimes can be a little complicated to understand even for oncologists who look at these reports on a daily basis? So could you tell us a little bit more about that, Dr. Kelley? Dr. Michael Kelley: Yeah, certainly. So the VA contracts for the sequencing service, currently we're contracting with Foundation Medicine and Tempus for the comprehensive genomic profiling. There are some other services, and before we started using Foundation, there were two other companies that we used. There is a molecular tumor board. Our molecular oncology tumor board is designed primarily for case-based education. But there's also an asynchronous on-demand consultation service that occurs electronically because we have a unified electronic health record system. So any oncology provider in the country can enter a request through what's called an interfacility consult. It comes to a team, that team vets that, discusses it with the appropriate experts; that includes molecular oncologists, molecular pathologists. A lot of oncology pharmacists have been trained at a course that's at the University of Kentucky.  And we have a lot of experience in doing this since that service was set up in 2016 as well, right from the beginning, because we understood the complexity of the data and the need for every oncologist across our enterprise to have access to the very best interpretation of that.  We also have educational sessions that are integrated into the molecular tumor board time slot we call primers in terms of the underlying science of why you do the interpretations the way you do. And then there's also some additional education that we'll be endeavoring to offer to our staff and our oncologists coming up this year. Dr. Rafeh Naqash: Excellent. It sounds like you definitely have taken this into a very multidisciplinary approach where you're incorporating oncologists, pharmacists, and perhaps even genetic counselors and then, obviously, keeping the patient at the center and trying to find the best possible therapies that are most relevant for that individual.   Now, going to Dr. Zhou's study here. Dr. Zhou, first of all, it's great to see a fellow lead a study and then especially, I think you're our first fellow on the podcast. We've had a lot of different individuals, but we have not had a fellow before. So thanks for coming.  Could you tell us, for our listeners, what drove your interest into NTRK fusions? As we know, they are rare, something that is not commonly seen, and we do have clinical trial data in this space. So what was the idea behind looking at a real-world data set? Did you start out with a hypothesis or were you just interested to see how targeting these fusions in the real-world setting, actually, what kind of results does it lead to? Dr. Katherine Zhou: Yeah, well, first of all, thanks for the question. And I do just want to mention that although I did sort of bring this project to the finish line, it was started by another fellow, Vishal Vashistha. So just wanted to mention that. And I think the interest was really just that NTRK is such a rare fusion and just a difficult one to be able to study, like you said, in the real-world setting. And we have the advantage of having so much data through the VA and through NPOP, specifically. And so having seen such great results with the TRK inhibitors and clinical trials, I think there's this big question of how that translates into the real-world setting. We have the ability to do that with our large patient population. Dr. Rafeh Naqash: Excellent. And again, it's nice to acknowledge the support that you had from the other individual who co-led this study. Now, since you would have, I'm guessing, done most of the analysis here and looked into the whole idea of the kind of results that you saw—and from my understanding, you looked at the entire VA data set and tried to understand first the incidence or frequency of NTRK fusions and also responses to treatment, which I think is the main message—but could you tell us a little bit more about the data set? How did you acquire the data set, and what it took to analyze? Because obviously every project has a very unique story, and I'm guessing there's one very unique story here, since as a fellow you have limited time to do all this interesting work. So how did you navigate that and analyze and work with some of the things that you had to look at to get to the results? Dr. Katherine Zhou: Yeah, so again, this was work that was done with multiple people involved, of course. And we used what we had, the resources we had available, some tools we had available through the VA. So first, looking at NPOP and looking at patients who are sequenced through NPOP, we could just find all the ones who had an NTRK rearrangement of some kind. The second way we went about finding patients was through the CDW or the Corporate Data Warehouse where we could see which patients were prescribed larotrectinib or entrectinib and kind of go backwards from there and see which of those patients had NTRK alterations or specifically NTRK rearrangements. And so we combined the patients from both of those different methods to come up with our cohort at the end of 33 patients with NTRK rearrangements and 12 patients who are treated with TRK inhibitors. Dr. Rafeh Naqash: Excellent. Could you walk us through what was the subsequent analysis as far as how many NTRK fusions? I know you mentioned in the paper about DNA versus RNA-based testing. So how many were DNA-based, how many were RNA-based? I think there's some element of ctDNA-based testing also, or what tumor types those people had so that we get an understanding of what's the landscape of the findings that you had. Dr. Katherine Zhou: Sure. Since this is a real-world setting, as you may expect, the vast majority of the sequencing was done through tissue DNA sequencing, and that was the case. So for the 25 patients who were sequenced through NPOP that we found who had NTRK rearrangements, 23 of them had tissue DNA sequencing. And then one was tissue DNA RNA, and one was cell-free DNA sequencing. And so using that and being able to go back and look at how many patients have been sequenced in NPOP in total, we could kind of come up with a yield, although the numbers are very small. But we do see that there does seem to be probably a lower yield, for example, with cell-free DNA sequencing, as one might expect.  And then looking at our total group of 33 patients, if we look at what types of cancers they had, we did have quite a few patients just based on prevalent tumors at the VA, I think, and in the population, prostate cancer was common, lung cancer, and then we had smaller numbers of colon and bladder, and I think there's a pancreatic cancer patient. We did have some of these rarer tumor types that more commonly have NTRK fusions as well, so like papillary thyroid carcinoma, and salivary gland cancers as well as soft tissue sarcomas. Dr. Rafeh Naqash: Question for you, Dr. Kelley, related to this data set: do you think that given that the denominator that you have is a unique population, the VA population, that's often males, they're usually above the age of 18, could the frequency have been influenced by that denominator where you may not have been able to capture, let's say, some of the rarer tumors that happen in the younger patient population, for that matter? Could that be a little bit of a bias here?  Dr. Michael Kelley: Definitely. The population of veterans that have cancer that is treated in the Veterans Health Administration do represent generally adult males in the United States, but there is some skewing in certain regards. One of them is towards a higher frequency of smoking status. So not current smoking, which is actually about the same as the national average of about 11%, but the former smoking rate is about twice as high as it is in the rest of the United States. So we may have a lower frequency of some actionable variants in cancers in general because there's a higher etiological role for tobacco smoke in our population. But overall, looking at adult men if we look at like EGFR mutations, our incidence of EGFR mutations in adenocarcinoma is similar to what is reported in other real-world evidence bases from the United States, which is significantly lower than that which is found in academic medical centers. Dr. Rafeh Naqash: Thank you. I'm a big fan personally of real-world data sets. I do a lot of this with some other collaborators and generally, I do phase I trials, which is why I'm interested in precision medicine. And two weeks back, actually, I had a patient with prostate cancer, who ended up having NTRK fusion on a liquid biopsy. Now, you do talk about some of this related to in-frame or out-of-frame fusions and how that can have interesting aspects related to the kinase domain functionality and RNA expression. Dr. Zhou, for the sake of our listeners, could you briefly describe why understanding some of that is important and what implications it has? Dr. Katherine Zhou: Yeah, so I think the oncogenic NTRK fusion that we think of and that's being targeted by the TRK inhibitors is a fusion 5-prime of a protein that forms a dimer and on the 3-prime end is the kinase domain of the tropomyosin receptor kinase. And so you have to have some kind of a gene fusion that results in not only the transcription of that RNA fusion, RNA transcript, but then the translation of that fusion protein. So that needs to be, like you mentioned, that has to be in frame so that the entire protein is translated and expressed and it needs to include the kinase domain. It can't be the other end of the NTRK gene. And both of the genes need to be in the same orientation, of course. And then also the partner gene probably matters in that the ones that we know that actually cause activation of this oncogene are the ones that sort of spontaneously dimerize. And so that's a lot of requirements that we don't necessarily see when we just get, for example, a DNA sequencing result that says there's an NTRK rearrangement. Dr. Rafeh Naqash: Excellent way to describe the importance of understanding the functionality of the activated oncogenic fusion. Now, I know here in most of the patients that you have is DNA sequencing and I'm sure you'll talk about some of the results. And when you connect the results to the kind of data that you have, do you think not having the RNA assessment played a role in not knowing perhaps whether those fusions were functionally active?  Dr. Katherine Zhou: Yes, I think we can't know for sure without having the RNA sequencing data. But certainly, that is a pattern in our small number of patients that we saw and something that makes sense just in terms of the mechanism of this oncogenic fusion protein. So I think that is a question of when should we be doing RNA sequencing to confirm that a fusion that we see on DNA sequencing is actually transcribed into RNA and how do we use RNA sequencing in a cost-effective and useful way to be able to detect more of these NTRK fusions that are actually clinically relevant. Dr. Rafeh Naqash: I absolutely agree with you and this is an ongoing debate. I know some platforms, commercial platforms that is, have incorporated RNA sequencing both bulk or whole transcriptome as part of their platform assessments, but it's still not made inroads into some other sequencing platforms that are commercially used. So it's an ongoing debate, but at the same time helping people understand that certain fusions need some level of RNA assessments to understand whether they're functionally active or not. Which again has implications, as you pointed out in terms of therapies are extremely relevant.   Now, going to the results, which again was very interesting, could you tell us about the findings from the therapeutic standpoint that you observed and what your thoughts are about why you saw those results which were very different from what one would have expected?  Dr. Katherine Zhou: Right. So in the clinical trials of larotrectinib and entrectinib, there were quite high objective response rates on the order of 60%, 70%, even almost 80%. In our very small real-world group of 12 patients who were treated with TRK inhibitors, nobody had an objective response and five patients had stable disease and everybody else, the other seven patients, progressed.  And so the question is why did we see such a big difference compared to the trials? I sort of think of this as two big buckets. One is the population that we were looking at. So this is a real-world population. For example, in the clinical trials, there were almost no Black or African American patients, whereas here we had about 30%-40% Black or African American patients.  Because it's a VA population, it was very heavily male, of course, the age groups are also different in that we didn't have children in the VA population whereas children were included in the trials. And the tumor types also differed because I think in the trials, which makes sense, there's a bias towards tumor types that have more NTRK fusions, and some of the tumor types we were looking at are just common tumor types like prostate and lung cancer where NTRK fusions are not common. But just because there are so many patients with these cancers, we did see them. And so certain of these groups, particularly certain racial and ethnic groups as well as certain tumor types, were not really represented in the trial to the extent that we can make conclusions about whether TRK inhibitors are effective in this population. So that's one.  The second part, I think we've already talked about some, is just the method of detecting these NTRK fusions and how many of these NTRK fusions were actually truly producing oncogenic fusion proteins. And I tried to sort of categorize some of these fusions as being canonical in that they've been more studied. We know the partner gene, they are known to produce an oncogenic protein and to respond to TRK inhibitors. But actually of the four patients who had what we called canonical fusions, all four of them had stable disease at least, whereas the ones that were noncanonical mostly did not have a response or have even stable disease and mostly just progressed. And so then you wonder whether they even had the actual target protein we thought we were targeting. So this is where the real-world setting we're not doing the RNA sequencing or this additional testing to confirm that it's an oncogenic fusion protein. Dr. Rafeh Naqash: And I do see in your results there's a patient especially—you pointed out canonical and noncanonical fusions—you have a patient with a papillary thyroid cancer that I believe had a stable disease for close to two years plus. Is there anything interesting apart from an NTRK fusion in that specific patient where certain co-mutation could have played a role or certain other factors that do you think played into the fact that this patient had stable disease but didn't respond on the TRK inhibitor? Dr. Katherine Zhou: I don't have a great answer for that. I think this is one of the cancers that was well represented in the trials and that commonly has NTRK, or more likely has NTRK fusions. And this was a well-studied canonical NTRK fusion. So I think those are all reasons. The question of co-mutations I think is really interesting. We didn't have the data for every single patient, but for the ones we looked at a lot of the time, NTRK fusions are mutually exclusive with other driver mutations. So we didn't see a whole lot of commutations that we could sort of differentiate between responders or stable disease and progression.  Dr. Rafeh Naqash: Thank you. Going to the toxicities, as a phase I trialist myself toxicity is the bane of my existence where we have to label toxicities, attribute toxicities, understand toxicities. The trial, obviously, as you very well know, that in the trials, they didn't have a lot of toxicities that caused patients to come off or required significant dose reductions, which is not the case compared to what you saw. Could you tell us a little bit about the landscape of toxicities for TRK inhibitors and what you saw in your cohort? That, again, I feel was interesting.  Dr. Katherine Zhou: Of the 12 patients, I think two-thirds of them had either dose reduction or interruption or discontinuation, or some combination of the above. The toxicities we saw were more common than, or at least led to discontinuation and interruption and dose reduction more commonly than in the trials. But the toxicities we saw were also seen in the clinical trials. So LFT elevations, creatinine elevations, neurotoxicity, some cytopenias. We didn't actually see a whole lot of that, but those were present as well, and then some sort of nonspecific things like fatigue. And so, as much as we could tell from retrospective trial review, at least these were severe enough to lead to holding the drug. Dr. Rafeh Naqash: Thank you so much, Dr. Zhou. Question for you, Dr. Kelley. Putting this into perspective, the analysis that you did, how would you connect it to other real-world questions that one could answer using these kinds of data sets? So basically, what are the lessons learned from this amazing program that you guys have run successfully and are, I'm guessing, expanding in different directions? And how can you use a program like this to look at some of these unique questions using real-world data sets? Dr. Michael Kelley: There are a couple of, I guess, next steps for us that are based off this study and other information that we've gotten in other analyses from our NPOP data set. So, first of all, access to an RNA-Seq test. So that has been resolved to some extent, in that we now have two options for comprehensive genomic profiling, one of which does have RNA-Seq.  And then the other approach that we're doing is to do more robust data generation. So we're going to be launching a study to collect prospective data on patients who are treated with off-label drugs. And as part of that, we will also have an on-label cohort for rare populations or any investigator in the VA who's interested in a particular drug or a particular genetic variant. They'll be able to tie into this protocol, and we will then collect data from across the system prospectively, which we think will improve the quality to some degree.  And then thirdly, I think there's an opportunity to merge the initial generation of data in rare genetic types or other populations, which are highly selected by doing a distributed type of clinical trial where patients can be enrolled in prospective treatment trials. So we're not just generating data based on their real-world exposure to FDA-approved drugs, but we're generating data as we're developing the new drugs, we can have a much more heterogeneous and representative population of patients enrolled in clinical trials. So this is called the decentralized clinical trial model. We're starting to launch some trials with industry partners in this area to test out the model. If it works, I think we'll be able to help contribute to the knowledge that we all can use in terms of the patient types, the patient characteristics, but also some of the different tumor characteristics, and also to bring clinical trial opportunities to a more representative group. A lot of the initial clinical trials are done in urban areas, rural populations in VA are about a third of our patients live in rural areas, compared to only 14% of the country. So we think this is a very important diversity issue that should be addressed. Those are some of the ways that we're taking a lesson from this trial and other data that we have to sort of bring it forward. Dr. Rafeh Naqash: Those are excellent next steps and I think the kind of work that the VA is doing and this specific program, Precision Oncology Program, the NPOP program is doing, it's definitely setting up a unique standard in the United States where we have been limited by not having a centralized database. So setting something up of this sort hopefully will help answer a lot of these unique, interesting questions as you have access to data. And then the fact that you mentioned decentralized clinical trials and trying to cater to this access issue for patients in the VA system, I think that would be huge.  And again, I congratulate you and your team on these efforts, and once again, thank you for joining us today and making JCO Precision Oncology a destination for your interesting work. We hope to see more of this work subsequently and hopefully, I get a chance to talk to you more about all the exciting stuff that you guys are leading within the VA health system.  Thank you for listening to JCO Precision Oncology Conversations. Don't forget to give us a rating or review and be sure to subscribe so you never miss an episode. You can find all ASCO shows at asco.org/podcast.  The purpose of this podcast is to educate and inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions.   Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Bios: Michael J. Kelley, MD, is Executive Director of Oncology for the Department of Veterans Affairs, Chief of Hematology-Oncology, Durham VA Medical Center, Professor of Medicine at Duke University School of Medicine and Member of the Duke Cancer Institute. Katherine I. Zhou, MD, PhD is a hematology-oncology fellow at Duke University. She also spends time at the Durham VA Medical Center as part of her fellowship training. COIs: Michael J. Kelley, MD Research Funding: Novartis (Inst), Bristol-Myers Squibb (Inst), Regeneron (Inst), Genentech (Inst), EQRx (Inst) Katherine I. Zhou, MD, PhD: No disclosures  

As biomarker testing can play a critical role in the diagnosis of rare cancers, such as NTRK gene fusion-positive cancers, hear what care teams need to know about identifying patients who may be eligible for this testing. In this episode, CANCER BUZZ speaks with Eric Konnick, MD, MS, associate professor of Laboratory Medicine and Pathology and associate director of Genetics and Solid Tumor Laboratory at the University of Washington Medical Center Fred Hutch Cancer Center about the importance of testing for NTRK gene fusions. “It's really important to test our patients for these [NTRK gene fusions] because there are very effective treatments now that can have dramatic effects on the outcome of these patients' disease course, so identifying patients that can be eligible for therapy is critical…” - Eric Konnick, MD, MS This is the first episode in a four-part podcast series developed in connection with the ACCC education program Emerging Biomarkers: Innovative Therapies for NTRK Gene Fusion Testing and was made possible with support by Bayer. Dr. Eric Konnick, MD, MS Associate Professor of Laboratory Medicine and Pathology Associate Director of Genetics and Solid Tumor Laboratory Director of Genetics Preanalytical Services Fred Hutch Cancer Center, University of Washington Medical Center Seattle, WA         Additional Reading/Sources: ·       Emerging Biomarkers: A Spotlight on NTRK Gene Fusion Testing (accc-cancer.org) ·       NTRKers Patient Community & Support (ntrkers.org) ·       NTRK Gene Fusion Infographic (ntrkers.org) ·       NTRK fusion-positive cancers and TRK inhibitor therapy

In This Episode, We Chat About: How we can teach our kids differently, from school to the example we set for them! The power of taking the time to understand the needs of each of your kids and getting the support to get them what they need. Resources + Links:  Follow Fusion Academy on Instagram @fusion_academy Learn more about Fusion Academy https://www.fusionacademy.com/   Learn more about our coaching services & upcoming events: https://www.girlsmentorship.com/   Join Girls Mentorship on Geneva https://app.geneva.com/invite/4fbd7746-217d-497d-853d-50386b9a2ed2   Connect with us on Instagram: Girls Mentorship | @girlsmentorship Jill Petersen | @jillphxsen Mary Frances | @msmaryfran   Join our Facebook Community | Girls Mentorship   Show Notes: I feel like we needed to start this episode with a team cheer! I guess we kind of do in the way we bring the energy, and today's guest showed up with mic drop moments around parenting and giving your kids the community, support, and resources they need! In this episode, we chat with our friend and Director of Outreach at Fusion Academy, Clarissa Abijaoude. We talk about the power of being in community, seeking out resources and camps that meet your kids needs, and modeling that healthy people ask for what they need. A motto we are a fan of every family adopting is “same team” mentality. There is so much gold in this episode about how to put that same team motto into practice in your home and every community you engage in!   04:00 Meet mama of two, and Director of Outreach at Fusion, Clarissa Abijaoude. 09:00 What is Fusion and how do they work as a 1-to-1 school? 15:15 Why we need to stop resisting asking for help and get the relief and support we need. 19:15 What pushback or hesitancy do you see around Fusions 1-to-1 model? 24:20 More details on the upcoming summer camp we have for your girls! 27:00 How are you empowering your kids with the resources and support they need? 33:30 Are you cultivating a “same team” mentality in your family and communities you are part of? 37:00 The power of asking for help and modeling that for your kids. 44:15 Do the hard thing and you can have an easy life. Do the easy thing, and have a hard life. 47:00 What has been your biggest WTF moment that you turned into a lesson? 50:00 How can you get involved in Fusion?

New scientific discoveries in physics and cognitive sciences confirm that consciousness is not merely the byproduct of our evolutionary biology but at the most fundamental level of the universe. This only confirms what people with strong faith already know: that consciousness has the power to influence external events in accordance with the will.   Learn more about the theory of consciousness, quantum theory, decorated permutations, and the software beyond the spacetime headset in this special episode of the Super Entrepreneurs Podcast. And what's even more important about this episode is the fact that you'll be among the first entrepreneurs to reach this knowledge and what it means in terms of doing business.   Who Is Donald Hoffman? Prepare to have your mind blown by the multi-talented Donald David Hoffman! Not only is he a renowned cognitive psychologist, but he's also a popular science author who can make the most complex concepts easy to understand. Currently, Don Hoffman is a professor in the Department of Cognitive Sciences at the University of California, Irvine, where he holds joint appointments in the Department of Philosophy, the Department of Logic and Philosophy of Science, and the School of Computer Science. This man is a true academic superstar! Make sure to watch his Ted Talk, titled “Do We See Reality?” after this episode. And now, he's Shahid's guest to explain all the interesting stuff he knows with the Super Entrepreneurs family! How is Donald Hoffman Super?   Donald Hoffman is super because he fully understands that we are not merely random objects in spacetime, but divine beings who channel the eternal consciousness of the ALL in the world of the senses. We create the universe as much as we're created by the universe.   Shahid Durrani's Key Insight:   This episode was enlightening to Shahid because it opened up a new horizon in terms of how to think about the universe. This new horizon opens up new vistas for entrepreneurs because we're the ones who pioneer everything. The new technology that will develop with these new scientific discoveries will change everything about how we live.   The same happened when Faraday and Nicola Tesla developed the technology that gave rise to modern communication technology.   Chapter Stamps:   00:00 Introductions: Who is Donald Hoffman and what is consciousness research? 00:44 Consciousness is hard to pi point by researchers (What is consciousness?) 05:35 Conscious agents and network information theory (Higher Intelligence) 10:16 The Large Hadron Collider of CERN (structures outside spacetime) 13:03 Decorated Permutations and the theory of consciousness 15:09 What's outside spacetime? ( and what's in it for entrepreneurs?) 18:13 The technology of the post-spacetime paradigm 19:12 Fusions of consciousness 22:25 Who won the 2022 Nobel Prize in physics and why? 29:05 Innermost superpower: We're not just objects in spacetime 32:20 What happened after we discovered electro magnetism 34:00 Final words   Pullout Quotes: “Spacetime (...) is just like a virtual reality headset.” “Once you get outside the headset, you start to be able to understand the software that's driving the virtual reality game in the headset.” “Working our way up.” “The moon only exists when you look.” “(we are) one consciousness that takes many avatars.”   Socials: Donald Hoffman books: https://www.amazon.com/Books-Donald-Hoffman/s?rh=n%3A283155%2Cp_27%3ADonald+Hoffman Fusions of Consciousness (Scientific paper): https://www.mdpi.com/1099-4300/25/1/129 LinkedIn: https://www.linkedin.com/in/donalddhoffman Twitter: https://twitter.com/donalddhoffman  

In this episode of Lung Cancer Considered, host Dr. Narjust Florez discusses ROS+1 Fusions in NSCLC, including diagnosis, treatment and new exciting research coming down the pipeline. Her guests are: Dr. Lorenza Landi, Director of Clinical Trials Unit: Phase 1 and Precision Medicine at the National Cancer Institute Regina Elena in Rome. Dr. Landi has extensive experience and is interested in targeted therapy in lung cancer with a focus on ALK, HER-2/EGFR positive and ROS+1 lung cancer. Dr. Shirish Gadgeel, Chief of the Division of Hematology and Oncology, at Henry Ford Cancer Institute in Detroit, Mich. Dr. Gadgeel is also part of the Lung Cancer steering committee for the Southwest Oncology Group and he is the Associate Editor of Clinical Lung Cancer and a reviewer for many journals.

In this episode of the Champion League Podcast, the champs attempt to discuss AI but are quickly sidetracked by some goofy fusions. It might be better to watch this one on YouTube lol

By looking back at Breath of the Wild, we can make predictions about Tears of the Kingdom.

Luke and Andrew stumble on an honest-to-gosh mystery outside Luke's apartment window. So they do what any good podcasters do: They get involved.

Go online to PeerView.com/JBE860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Less common genomic alterations such as gene fusions represent actionable and important therapeutic targets in a substantial proportion of patients with non–small cell lung cancer (NSCLC). Although they are relatively rare, it is essential to conduct appropriate biomarker testing to identify these alterations because highly effective targeted therapies have become available that can significantly improve patient outcomes versus older targeted therapies or cytotoxic agents. RET fusion–positive NSCLC is one such example. Next-generation, more selective tyrosine kinase inhibitors (TKIs) have demonstrated remarkable efficacy and improved safety in patients with tumors exhibiting RET fusions. However, testing for these fusions and other less common alterations as well as interpreting reports of testing results can be challenging, which can lead to missed opportunities to offer the best possible therapy to patients who could benefit from them. This educational activity is designed to help professionals involved in the testing and treatment of patients with NSCLC develop their knowledge and skills to bridge the current gaps in the care of patients with lung cancer. Expert faculty provide practical guidance on how to select the correct biomarker testing approach and platform to identify gene fusions and other less common alterations in NSCLC, implement the testing in-house or externally, and decipher the results or interpret the information in send-out testing reports. The experts also share tips and case-based examples of effectively collaborating with multidisciplinary and interprofessional colleagues to identify suitable candidates for the latest targeted therapies matched to the results of biomarker testing and, consequently, positively impact the outcomes of these patients. Upon completion of this activity, participants should be better able to: Describe the role of gene fusions and other less common alterations in NSCLC, importance of appropriate biomarker testing to identify patients with these alterations, and clinical evidence supporting the use of matched targeted therapies to optimize patient outcomes; Implement team-based strategies to identify patients with NSCLC for biomarker testing, select appropriate tests to capture all actionable genomic alterations, and interpret testing results to guide treatment selection; Apply the latest evidence and guidelines to individualize targeted therapy for patients with lung cancers harboring uncommon gene fusions and other alterations; and Educate patients about the role of biomarker testing in lung cancer, risks and benefits of targeted therapies, and importance of selecting optimal therapy based on biomarker testing results and patient needs, values, and preferences.

Go online to PeerView.com/JBE860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Less common genomic alterations such as gene fusions represent actionable and important therapeutic targets in a substantial proportion of patients with non–small cell lung cancer (NSCLC). Although they are relatively rare, it is essential to conduct appropriate biomarker testing to identify these alterations because highly effective targeted therapies have become available that can significantly improve patient outcomes versus older targeted therapies or cytotoxic agents. RET fusion–positive NSCLC is one such example. Next-generation, more selective tyrosine kinase inhibitors (TKIs) have demonstrated remarkable efficacy and improved safety in patients with tumors exhibiting RET fusions. However, testing for these fusions and other less common alterations as well as interpreting reports of testing results can be challenging, which can lead to missed opportunities to offer the best possible therapy to patients who could benefit from them. This educational activity is designed to help professionals involved in the testing and treatment of patients with NSCLC develop their knowledge and skills to bridge the current gaps in the care of patients with lung cancer. Expert faculty provide practical guidance on how to select the correct biomarker testing approach and platform to identify gene fusions and other less common alterations in NSCLC, implement the testing in-house or externally, and decipher the results or interpret the information in send-out testing reports. The experts also share tips and case-based examples of effectively collaborating with multidisciplinary and interprofessional colleagues to identify suitable candidates for the latest targeted therapies matched to the results of biomarker testing and, consequently, positively impact the outcomes of these patients. Upon completion of this activity, participants should be better able to: Describe the role of gene fusions and other less common alterations in NSCLC, importance of appropriate biomarker testing to identify patients with these alterations, and clinical evidence supporting the use of matched targeted therapies to optimize patient outcomes; Implement team-based strategies to identify patients with NSCLC for biomarker testing, select appropriate tests to capture all actionable genomic alterations, and interpret testing results to guide treatment selection; Apply the latest evidence and guidelines to individualize targeted therapy for patients with lung cancers harboring uncommon gene fusions and other alterations; and Educate patients about the role of biomarker testing in lung cancer, risks and benefits of targeted therapies, and importance of selecting optimal therapy based on biomarker testing results and patient needs, values, and preferences.

Moderator: Ron G. Ray, DPM, FACFAS   Panelists: Brett D. Sachs, DPM, FACFAS; Michael A. Gentile, DPM, FACFAS; Matthew E. Williams, DPM, FACFAS   Listen in as the panel discusses managing patients with multiple medial column joint fusions. They talk about expertise needed, techniques and positioning issues, and functional limitations patients may experince following these procedures.   Running time: 43m 41s

durée : 00:28:19 - Les orchestres néerlandais (4/4) : Dissolutions et fusions - par : Christian Merlin - Il y a bien sûr le Concertgebouw d'Amsterdam, que l'on passera pour une fois sous silence. Car on néglige trop le Philharmonique de Rotterdam, l'Orchestre de la Résidence de La Haye, le Philharmonique néerlandais, sans parler de Groningen, Eindhoven ou Arnhem. Un paysage orchestral malmené. - réalisé par : Marie Grout

Chef Tala Bashmi visits Google to discuss her successful culinary career and how she is bringing cuisine from the Gulf region to the forefront of the global food industry. Tala Bashmi started her culinary career by joining The Gulf Hotel Bahrain as a trainee and eventually working her way up the ranks. She studied at the Culinary Arts Academy in Lucerne, Switzerland, where she received her Masters of International Business in Culinary Management. Returning to the Middle East, she joined the cast of Top Chef, Middle East & North Africa, as a contestant, where she finished in the finals and showcased the modernized Bahraini cuisine that she would become famous for. Chef Tala then opened her inaugural restaurant Fusions by Tala in her home country of Bahrain, where she prides herself in her daring and willingness to experiment with a range of ingredients and techniques that come from different parts of the world. Visit http://g.co/TalksAtGoogle/TalaBashmi to watch the video.

Mike and Robbie discuss their latest Rockin' and Coppin' and which Jordan Fusions they would wear if they had to. Watch this episode on YouTube: https://youtu.be/JTl3ZrMy3bM Join our Discord: https://discord.gg/xJFyWmWgza Support the Pod: https://patreon.com/sneakerhistory Subscribe on Twitch: https://twitch.com/sneakerhistory Check out our new Formula 1 show, Exhaust Notes: https://exhaustnotes.fm Check out our new Fitted Hats show, Crown and Stitch: https://crownandstitch.com —–––– EXCLUSIVE DEALS FOR YOU FROM OUR PARTNERS —–––– 10% Off Kicks with Vee Hot Sauce Use Code SNEAKERHISTORY10 for 10% off your order: https://kickswithveehots.com/ 10% Off Sneaker Throne Display Cases: https://bit.ly/snkrthrne Use code HISTORY for 10% off all orders 10% Off at PROSPECT: http://bit.ly/shpdcst Use code HISTORY10 for 10% Off All Orders [Links contain affiliate links, we may receive a small commission if you make a purchase after clicking a link. A great way to support the pod!] —––––—––––—––––—––––—––––—––––—––––—–––– Our podcast is proudly... Livestreamed with StreamYard: https://streamyard.com?pal=6514386237915136 Recorded on Riverside: http://www.riverside.fm/?via=sneakerhistory Distributed By Captivate: https://bit.ly/3j2muPb Follow The Hosts: Robbie https://instagram.com/rahbee702 Mike https://instagram.com/madwatcher789 Rohit: https://instagram.com/rohitm13 Nick: https://instagram.com/nickengvall Livestream Team: Greg: https://www.instagram.com/gregatronx/ Dalton: https://www.instagram.com/sneaker_saiyan/ AJ: https://www.instagram.com/gooberdeluxe Disclaimer: The views and opinions expressed in this program are those of the speakers and do not necessarily reflect the views or positions of any entities they represent.