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Tanner M. Johanns, Cole J. Ferguson, Patrick M. Grierson, Sonika Dahiya, and George Ansstas

glioblastoma reveals a subset of biologically favorable tumors with associated molecular prognostic markers . Acta Neuropathol 2015 ; 129 : 669 – 678 . 33. Bautista F Paci A Minard-Colin V . Vemurafenib in pediatric patients with BRAFV600E

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David R. Braxton

results, with not all histologies responding to targeted therapy against a particular mutation. For instance, many BRAF V600E–mutant nonmelanoma histologies respond to vemurafenib; however, BRAF V600E–mutant colorectal cancers did not display any

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Daniel G. Coit, John A. Thompson, Mark R. Albertini, Christopher Barker, William E. Carson III, Carlo Contreras, Gregory A. Daniels, Dominick DiMaio, Ryan C. Fields, Martin D. Fleming, Morganna Freeman, Anjela Galan, Brian Gastman, Valerie Guild, Douglas Johnson, Richard W. Joseph, Julie R. Lange, Sameer Nath, Anthony J. Olszanski, Patrick Ott, Aparna Priyanath Gupta, Merrick I. Ross, April K. Salama, Joseph Skitzki, Jeffrey Sosman, Susan M. Swetter, Kenneth K. Tanabe, Evan Wuthrick, Nicole R. McMillian, and Anita M. Engh

and safety data from prospective randomized controlled trials testing some of these immune checkpoint inhibitors (ipilimumab, nivolumab, pembrolizumab) and targeted therapies (vemurafenib, dabrafenib/trametinib) for adjuvant treatment of high

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Tanner M. Johanns, George Ansstas, and Sonika Dahiya

. 10 , 18 – 24 In total, adult HGG or GBM cases were composed of 4 GBM/eGBM, 9 aPXA, and 1 anaplastic ganglioglioma, with 10 patients treated with single-agent BRAFi (5 with vemurafenib, 5 with dabrafenib) and 4 treated with combination BRAFi/MEKi (all

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Axel Grothey and Alan P. Venook

, 10 progression-free survival was doubled with the triplet of cetuximab/vemurafenib/irinotecan. The NCCN Colon Cancer Panel, therefore, recommends combination therapy for tumors with BRAF V600E mutations, including irinotecan/cetuximab/vemurafenib

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Anirban Maitra

cancers treated with vemurafenib. 8 Within the PDAC genomic landscape, probably the most prevalent actionable subtype (currently estimated at between 5% and 10% of cases) is composed of tumors with defective DNA damage repair (“DDR-defective” PDAC), which

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Richard D. Carvajal, Sharon A. Spencer, and William Lydiatt

conducted specifically in patients with advanced MM, anecdotal cases of benefit have been observed. Vemurafenib, a small molecule inhibitor with specificity for BRAF harboring a substitution of glutamic acid for valine at position 600 (V600E), was approved

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Silviya K. Meletath, Dean Pavlick, Tim Brennan, Roy Hamilton, Juliann Chmielecki, Julia A. Elvin, Norma Palma, Jeffrey S. Ross, Vincent A. Miller, Philip J. Stephens, George Snipes, Veena Rajaram, Siraj M. Ali, and Isaac Melguizo-Gavilanes

600E, activates MEK-ERK signaling 18 and is sensitive to BRAF V600E mutant-specific inhibitors such as vemurafenib and dabrafenib. 19 , 20 BRAF V600E mutations are also found in other low-grade pediatric gliomas, such as pleomorphic

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Barbara Burtness

as sorafenib and vemurafenib, have been associated with hand-foot skin reaction (HFSR), 5 and the newer BRAF inhibitor regorafenib “has some pretty dramatic skin manifestations,” noted Dr. Burtness. mTOR inhibitors, such as temsirolimus and

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John A. Thompson

patients. The most recent major trial of the BRAF inhibitor vemurafenib showed an overall response rate of 53%, a median PFS of almost 7 months, and a median OS approaching 16 months. 7 The BRAF inhibitor dabrafenib produced a 50% response rate in a