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Rohan Maniar, Stephanie M. Gallitano, Sameera Husain, Golnaz Moazami, Michael J. Weiss, and Catherine A. Shu

painful eruption over the bilateral lower extremities. First-line treatment with a BRAF inhibitor, dabrafenib at 150 mg twice daily, and an MEK inhibitor, trametinib at 2 mg daily, had been initiated 3 months prior. She had no pertinent dermatologic

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

(LGGs; Table 1 ). This report describes the use of combination dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor) in 2 adults with high-grade gliomas (HGGs). The first patient was treated at time of diagnosis, whereas the second was treated at

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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

dabrafenib and TTFields resulted in a durable complete response of more than 2 years. Case Presentation We reviewed the medical records of a male patient who is undergoing treatment at the Department of Neuro-Oncology at Baylor University Medical

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James S. Blachly, Gerard Lozanski, David M. Lucas, Michael R. Grever, Kari Kendra, and Leslie A. Andritsos

small molecule BRAF inhibitor vemurafenib. 7 , 10 The newer BRAF inhibitor dabrafenib has also been approved for use in melanoma. This report presents the first case of the cooccurrence of malignant melanoma and HCL, both harboring the BRAF p

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Anastasia Drobysheva, Laura J. Klesse, Daniel C. Bowers, Veena Rajaram, Dinesh Rakheja, Charles F. Timmons, Jason Wang, Korgun Koral, Lynn Gargan, Erica Ramos, and Jason Y. Park

treatment of low- and high-grade gliomas with BRAF inhibitors (vemurafenib and dabrafenib). 8 – 13 There is only a single report of 2 patients with PAs who were treated with trametinib, a MAPK pathway inhibitor, 5 and no reports on MAPK pathway

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Victor T.G. Lin, Lisle M. Nabell, Sharon A. Spencer, William R. Carroll, Shuko Harada, and Eddy S. Yang

was identified. After discussion by the UAB MTB, 1 he was started on targeted therapy with the BRAF inhibitor dabrafenib and the MEK inhibitor trametinib, in addition to zoledronic acid for his bony metastases ( Figure 1 ). Dabrafenib and trametinib

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Rishi Agarwal, Jiang Wang, Keith Wilson, William Barrett, and John C. Morris

dabrafenib and trametinib, and experienced a response. Case Report A 47-year-old woman with a history of moderately severe rheumatoid arthritis treated with infliximab and methotrexate presented with a 1-month history of a rapidly enlarging left neck

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Presenter: Genevieve Boland

adjuvant therapy trials of immune checkpoint inhibitors (ICIs) in stage III–IV melanoma and their outcomes. Figure 1. Adjuvant therapy in stage III–IV melanoma. Abbreviations: D/T, dabrafenib + trametinib; DMFS, distant metastasis–free survival; HR

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Jarred Burkart, Dwight Owen, Manisha H. Shah, Sherif R. Z. Abdel-Misih, Sameek Roychowdhury, Robert Wesolowski, Sigurdis Haraldsdottir, Julie W. Reeser, Eric Samorodnitsky, Amy Smith, and Bhavana Konda

Klempner et al, 2 the patient was initiated on oral treatment with off-label dabrafenib, 150 mg twice daily, and trametinib, 2 mg daily. Restaging scans performed 8 weeks after initiation of dabrafenib/trametinib combination therapy demonstrated

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Daniel G. Coit, John A. Thompson, Robert Andtbacka, Christopher J. Anker, Christopher K. Bichakjian, William E. Carson III, Gregory A. Daniels, Adil Daud, Dominick DiMaio, Martin D. Fleming, Rene Gonzalez, Valerie Guild, Allan C. Halpern, F. Stephen Hodi Jr, Mark C. Kelley, Nikhil I. Khushalani, Ragini R. Kudchadkar, Julie R. Lange, Mary C. Martini, Anthony J. Olszanski, Merrick I. Ross, April Salama, Susan M. Swetter, Kenneth K. Tanabe, Vijay Trisal, Marshall M. Urist, Nicole R. McMillian, and Maria Ho

%, respectively). 3 Treatment options for patients harboring BRAF V600 mutations are increasing with the approval of additional targeted inhibitors, dabrafenib and trametinib. However, because of the rapid development of therapeutic resistance after initial