Podcasts about taxane

Dr. Shannon Westin and her guest, Dr. Bryan Schneider discuss the article “ECOG-ACRIN EAZ171: Prospective Validation Trial of Germline Predictors of Taxane-induced Peripheral Neuropathy in Black Women with Early Stage Breast Cancer” recently published in the JCO and presented at the 2024 ASCO Annual Meeting. TRANSCRIPT  The guest on this podcast episode has no disclosures to declare. Shannon Westin: Hello, everyone, and welcome to another episode of JCO After Hours, the podcast where we get in depth on manuscripts published in the Journal of Clinical Oncology. I am your host, Shannon Westin, GYN Oncology Extraordinaire and also the Social Media Editor of the Journal of Clinical Oncology. And it is my great pleasure to present some really incredible work today that is going to be a dual publication in the Journal Clinical Oncology and a presentation at the American Society of Clinical Oncology Annual Meeting on Monday, June 3. And this is the “ECOG-ACRIN EAZ171: Prospective Validation Trial of Germline Predictors of Taxane-induced Peripheral Neuropathy in Black Women with Early Stage Breast Cancer.” And I am joined today by the senior author on the presentation and the primary author on the manuscript, Dr. Bryan Schneider. He is the Vera Bradley Professor of Oncology, the Professor of Medicine and Medical Molecular Genetics at the Indiana University Melvin and Bren Simon Comprehensive Cancer Center in Indianapolis. Welcome, Dr. Schneider. Dr. Bryan Schneider: Dr. Westin, thank you for having me on today. Shannon Westin: We're so excited and we're really excited to really summarize this incredible work that's being presented today. So, first, let's just levelset. Can you speak a little bit about peripheral neuropathy and the most common causes in patients with cancer? Dr. Bryan Schneider: Yeah, I mean, I think for those of us who treat patients using the taxanes, we recognize probably one of the most important and common side effects that we deal with is peripheral neuropathy, and one that can, I think, impact both quality of life, but also impacts the ability to maintain dose intensity. When we think about risk factors for neuropathy, historically, I think obesity has been reported as a potential risk factor, as has diabetes and other conditions which put people at risk for neuropathy. Shannon Westin: And prior to your work that you'll discuss with us today, what do we know about the incidence of peripheral neuropathy in patients that identify as black? Dr. Bryan Schneider: Yeah. So, interestingly, I think we've recognized that patients who self identify as black have disparate outcomes in terms of inferior survival and more aggressive subtypes of breast cancer, like triple negative breast cancer. But I think the idea of toxicity being a disparate factor as well is probably a more recent one. Interestingly, as we set out to identify biomarkers to predict outcomes in the large adjuvant trial E5103, we weren't really setting out to look at this by race. We were using at that time, genome-wide approaches to identify biomarkers for toxicity and also efficacy. But what was interesting as we did that one of the most important predictors, as we looked across a number of important toxicities, was ancestry. And really the science spoke to us, it was very clear that patients of African ancestry had higher rates of bev-induced hypertension, anthracycline-induced cardiomyopathies and also peripheral neuropathy. Shannon Westin: That's so interesting. We have so much overlap in gynecologic oncology and breast cancer. And I don't know that I've ever seen work like this. And now it's making me very intrigued and making me want to move forward to that. Can you talk a little bit more about this ECOG-ACRIN E5103, like briefly about the study and what it demonstrated specifically? Dr. Bryan Schneider: Yeah. So E5103 was an adjuvant breast cancer trial that really set out to look at the impact of bevacizumab in the curative setting. This was a 5000 patient trial that randomized patients the standard backbone of chemotherapy. So everyone received four cycles of doxorubicin and cyclophosphamide, followed by weekly paclitaxel, and then with or without the addition of bevacizumab. So the parent clinical trial showed, as we know now, bevacizumab didn't add benefit, but certainly this was a fertile ground for us to use genomic markers to try to identify a number of other important factors and predictors. Shannon Westin: And what did you find genomically in that study that led to kind of where we are now? Dr. Bryan Schneider: Initially, what we found is that ancestry was a major predictor of neuropathy. And in that trial we saw essentially a doubling of the risk of grade 2 and above and a doubling of the risk of grade 3 and above neuropathy. When we then looked comprehensively across the genome for common variants that might put patients at risk for neuropathy, we had enough patients in the black population to identify some markers that seemed to differentially predict the risk of neuropathy in the patients of African ancestry. So there we found a variant in the gene FCAMR, which appeared to be protected from neuropathy, and FCAMR is known to have an immune modulatory effect. But importantly, we also found that rare variants, so we did this using an exome wide approach in a gene called SPF2, predicted an increased risk of neuropathy. Now, interestingly, that gene SPF2 is also thought to contribute to a hereditary form of neuropathy, Charcot-Marie-Tooth. Here, what we found, obviously, is that if you inherit two of these variants, you probably have a hereditary neuropathy, but if you inherit one, you may not have neuropathy at baseline, but if exposed to a neurotoxin, much more predisposed to that event. Shannon Westin: That is so intriguing and makes so much physiologic sense. So, can you talk a little bit about how that led to the development of the current study, the objectives design, that type of thing? Dr. Bryan Schneider: Yeah. I think, overarching question and concern is, and we see this with all clinical trials in the United States, is that we're seeing disparate outcomes in a population that are largely underrepresented in our clinical trials. And so one of the first things we wanted to do was really focus on the population that was being disparately affected. So EAZ171 was set out to accrue patients, and in fact, only accrue patients who were self described as a Bck race or African American. So the goal of this trial then was to see if, number one, we could further predict which patients were going to get neuropathy based on our germline genotyping, and then also to better personalize the type of taxane based, again on genomics, but also on the risk of dose reductions, risk of neuropathy, impact on financial toxicity, quality of life, and a number of other, what we felt to be, important clinical variables. Shannon Westin: So let's get into the details. What did you find regarding the incidence of neuropathy in the study, and how was it impacted by the type of chemotherapy the patient received? Dr. Bryan Schneider: Yeah. So the starting point, the primary objective of that study, was to try to validate a high and low risk composite score for neuropathy. And the trial was negative, meaning our genotypes did not predict significantly differences based on the germline genotyping. Now, interestingly, the genotyping did numerically separate, meaning those in the high risk category had about a 12% higher risk of neuropathy, but this did not meet statistical significance. Another major or key secondary endpoint, though, was to look at the type of taxane and its impact in this population. And indeed, what we found is that patients who received paclitaxel had a markedly and statistically significantly higher risk of both grade 2 and above and grade 3 and above peripheral neuropathy. And in addition, we saw more dose reductions, both because of TIPN and all causes in the paclitaxel arm. Shannon Westin: So why do you think you were unable to validate the genomic predictors in the current study? Dr. Bryan Schneider: This is an incredibly important question. So, number one, I mean, we were happy to see the directionality of our preliminary data be correct. But I do think that neuropathy is a very complicated toxicity, and it's probably a multigenic effect, and it probably is also impacted a lot by a variety of clinical factors. So some of the future work we'll be doing is looking at polygenic risk scores and other known genes that may be impactful, and also melding that with a number of really important clinical variables, because I still think we have the potential to predict this ahead of time. Shannon Westin: I know that this was such a patient driven topic, really focused on the patient experience and how to improve not only survival outcomes, but also toxicities and quality of life. Can you speak a little bit about the role of patients in the design of this trial, and maybe with helping it be as successful as it was with accrual? Dr. Bryan Schneider: Yeah. This has truly been one of the most exciting projects I've ever embarked on, and largely because of the incredible team atmosphere and contributions by so many people. Real thanks to the late Worta McCaskill-Stevens and also the late Edith Mitchell, who were two really fundamental disparities experts who really helped motor this trial to where it was. And also our patient advocates and the community at large really were part of the design and part of this from the very beginning, all the way through the publication, I think, have made it a clinically relevant study, and one that I think we're all very proud of. Shannon Westin: Is paclitaxel typically, what is the go-to? Or are more people using, let's say, docetaxel? Dr. Bryan Schneider: I think it depends a little bit on the disease setting and type. And again, is a function of historical clinical trials. One of the pivotal trials, E1199, actually compared a number of these. So it compared weekly paclitaxel to every three week paclitaxel to weekly docetaxel to every three week docetaxel in a two by two design. And essentially the conclusion there is that weekly paclitaxel and every three week docetaxel both outperformed what at the time was a standard of care, every three week paclitaxel. Now, weekly paclitaxel, at least through ECOG-ACRIN, has been adopted as kind of the standard reference therapy and schedule of choice, but largely because of the side effect profile. And again, this is based predominantly on white patients, where the tolerability is much better. Shannon Westin: Well, I mean, I think that this leads to really great information around how we're designing these trials and how we're potentially making those differences. What are your next steps here? Dr. Bryan Schneider: So I think one of the things this clinical trial did was first validate that we do see high rates of peripheral neuropathy in Black patients with breast cancer. This was a prospective study using both physician and patient adjudicated variables. So I think this is a really nice validation that this is a problem in this population. I think it also shows us that docetaxel is probably a more tolerable drug for black patients with breast cancer. The goal, though, I think in our future work, is really going to try to bring equity in terms of outcome and side effects. So we're working with ECOG-ACRIN now on our second trial, where really the primary endpoint is going to be to nullify the disparities and try to bring equity in terms of toxicity. One of the other pieces of work we're really excited about is we're doing some ex vivo work. So from patients in EAZ171, we have a blood stick where we're taking white blood cells and differentiating those into peripheral neurons. And here we're hoping to look at really important changes in both gene expression and epigenetics that might lead us to a little bit deeper understanding of the mechanism of the disparities in neuropathy, maybe what's causing some of the neuropathy. And we hope ultimately, these may lead to nice drug targets to help prevent or treat neuropathy down the road. Shannon Westin: Those are some really great ideas. The other thing that really caught my eye around your findings was what you all found regarding the physician reported and patient reported toxicity. I'd love for you to summarize that, because I think that's always a concern as well. Dr. Bryan Schneider: Historically, I think we recognize that physicians probably underreport side effects. And so we felt, and our team felt, that having patient reported outcomes would be a really critical piece to this study. What was fairly astonishing to me, if you look at the CTCAE, both patient and physician reported outcomes, they were actually pretty similar. And I think what this is a testament to is if physicians are actually thinking about the side effect, they do a pretty good job of predicting it. Now, one thing we're looking very forward to is that we have a long term follow up out to three years. So it'll be interesting to see if physicians continue to pay close attention to neuropathy, because I know the patients will be. So we'll be looking at the discordance at these longer term follow up time points as well. Shannon Westin: Well, great. This is such incredible work, and I'm like literally taking notes to get in touch with people I know that do this type of work and gynecological malignancies because I think that this is going to have far reaching consequences. So just thank you so much for taking the time to review this and congratulations on the JCO publication and ASCO presentation. It's very well deserved. Dr. Bryan Schneider: Thank you Dr. Westin. Shannon Westin: And thank you to all of our listeners. Again, we have been discussing the “ECOG-ACRIN EAZ171: Prospective Validation Trial of Germline Predictors of Taxane-induced Peripheral Neuropathy in Black Women with Early Stage Breast Cancer.” We're so grateful you joined us, and please do check out our other offerings wherever you get your podcasts. Have an awesome day. The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Disclosures Research Funding Company name: Genentech/Roche Company name: Pfizer Company name: Foundation Medicine      

Drs Sandhya Srinivas and Oliver Sartor discuss the VISION study, new therapies for patients with metastatic castrate-resistant prostate cancer, and PSMA biomarker-based imaging. Relevant disclosures can be found with the episode show notes on Medscape (https://www.medscape.com/viewarticle/988736). The topics and discussions are planned, produced, and reviewed independently of advertisers. This podcast is intended only for US healthcare professionals. Resources Lutetium-177-PSMA-617 for Metastatic Castration-resistant Prostate Cancer https://pubmed.ncbi.nlm.nih.gov/34161051/ Prostate Cancer Theranostics: PSMA Targeted Therapy https://pubmed.ncbi.nlm.nih.gov/34053583/ Piflufolastat F-18 (18F-DCFPyL) for PSMA PET Imaging in Prostate Cancer https://pubmed.ncbi.nlm.nih.gov/35603510/ NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) in Prostate Cancer https://www.nccn.org/professionals/physician_gls/pdf/prostate.pdf German Multicenter Study Investigating 177Lu-PSMA-617 Radioligand Therapy in Advanced Prostate Cancer Patients https://pubmed.ncbi.nlm.nih.gov/27765862/ Results of a Prospective Phase 2 Pilot Trial of 177Lu-PSMA-617 Therapy for Metastatic Castration-resistant Prostate Cancer Including Imaging Predictors of Treatment Response and Patterns of Progression https://pubmed.ncbi.nlm.nih.gov/30425003/ Effect of Radium-223 Dichloride on Symptomatic Skeletal Events in Patients With Castration-resistant Prostate Cancer and Bone Metastases: Results From a Phase 3, Double-blind, Randomised Trial https://pubmed.ncbi.nlm.nih.gov/24836273/ Long-term Follow-up and Outcomes of Retreatment in an Expanded 50-patient Single-center Phase II Prospective Trial of 177Lu-PSMA-617 Theranostics in Metastatic Castration-resistant Prostate Cancer https://pubmed.ncbi.nlm.nih.gov/31732676/ [177Lu]Lu-PSMA-617 Versus Cabazitaxel in Patients With Metastatic Castration-resistant Prostate Cancer (TheraP): A Randomised, Open-label, Phase 2 Trial https://pubmed.ncbi.nlm.nih.gov/33581798/ Prednisone Plus Cabazitaxel or Mitoxantrone for Metastatic Castration-resistant Prostate Cancer Progressing After Docetaxel Treatment: A Randomised Open-label Trial https://pubmed.ncbi.nlm.nih.gov/20888992/ [177Lu]Lu-PSMA-617 in PSMA-positive Metastatic Castration-resistant Prostate Cancer: Prior and Concomitant Treatment Subgroup Analyses of the VISION Trial https://ascopubs.org/doi/10.1200/JCO.2022.40.16_suppl.5001 PSMAfore: A Phase 3 Study to Compare 177Lu-PSMA-617 Treatment With a Change in Androgen Receptor Pathway Inhibitor in Taxane-naïve Patients With Metastatic Castration-resistant Prostate Cancer https://ascopubs.org/doi/abs/10.1200/JCO.2022.40.6_suppl.TPS211

In der Studie geht es um genomische Biomarker, die das Ansprechen einer Therapie mit Taxane versus NHT beim kastrationsresitenten metastasierten Prostatakarzinom vorhersagen sollen. Den Patienten wurden dabei vor der Behandlung Gewebeproben entnommenen und in die retroperspektivische Auswertung mit einbezogen. Welche Biomarker ausfindig gemacht wurden, mittels welchem Test und warum das real-world-setting bei dieser Studie so besonders ist, besprechen Hans Heinzer und Markus Graefen und gehen dabei auch auf die Limitationen ein.

Dr. Neeraj Agarwal, ASCO Daily News editor-in-chief, and director of the Genitourinary Cancers Program at the University of Utah's Huntsman Cancer Institute, shares key takeaways from the PROpel and MAGNITUDE trials in mCRPC, featured at the 2022 ASCO Genitourinary Cancers Symposium.   Transcript: ASCO Daily News: Hello and welcome to the ASCO Daily News Podcast. I'm Geraldine Carroll, a reporter for the ASCO Daily News. Today, in our continuing coverage of the 2022 ASCO Genitourinary (GU) Cancers Symposium, Dr. Neeraj Agarwal, the editor-in-chief of the ASCO Daily News will highlight promising advances in metastatic castration-resistant prostate cancer. Dr. Agarwal has no conflicts relating to the topic of this episode, and his full disclosures are available in the show notes. Disclosures of all guests on the podcast can be found in our transcripts at asco.org/podcasts.   Dr. Neeraj Agarwal: Hello and welcome to the ASCO Daily News Podcast. I'm Dr. Neeraj Agarwal, the director of the Genitourinary Cancer Program, and professor of medicine at the University of Utah Huntsman Cancer Institute, and editor in chief of the ASCO Daily News. I'd like to start with the PROpel trial followed by a discussion on the MAGNITUDE trial. So, Abstract 11 was on the results of the PROpel trial and presented by Dr. Fred Saad from the University of Montreal. PROpel is a randomized phase 3 trial, which evaluated the efficacy and safety of olaparib, a PARP inhibitor plus abiraterone versus this placebo plus abiraterone in the first-line metastatic castration-resistant prostate cancer setting. Patients were allowed to have docetaxel chemotherapy is given in a metastatic castration-sensitive prostate cancer setting. Enrollment in the study was independent of the effects in the homologous recombination repair pathway. The primary endpoint was investigator-assessed radiographic progression-free survival (PFS) with multiple secondary endpoints, including overall survival and safety.   Approximately 800 patients were randomly assigned to the novel combination of olaparib plus abiraterone or placebo plus abiraterone. Baseline characteristics were well-balanced between the treatment arms, including homologous recombination repair or HRR mutation status. At the pre-planned interim analysis results show the trial meets its primary endpoint with significant improvement in radiographic PFS for all patients receiving the combination therapy versus control, regardless of the presence of homologous recombination repair gene mutations. Median PFS was 24.8 months versus 16.6 months for patients receiving olaparib plus abiraterone versus placebo plus abiraterone respectively with the hazard ratio of 0.66, and a P < 0.0001. This translates into a 34% reduction in risk of progression or death. Overall survival results are still immature with only 29% [of patients experiencing events] thus far. It is interesting that even patients deemed negative for homologous recombination repair gene mutations showed significant improvement in radiographic PFS when treated with the combination of olaparib plus abiraterone versus placebo plus abiraterone.   Regarding the adverse effects, they were what you would expect from the combination of a PARP inhibitor, such as olaparib and abiraterone. We saw a higher sequence of all great events of anemia, fatigue, and nausea in the combination arm. While anemia was the only grade 3-4 adverse event observed at a significantly high frequency in the combination arm. It is also important [that] we get a better understanding of the molecular mechanism by which patients who are homologous recombination repair mutation-negative are benefiting from the combination treatment as well.   The next trial in this context, or this team, was the MAGNITUDE trial. Abstract 12 was presented by Dr. Kim Chi from British Columbia Cancer Center in Vancouver, Canada. MAGNITUDE is a randomized phase 3 trial evaluating the efficacy and safety of niraparib plus abiraterone plus placebo plus abiraterone in the first-line metastatic castration-resistant prostate cancer setting. The study population was slightly different from what we saw in PROpel trial. Taxane chemotherapy, as well as novel hormonal therapy, was allowed in metastatic castration-sensitive prostate cancer, as well as a prior novel hormonal therapy was allowed in the non-metastatic castration-resistant prostate cancer.   Also, patients were allowed up to 4 months of treatment with abiraterone in the first-line metastatic castrate-resistant prostate cancer. Prospective selection of patients with, and without homologous recombination repair (HRR) gene mutations were required. The primary endpoint was radiographic PFS by central review with multiple secondary endpoints, including overall survival and safety. A pre-specified fertility analysis was planned after enrolling 233 patients who were randomly assigned to niraparib plus abiraterone or placebo plus abiraterone. Evaluation of fertility was based on the composite PFS of PSA or radiographic progression, whichever occurred first. The pre-planned fertility analysis showed no benefit in the biomarker negative cohort. And thus the trial did not pursue further enrollment of those patients who were not positive for homologous recombination repair gene mutations.   Coming to the HRR positive cohort, 423 patients were randomly assigned to either niraparib plus abiraterone or placebo plus abiraterone. At the pre-planned interim analysis primary endpoint was met with a significant improvement in radiographic PFS for BRCA1 and BRCA2 and all patients who are homologous recombination repair mutation-positive, receiving the novel combination of niraparib plus abiraterone. Overall survival results are still immature. It is important to note that in the patients who are HRR positive, approximately 50% were BRCA1 and 2 positive. And these patients clearly derived the most benefit with a combination with an approximate 47% reduced risk of death. And if you look at other patients who are biomarker positive, there was a clear benefit and a significant improvement in median PFS (radiographic progression-free survival) with a hazard ratio of 0.73, which translates to a 27% reduction in the risk of death or progression. With the caveat of subgroup analysis, being underpowered following groups of patients seem to derive less benefit with the combination than the overall cohort with the combination of niraparib plus abiraterone. And these patients included patients who were age 65 or younger, or less than age 65, patients with visceral metastatic disease, patients with prior abiraterone or taxane chemotherapy, [and] patients who had a PSL level below the median, and patients with non-BRCA homologous recombination repair mutations.   In conclusion, the combination of niraparib plus abiraterone shows a significant improvement in the radiographic PFS for patients who are HRR positive in the first-line metastatic CRPC. Based on the available data in the public domain, without any doubt that both PROpel and MAGNITUDE trials established a combination of a PARP inhibitor with abiraterone in the first-line metastatic CRPC setting for patients who are positive for HRR mutation improve radiographic progression-free survival. Even though overall survival data are immature for both trials, I expect both combinations will be approved by the U.S. Food and Drug Administration in the near future and will be available to our patients. Regarding the HRR negative cohort in the PROpel trial, which also seems to derive significant benefit with the combination of abiraterone plus olaparib, I'm looking forward to the data on confirmation of HRR negative status by tissue-based genomic profiling results in the full-length publication which we expect to be published soon. If indeed confirmed by the tissue-based genomic profiling, I see the combination of abiraterone plus olaparib to be a reasonable option in the patients who are HRR negative in the first-line metastatic CRPC setting.   With this, I would like to conclude my discussion on the 2 practice-changing trials presented in the 2022 ASCO GU meeting, which were the PROpel and MAGNITUDE trials. Thank you very much for your kind attention. ASCO Daily News: That was Dr. Neeraj Agarwal of the University of Utah's Huntsman Cancer Institute. Thanks for joining us today. If you're enjoying the content on the podcast, please take a moment to rate and review us wherever you get your podcast.   Disclosures: Dr. Neeraj Agarwal: Consulting or Advisory Role: Pfizer, Medivation/Astellas, Bristol-Myers Squibb, AstraZeneca, Nektar, Lilly, Bayer, Pharmacyclics, Foundation Medicine, Astellas Pharma, Lilly, Exelixis, AstraZeneca, Merck, Novartis, lily, Eisai, Seattle Genetics, EMD Serono, Janssen Oncology, AVEO, Calithera Biosciences, MEI Pharma, Genentech, Astellas Pharma, Foundation Medicine, and Gilead Sciences Research Funding (Institution): Bayer, Bristol-Myers Squibb, Takeda, Pfizer, Exelixis, Amgen, AstraZeneca, Calithera Biosciences, Celldex, Eisai, Genentech, Immunomedics, Janssen, Merck, Lilly, Nektar, ORIC Pharmaceuticals, ORIC Pharmaceuticals, CRISPR therapeutics, and Arvinas Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.  

Track 1: Introduction to Rus and our topic on the YewTip What is the Yew How big of an area Northern California up to the coast into Canada January 1991 when he started the business Outfitter Asked about Yew Tree in MT - originally used to make archery equipment “Taxol” cancer drug National Cancer Institute in Washington, DC Who is involved? —> Bristol Meyer Squibb 1991 + 1992 + 1993 until February 1994 13,000 lbs, 90,000 lbs, 200,000 lbs. BMS: rights to Yew on all Federal Land in 1992: Rus heard stories about people making Yew-Tea 7 types of Yew Trees in Northern Hemisphere Pacific Yews are NOT poisonous European and Asian Yews are VERY poisonous - Taxane causes your heart to stop - most trees you buy in nursery are European and Asian Yews or a mix of the two… When then drink yew tea their cancer went down. Start of prostate story - continued in Track 2. Start Track 2: 21:12 Track 2: Story about friend with stage 4 prostate cancer spreading to the bones and liver. Started 4-6 cups daily 6 months later cancer FREE Story about Vietnam vet tumor at base of spine —> healed February 1994 BMS Stopped the operation Was directed Mildred Melson Clinical Nurse in Biomedical Clinic in Tijuana After using the tea she came to MT to see the trees She suggested to test the tips (10-12 inches) more effective than the bark Went completely Yew Tip in 1995 Call about bladder cancer being healed Tax species —> containing taxanes 100's of them - they peaked at the height of summer What Taxanes do: Most important part is using Anti Cancer Diet: No sugar Call about where to find more information: bighornbotanicals.com online or in our store here in Bozeman, MT Discussion on recommending dosage   Start Track 3: 45:20 Track 3: Quick Recap of show so far Registered with FDA 41 page compliance regulations Different products most popular: capsules tincture = alcohol extract mixed with juice oil = nonalcoholic liquid internal or external usage options Equal parts of yew tip extract w/ equal parts organic olive oil made in crockpot on low 1/8 tsp pwd 1 mL of tincture/oil = 1 300mg capsule For dogs and cats: use Yew 1 mL/ 1 dropper per 10th of weight mix with food cut the dosage in half for inflammation How long does it take for Yew Trees to grow back? Sustainability Start   Start Track 4: 1:03:01 Track 4: Sustainability continued Nan Vance, PhD (Oregon) Rus explains how fast + how Yew trees regrow Give them at least 4 years Rus goes back every 5th year Rus keeps track of every patch How does he work with the Forest Service? internal products: capsules powered tea tincer oil External products: salve lotion soap lip balm Not all taxanes are in the tree Oil is tasting good What expiration dates on products? You need stability study Call about kidneys   Start Track 5: 1:26:20 Track 5: Recap of the show Harvesting is seasoned End of June - End of August Different Types Taxans Caratenoids Flavonoids Lignans Phytosterols All types are antiviral, anti-fungal & antibacterial Testimonials: How the Salve became to be because of Mildred Nelson, RN Rus broke his hip From friend with Henry (w/Melanoma) Salve is used for anything external Repeat how Taxanes affect spindle fibers in cancer cells   Start Track 6: 1:44:26 Track 6: All different compounds in Yew, coming from soil Visits from FDA What happens Big Horn Botanicals First + Only One

ONS member Rae Norrod, MS, RN, AOCN®, CNS, manager of the oncology service line at Kettering Health Network in Kettering, OH, and member of the West Central Ohio ONS Chapter, joins Stephanie Jardine, BSN, RN, oncology clinical specialist at ONS, to discuss how to safely administer taxane chemotherapy treatments. This episode is part of an ongoing series about chemotherapy administration. The others are linked in the episode notes. Music Credit: "Fireflies and Stardust" by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0 Earn 0.5 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at myoutcomes.ons.org by March 5, 2023. The planners and faculty for this episode have no conflicts to disclose, and the episode has no commercial support. ONS is accredited as a provider of NCPD by the American Nurses Credentialing Center's Commission on Accreditation. Episode Notes Check out these resources from today's episode: Complete this evaluation for free NCPD. Oncology Nursing Podcast Episode 92: Doxorubicin: The Infamous Red Devil Oncology Nursing Podcast Episode 143: Administer FOLFOX Chemotherapy Regimens With Confidence Clinical Journal of Oncology Nursing article: Extremity Cooling: A Synthesis of Cryotherapy Interventions to Reduce Peripheral Neuropathy and Nail Changes From Taxane-Based Chemotherapy ONS book: Chemotherapy and Immunotherapy Guidelines and Recommendations for Practice ONS Communities thread on cryotherapy ONS Communities thread on safely administering exfoliants ONS course: Safe Handling Basics ONS course: Fundamentals of Chemotherapy Immunotherapy Administration ONS position statement: Education of the Registered Nurse Who Administers and Cares for the Individual Receiving Antineoplastic Therapies Journal of Oncology Pharmacy Practice article: Administration Sequence for Multi-Agent Oncolytic Regimens National Cancer Institute resources on taxanes

Demodicosis in children – Multiple pilomatricoma syndromes – Topical metformin for CCCA – Dermatology cancer Tx AEs: Taxane-induced onycholysis TEMPI syndrome - Pediatric LS&A persists beyond childhood Luke and Michelle report no conflicts of interest. http://www.dermaspherepodcast.com

Today, I talk breast cancer and how Odonate's oral Taxane (Tesataxel) could garner the attention of doctor's looking to alleviate the burden of IV chemotherapy infusion in their patients. I discuss the latest macro news, biotech news, and compare previous Taxane revenue to see if my model is reasonable.www.breakingbiotech.com biotech #breakingbiotech #odonate This is not investment advice, but for entertainment purposes. I am not liable for any losses you generate from trading.Support Breaking Biotech by donating to their Tip Jar: https://tips.pinecast.com/jar/breaking-biotech

Dr Emmanuel Antonarakis talks to ecancertv at ASCO GU 15 about the results of his small prospective study on the correlation between androgen receptor V7 status and resistance to taxane chemotherapy in men with metastatic castration-resistant prostate cancer.

Dr. Jack West, Swedish Cancer Institute, reviews the choices for a first-line chemotherapy regimen based on a squamous histology.

Dr. Jack West, Swedish Cancer Institute, reviews the choices for a first-line chemotherapy regimen based on a squamous histology.

Dr. Jack West, Swedish Cancer Institute, reviews the choices for a first-line chemotherapy regimen based on a squamous histology.

Dr. Jack West, Swedish Cancer Institute, addresses the issue of choosing a first-line chemotherapy regimen based on an adenocarcinoma histology.

Dr. Jack West, Swedish Cancer Institute, addresses the issue of choosing a first-line chemotherapy regimen based on an adenocarcinoma histology.

Dr. Jack West, Swedish Cancer Institute, addresses the issue of choosing a first-line chemotherapy regimen based on an adenocarcinoma histology.

Although historically toxicity was often thought to be a biomarker of efficacy, often it appears to be a marker of dose intensity and individual susceptibility as is the case in this retrospective study of taxane induced peripheral neuropathy and breast cancer outcome.

Background: Data from meta-analyses have shown taxane-containing therapies to be superior to anthracycline-based treatments for high-risk breast cancer. Patients and Methods: The ADEBAR trial was a multicenter phase Ill trial in which patients with lymph node-positive breast cancer were prospectively randomized for either sequential anthracycline-taxane or FEC120 therapy. Patients received 4x epirubicin (90 mg/m(2)) and cyclophosphamide (600 mg/m(2)) every 3 weeks (q3w), followed by 4x docetaxel (100 mg/m(2)) q3w (EC-Doc arm), or 6x epirubicin (60 mg/m(2)) and 5-fluorouracil (500 mg/m(2)) on days 1 and 8 and cyclophosphamide (75 mg/m(2)) on days 1-14, q4w (FEC arm). We compared both arms with respect to toxicity and feasibility. Results: Hematological toxicity was found significantly more often in the FEC arm. Febrile neutropenia was seen in 11.3% of patients in the FEC arm and in 8.4% of patients in the EC-Doc arm (p = 0.027). Non-hematological side effects of grade 3/4 were rarely seen in either arm. Therapy was terminated due to toxicity in 3.7% of the patients in the EC-Doc arm and in 8.0% of the patients in the FEC arm (p = 0.0009). Conclusion: The sequential anthracycline-taxane regimen is a well-tolerated and feasible alternative to FEC120 therapy.

Introduction Despite the fact that people older than 65 years of age have the highest incidence of developing breast cancer, these patients are excluded from clinical trials in most cases. Furthermore, most physicians tend towards therapy regimens without the use of dose-dense, highly active taxane-based treatments because of a lack of data regarding toxicities of these compounds in older patients. Methods Pooled side-effect data were analyzed from four prospective, randomized clinical trials in which patients of different age groups (60 years, between 60 and 64 years, and 64 years) with primary breast cancer received taxane-based chemotherapy. Results Dose delays, dose reductions, hospitalization, and therapy discontinuation increased with age. Hematologic toxicities and some nonhematologic toxicities were generally more common in older patients. Leucopenia increased from 55.3% in patients aged 60 years to 65.5% in patients aged 64 years (P

Oncology, December 13th, 2007 Reporting from: San Antonio Breast Cancer Symposium, 13-16 December, 2007 Early Breast Cancer: Survival Benefit For Adjuvant Docetaxel/Cyclophosphamide STEPHEN JONES, US Oncology Research, Houston REFERENCE: ABSTRACT 12 Long term data from an early breast cancer trial involving cyclophosphamide combined with docetaxel or doxorubicin have shown a survival advantage for the taxane. As Stephen Jones of US Oncology Research explained to Derek Thorne, this advantage was also seen in patients over 65.

BreastCancerUpdate.com/ThinkTank – Proceedings from a Clinical Investigator “Think Tank.” Selection of a Taxane in the Adjuvant and Metastatic Settings. Interviews conducted by Neil Love, MD. Produced by Research To Practice.