Asco Meeting 2006

Asco Meeting 2006 Average ratng: 7,3/10 1771reviews
Asco Meeting 2006

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Course Name: 6 th Annual Lung Cancer Symposium. Course Date: Friday, March 2, 2. Course Co- Directors and Planners : Ralph Zinner, MD; Gregory Kane, MD; Judith Alberto, RPh; Rita Axelrod, MD; Stephanie Bork, MSN, CRNP; Nathaniel R.

Bayer is a global enterprise with core competencies in the Life Science fields of health care and agriculture. ASCO’s growing roster of cutting-edge journals serves readers as the most credible, authoritative, peer-reviewed resources for significant clinical oncology. Journal of Clinical Oncology (JCO) is a high-impact, peer-reviewed medical journal that publishes significant clinical oncology research along with editorials. Acronym expansions, definitions, links, and opinions. About a fifth of the entries are American Societies of this or that, especially that. Why is it that at a meeting minutes are kept but the hours are lost? The Society for Immunotherapy of Cancer (SITC) Annual Meeting & Pre-Conference Programs brings together stakeholders across the cancer immunotherapy field to advance.

Original Article. Intraperitoneal Cisplatin and Paclitaxel in Ovarian Cancer. Deborah K. Armstrong, M.D., Brian Bundy, Ph.D., Lari Wenzel, Ph.D., Helen Q. Huang, M.S. The 2017 ASCO Annual Meeting will soon unveil top-line findings across the field of oncology. Pivotal research in immunotherapy, targeted agents, and supportive care. ASCO Recommendations for Use of White Blood Cell Growth Factors: What Remains the Same and What Has Been Modified. School Girl Costume Ideas Adults on this page. By Gary H. Lyman, MD, MPH November 10, 2015.

Sunitinib - Wikipedia. Sunitinib. Clinical data.

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YKey: WINHZLLDWRZWRT- ATVHPVEESA- N Y NY (what is this?)  (verify)Sunitinib (marketed as Sutent by Pfizer, and previously known as SU1. RTK) inhibitor that was approved by the FDA for the treatment of renal cell carcinoma (RCC) and imatinib- resistant gastrointestinal stromal tumor (GIST) on January 2.

Sunitinib was the first cancer drug simultaneously approved for two different indications.[1]Mechanism of action[edit]Sunitinib inhibits cellular signaling by targeting multiple receptor tyrosine kinases (RTKs). These include all receptors for platelet- derived growth factor (PDGF- Rs) and vascular endothelial growth factor receptors (VEGFRs), which play a role in both tumor angiogenesis and tumor cell proliferation. The simultaneous inhibition of these targets therefore reduces tumor vascularization and triggers cancer cell apoptosis and thus results in tumor shrinkage. Sunitinib also inhibits CD1. KIT),[2] the receptor tyrosine kinase that (when improperly activated by mutation) drives the majority of gastrointestinal stromal cell tumors.[3] It has been recommended as a second- line therapy for patients whose tumors develop mutations in c- KIT that make them resistant to imatinib, or who the cannot tolerate the drug.[4][5]In addition, sunitinib binds other receptors.[6] These include: The fact that sunitinib targets many different receptors, leads to many of its side effects such as the classic hand- foot syndrome, stomatitis, and other dermatologic toxicities. Indications[edit]Gastrointestinal stromal tumor[edit]Like RCC, GIST does not generally respond to standard chemotherapy or radiation.

Imatinib was the first cancer agent proven effective for metastatic GIST and represented a major development in the treatment of this rare but challenging disease. However, approximately 2. Prior to sunitinib, patients had no therapeutic option once they became resistant to imatinib.[7]Sunitinib offers patients with imatinib- resistant GIST a new treatment option to stop further disease progression and, in some cases, even reverse it. This was shown in a large, Phase III clinical trial in which patients who failed imatinib therapy (due to primary resistance, secondary resistance, or intolerance) were treated in a randomized and blinded fashion with either sunitinib or placebo.[7]The study was unblinded early, at the very first interim analysis, due to the clearly emerging benefit of sunitinib.

At that time, patients receiving placebo were offered to switch over to sunitinib. In the primary endpoint of this study, median time to tumor progression (TTP) was more than four- fold longer with sunitinib (2. P<. 0. 00. 1). These are based on the assessments of an independent radiology lab assessment. The benefit of sunitinib remained statistically significant when stratified for a multitude of prespecified baseline factors.[7]Among the secondary endpoints, the difference in progression- free survival (PFS) was similar to that in TTP (2. P<. 0. 00. 1). Seven percent of sunitinib patients had significant tumor shrinkage (objective response) compared with 0% of placebo patients (P=. Another 5. 8% of sunitinib patients had disease stabilization vs.

The median time to response with sunitinib was 1. Sunitinib reduced the relative risk of disease progression or death by 6. The difference in survival benefit may be diluted because placebo patients crossed over to sunitinib upon disease progression, and most of these patients subsequently responded to sunitinib.[7]Sunitinib was relatively well tolerated. About 8. 3% of sunitinib patients experienced a treatment- related adverse event of any severity, as did 5.

Serious adverse events were reported in 2. Adverse events were generally moderate and easily managed by dose reduction, dose interruption, or other treatment.

Nine percent of sunitinib patients and 8% of placebo patients discontinued therapy due to an adverse event.[7]Fatigue is the adverse event most commonly associated with sunitinib therapy. In this study, 3.

Oncology Leaders Pick Their Top Abstracts. The 2. 01. 7 ASCO Annual Meeting will soon unveil top- line findings across the field of oncology. Pivotal research in immunotherapy, targeted agents, and supportive care are among the much- discussed abstracts this year. Key opinion leaders spoke with Onc.

Live to share the top- 5 abstracts they find to be the most exciting and/or potentially practice- changing across breast cancer, lung cancer, genitourinary cancers, gastrointestinal cancers, hematologic malignancies, and supportive care. H. “Jack” West, MD, thoracic oncologist, Swedish Cancer Institute at Swedish Medical Center. Alectinib (Alecensa) versus crizotinib (Xalkori) in treatment- naive advanced ALK- positive non–small cell lung cancer (NSCLC): primary results of the global phase III ALEX study (LBA9. H. Jack West, MD. The open- label study (NCT0. ALK- positive NSCLC in a 1: 1 ratio to alectinib or crizotinib. Progression- free survival (PFS) was the primary endpoint of the international study.

Genentech (Roche), the developer of the second- generation ALK inhibitor alectinib, announced in April 2. Coming on the heels of the smaller, Japanese- only J- ALEX trial that demonstrated overwhelmingly clear superiority of alectinib over crizotinib in terms of extracranial and intracranial efficacy, as well as better tolerability with alectinib (at a lower dose of alectinib than is the current standard around the world), the ALEX trial results will change our standard of care for first- line treatment of ALK- positive advanced NSCLC to alectinib if the results are even in the ballpark of the remarkable benefits seen with alectinib in the J- ALEX trial.”Gefitinib (Iressa) versus vinorelbine+cisplatin as adjuvant treatment in stage II- IIIA (N1- N2) NSCLC with EGFR- activating mutation (ADJUVANT): a randomized, phase III trial (CTONG 1. Abstract 8. 50. 0)CTONG 1. EGFR tyrosine kinase inhibitor (TKI) gefitinib with vinorelbine/cisplatin—the standard of care in the adjuvant setting for patients with stage II- IIIA NSCLC with EGFR mutations. Prior studies, including BR1.

RADIANT, have shown that EGFR TKIs have not demonstrated benefit in the adjuvant setting for patients with unselected resected NSCLC. In CTONG 1. 10. 4, gefitinib significantly prolonged disease- free survival (DFS) versus standard chemotherapy.“These provocative findings may be interpreted as supporting use of an EGFR TKI as adjuvant therapy, but many might favor an approach of giving sequential adjuvant chemotherapy, as an established standard of care with a demonstrated survival benefit, followed by EGFR TKI therapy.

At the same time, this trial will raise the critical question of whether we need to see a significant improvement in overall survival (OS) before adopting a new therapy approach in the curative setting—especially when we are considering recommending years of treatment, with the attendant side effects and costs, for patients who may well already be cured without it.”Nivolumab (Opdivo) with or without ipilimumab (Yervoy) in advanced small cell lung cancer (SCLC): first report of a randomized expansion cohort from Check. Mate- 0. 32 (Abstract 8. This phase I/II study is exploring multiple regimens of nivolumab with or without ipilimumab across several solid tumors, one of which is advanced SCLC. Following standard first- line platinum- based chemotherapy, patients with SCLC have a poor prognosis and limited treatment options. Early results demonstrated tolerability and efficacy for both the immunotherapy combination and nivolumab alone in patients with SCLC.“Though only reporting results from a phase II trial, this presentation will have an outsized impact because nivolumab, with or without ipilimumab, is now being widely adopted as a leading treatment consideration in relapsed SCLC based on the inclusion of this option in the NCCN guidelines and the lack of enthusiasm felt for standard second- line topotecan. With immunotherapy more readily available than other potentially promising treatments only available in clinical trials, these results will be of great interest despite the lack of systematic evaluation of immunotherapy compared to better established standards in this setting.”Impact of atezolizumab (Tecentriq) treatment beyond disease progression in advanced NSCLC: results from the randomized phase III OAK study (Abstract 9.