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• W2807164879 abstract "Emerging Therapeutics for Melanoma Which therapy for which patient?Antoni RibasAntoni RibasAntoni Ribas is Professor of Medicine at the University of California (UCLA; CA, USA) in the Division of Hematology/Oncology, with additional appointments in the Department of Surgery and Department of Molecular and Medical Pharmacology. He joined UCLA in 1996 from the Hospital Vall d’Hebron, Autonomous University of Barcelona in Spain, where he earned both his medical and doctoral degrees. His research includes laboratory and clinical translational research in melanoma, with work in the adoptive cell transfer therapy using T-cell-receptor-engineered lymphocytes designed to seek out melanoma cells, incorporating molecular imaging and advanced immune monitoring platforms. He is also testing, both in the laboratory and the clinic, novel targeted therapies blocking melanoma driver cancer events, as well as clinical applications of nanoparticle delivery of siRNA, which interferes with gene expression related to cancer. He is Director of the Tumor Immunology Program at the UCLA’s Jonsson Comprehensive Cancer Center and a member of the Center’s Cancer Molecular Imaging Program. He is also a member of the Institute for Molecular Medicine, the Broad Stem Cell Research Center and the Jules Stein Eye Institute. He also is an elected member of the American Society of Clinical Investigation and a permanent committee member of the National Cancer Institute grant review panels.Search for more papers by this authorPublished Online:18 Jan 2012https://doi.org/10.2217/ebo.11.97AboutSectionsView ArticleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinkedInReddit View chapterAbstract: The recent approval of two new agents for the treatment of metastatic melanoma, both with demonstrated improvements in overall survival compared with standard of care therapies, results in a new era in the treatment of this disease. Both agents have markedly different mechanisms of action and benefits to patients. The anti-CTLA-4 antibody ipilimumab is an immune-modulating antibody leading to low but very durable response rates. The BRAF inhibitor, vemurafenib, is an oncogene-targeted therapy only active in approximately 50% of melanomas with the BRAF V600 mutation, which leads to very high response rates but usually of limited durability. In this chapter, we discuss how these different treatment approaches and their perceived benefits can help in deciding which treatment to use for which patient. References1 Hodi FS , O’Day SJ , McDermott DF et al. Improved survival with ipilimumab in patients with metastatic melanoma. . N. Engl. J. Med. 363 (8) , 711 – 723 (2010) . Crossref, Medline, CAS, Google Scholar2 Robert C , Thomas L , Bondarenko I et al. Ipilimumab plus dacarbazine for previously untreated metastatic melanoma . N. Engl. J. Med. 364 (26) , 2517 – 2526 (2011) . Crossref, Medline, CAS, Google Scholar3 O’Day SJ , Maio M , Chiarion-Sileni V et al. Efficacy and safety of ipilimumab monotherapy in patients with pretreated advanced melanoma: a multicenter single-arm Phase II study . Ann. Oncol. 21 (8) , 1712 – 1717 (2010) . Crossref, Medline, Google Scholar4 Ribas A , Glaspy JA , Lee Y et al. Role of dendritic cell phenotype, determinant spreading, and negative costimulatory blockade in dendritic cell-based melanoma immunotherapy . J. Immunother. 27 (5) , 354 – 367 (2004) . Crossref, Medline, CAS, Google Scholar5 Agarwala SS , Ribas A . Current experience with CTLA4- blocking monoclonal antibodies for the treatment of solid tumors . J. Immunother. 33 (6) , 557 – 569 (2010) . Crossref, Medline, CAS, Google Scholar6 Ribas A , Hauschild A , Kefford R et al. PhaseIII, open-label, randomized, comparative study of tremelimumab (CP-675,206) and chemotherapy (temozolomide or dacarbazine) in patients with advanced melanoma . J. Clin. Oncol. 26 (Suppl.) (2008) . (Abstract LBA9011) . Google Scholar7 Flaherty KT , Puzanov I , Kim KB et al. Inhibition of mutated, activated BRAF in metastatic melanoma . N. Engl. J. Med. 363 (9) , 809 – 819 (2010) . Crossref, Medline, CAS, Google Scholar8 Ribas A , Kim K , Schuchter L et al. BRIM-2: an open-label, multicenter Phase II study of RG7204 (PLX4032) in previously treated patients with BRAF V600E mutation-positive metastatic melanoma . J. Clin. Oncol. 29 (Suppl.) (2011) (Abstract 8509) . Google Scholar9 Kim KB , Flaherty KT , Chapman PB et al. Pattern and outcome of disease progression of Phase I study of PLX4032 (RG7204) in patients with metastatic melanoma . J. Clin. Oncol. 29 (Suppl.) (2011) (Abstract 8519) . Google Scholar10 Johannessen CM , Boehm JS , Kim SY et al. COT drives resistance to RAF inhibition through MAP kinase pathway reactivation . Nature 468 (7326) , 968 – 972 (2010) . Crossref, Medline, CAS, Google Scholar11 Wagle N , Emery C , Berger MF et al. Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling . J. Clin. Oncol. 29 (22) , 3085 – 3096 (2011) . Crossref, Medline, CAS, Google Scholar12 Nazarian R , Shi H , Wang Q et al. Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation . Nature 468 (7326) , 973 – 977 (2010) . Crossref, Medline, CAS, Google Scholar13 Villanueva J , Vultur A , Lee JT et al. Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K . Cancer Cell 18 (6) , 683 – 695 (2010) . Crossref, Medline, CAS, Google Scholar14 Heidorn SJ , Milagre C , Whittaker S et al. Kinase-dead BRAF and oncogenic RAS cooperate to drive tumor progression through CRAF . Cell 140 (2) , 209 – 221 (2010) . Crossref, Medline, CAS, Google Scholar15 Poulikakos PI , Zhang C , Bollag G , Shokat KM , Rosen N . RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF . Nature 464 (7287) , 427 – 430 (2010) . Crossref, Medline, CAS, Google Scholar16 Ribas A , Flaherty KT . BRAF targeted therapy changes the treatment paradigm in melanoma . Nature Rev. Clin. Oncol. 8 (7) , 426 – 433 (2011) . Crossref, Medline, CAS, Google Scholar17 Chapman PB , Hauschild A , Robert C et al. Improved survival with vemurafenib in melanoma with. BRAF V600E mutation . N. Engl. J. Med. 364 (26) , 2507 – 2516 (2011) . Crossref, Medline, CAS, Google Scholar18 Kefford R , Arkenau H , Brown MP et al. Phase I/II study of GSK2118436, a selective inhibitor of oncogenic mutant BRAF kinase, in patients with metastatic melanoma and other solid tumors. Presented at: American Society of Clinical Oncology. Chicago, IL, USA, 4–8 June 2010 . Google Scholar19 Infante JR , Falchook GS , Lawrence DP et al. Phase I/II study to assess safety, pharmacokinetics, and efficacy of the oral MEK 1/2 inhibitor GSK1120212 (GSK212) dosed in combination with the oral BRAF inhibitor GSK2118436 (GSK436) . J. Clin. Oncol. 29 (Suppl.) (2011) (Abstract CRA8503) . Google Scholar20 Gray-Schopfer V , Wellbrock C , Marais R . Melanoma biology and new targeted therapy . Nature 445 (7130) , 851 – 857 (2007) . Crossref, Medline, CAS, Google Scholar21 Curtin JA , Fridlyand J , Kageshita T et al. Distinct sets of genetic alterations in melanoma . N. Engl. J. Med. 353 (20) , 2135 – 2147 (2005) . Crossref, Medline, CAS, Google Scholar22 Curtin JA , Busam K , Pinkel D , Bastian BC . Somatic activation of KIT in distinct subtypes of melanoma . J. Clin. Oncol. 24 (26) , 4340 – 4346 (2006) . Crossref, Medline, CAS, Google Scholar23 Beadling C , Jacobson-Dunlop E , Hodi FS et al. KIT gene mutations and copy number in melanoma subtypes . Clin. Cancer Res. 14 (21) , 6821 – 6828 (2008) . Crossref, Medline, CAS, Google Scholar24 Hodi FS , Friedlander P , Corless CL et al. Major response to imatinib mesylate in KIT-mutated melanoma . J. Clin. Oncol. 26 (12) , 2046 – 2051 (2008) . Crossref, Medline, CAS, Google Scholar25 Carvajal RD , Antonescu CR , Wolchok JD et al. KIT as a therapeutic target in metastatic melanoma . JAMA 305 (22) , 2327 – 2334 (2011) . Crossref, Medline, CAS, Google ScholarFiguresReferencesRelatedDetails Emerging Therapeutics for MelanomaMetrics Downloaded 15 times History Published online 18 January 2012 Published in print January 2012 Information©Future Medicine Ltd© 2011 Future Medicine LtdPDF download" @default.
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