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Jaffer A. Ajani, Thomas A. D’Amico, David J. Bentrem, David Cooke, Carlos Corvera, Prajnan Das, Peter C. Enzinger, Thomas Enzler, Farhood Farjah, Hans Gerdes, Michael Gibson, Patrick Grierson, Wayne L. Hofstetter, David H. Ilson, Shadia Jalal, Rajesh N. Keswani, Sunnie Kim, Lawrence R. Kleinberg, Samuel Klempner, Jill Lacy, Frank Licciardi, Quan P. Ly, Kristina A. Matkowskyj, Michael McNamara, Aaron Miller, Sarbajit Mukherjee, Mary F. Mulcahy, Darryl Outlaw, Kyle A. Perry, Jose Pimiento, George A. Poultsides, Scott Reznik, Robert E. Roses, Vivian E. Strong, Stacey Su, Hanlin L. Wang, Georgia Wiesner, Christopher G. Willett, Danny Yakoub, Harry Yoon, Nicole R. McMillian, and Lenora A. Pluchino

-H (≥10 mutations/megabase) tumors, 149 entrectinib or larotrectinib for NTRK gene fusion-positive tumors, 150 , 151 dabrafenib and trametinib for BRAF V600E mutated tumors, 152 and selpercatinib for RET gene fusion positive tumors. 153 See next

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Philip E. Lammers, Christine M. Lovly, and Leora Horn

may prove fruitful in NSCLC. Dabrafenib, a BRAF inhibitor, showed activity in 17 patients with BRAF V600E mutations, 9 and case reports have documented responses of BRAF -mutant lung cancer to the BRAF inhibitor vemurafenib. 10 In addition

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Daniel G. Coit and Anthony J. Olszanski

progression-free survival was 9.4 months with the combination of dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor), versus 5.8 months for dabrafenib monotherapy ( P <.001). 13 The combination is also associated with less skin toxicity, although

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Christopher A. Barker and April K. Salama

ipilimumab for resected stage IIIB/C melanoma. For patients with sentinel node metastasis >1 mm, the NCCN Guidelines recommend dabrafenib/trametinib (for patients with BRAF V600–mutated disease), in addition to nivolumab. Second-Line Therapies for

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Vaia Florou, Christopher Nevala-Plagemann, Jonathan Whisenant, Patricia Maeda, Glynn W. Gilcrease, and Ignacio Garrido-Laguna

NTRK1 . JCO Precis Oncol 2020 ; 4 : 79 – 90 . 32133433 10.1200/PO.19.00287 24. Long GV , Flaherty KT , Stroyakovskiy D , Dabrafenib plus trametinib versus dabrafenib monotherapy in patients with metastatic BRAF V600E/K-mutant melanoma

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Céline Mascaux, Ming-Sound Tsao, and Fred R. Hirsch

rearrangements, which are mainly observed in nonsmokers. 24 For patients with BRAF V600E mutations, the NCCN Guidelines for NSCLC recommend the combination of dabrafenib with trametinib in the first-line setting. 25 Both dabrafenib and vemurafenib as

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Ronald S. Go, Eric Jacobsen, Robert Baiocchi, Ilia Buhtoiarov, Erin B. Butler, Patrick K. Campbell, Don W. Coulter, Eli Diamond, Aron Flagg, Aaron M. Goodman, Gaurav Goyal, Dita Gratzinger, Paul C. Hendrie, Meghan Higman, Michael D. Hogarty, Filip Janku, Reem Karmali, David Morgan, Anne C. Raldow, Alexandra Stefanovic, Srinivas K. Tantravahi, Kelly Walkovich, Ling Zhang, Mary Anne Bergman, and Susan D. Darlow

keratosis (8%). All patients required dose reduction due to toxicities. Encouraging results from a case series also support the use of dabrafenib, a second-generation BRAF inhibitor, in adults with LCH. Dabrafenib may be better tolerated than vemurafenib

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Chloe E. Atreya, Claire Greene, Ryan M. McWhirter, Nabia S. Ikram, I. Elaine Allen, Katherine Van Loon, Alan P. Venook, Benjamin M. Yeh, and Spencer C. Behr

-mutated colorectal cancer . J Clin Oncol 2015 ; 33 : 4032 – 4038 . 40. Corcoran RB Atreya CE Falchook GS . Combined BRAF and MEK inhibition with dabrafenib and trametinib in BRAF V600-mutant colorectal cancer . J Clin Oncol 2015 ; 33 : 4023 – 4031

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Cary P. Gross, Craig S. Meyer, Sarika Ogale, Matthew Kent, and William B. Wong

, 2011 (crizotinib); EGFR : May 14, 2013 (erlotinib); ROS1 : March 11, 2016 (crizotinib); PD-L1: October 2, 2015 (pembrolizumab); and BRAF : June 27, 2017 (dabrafenib + trametinib). We identified first-line (1L) therapy occurring within 4 months

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Alan P. Venook, Maria E. Arcila, Al B. Benson III, Donald A. Berry, David Ross Camidge, Robert W. Carlson, Toni K. Choueiri, Valerie Guild, Gregory P. Kalemkerian, Razelle Kurzrock, Christine M. Lovly, Amy E. McKee, Robert J. Morgan, Anthony J. Olszanski, Mary W. Redman, Vered Stearns, Joan McClure, and Marian L. Birkeland

melanomas. 42 Most of these mutations are the result of valine (V) to glutamate (E) or lysine (K) substitutions at amino acid position 600, resulting in a constitutively active form of the kinase. 43 Vemurafenib and dabrafenib are selective kinase