Literature DB >> 23020132

Combined BRAF and MEK inhibition in melanoma with BRAF V600 mutations.

Keith T Flaherty1, Jeffery R Infante, Adil Daud, Rene Gonzalez, Richard F Kefford, Jeffrey Sosman, Omid Hamid, Lynn Schuchter, Jonathan Cebon, Nageatte Ibrahim, Ragini Kudchadkar, Howard A Burris, Gerald Falchook, Alain Algazi, Karl Lewis, Georgina V Long, Igor Puzanov, Peter Lebowitz, Ajay Singh, Shonda Little, Peng Sun, Alicia Allred, Daniele Ouellet, Kevin B Kim, Kiran Patel, Jeffrey Weber.   

Abstract

BACKGROUND: Resistance to therapy with BRAF kinase inhibitors is associated with reactivation of the mitogen-activated protein kinase (MAPK) pathway. To address this problem, we conducted a phase 1 and 2 trial of combined treatment with dabrafenib, a selective BRAF inhibitor, and trametinib, a selective MAPK kinase (MEK) inhibitor.
METHODS: In this open-label study involving 247 patients with metastatic melanoma and BRAF V600 mutations, we evaluated the pharmacokinetic activity and safety of oral dabrafenib (75 or 150 mg twice daily) and trametinib (1, 1.5, or 2 mg daily) in 85 patients and then randomly assigned 162 patients to receive combination therapy with dabrafenib (150 mg) plus trametinib (1 or 2 mg) or dabrafenib monotherapy. The primary end points were the incidence of cutaneous squamous-cell carcinoma, survival free of melanoma progression, and response. Secondary end points were overall survival and pharmacokinetic activity.
RESULTS: Dose-limiting toxic effects were infrequently observed in patients receiving combination therapy with 150 mg of dabrafenib and 2 mg of trametinib (combination 150/2). Cutaneous squamous-cell carcinoma was seen in 7% of patients receiving combination 150/2 and in 19% receiving monotherapy (P=0.09), whereas pyrexia was more common in the combination 150/2 group than in the monotherapy group (71% vs. 26%). Median progression-free survival in the combination 150/2 group was 9.4 months, as compared with 5.8 months in the monotherapy group (hazard ratio for progression or death, 0.39; 95% confidence interval, 0.25 to 0.62; P<0.001). The rate of complete or partial response with combination 150/2 therapy was 76%, as compared with 54% with monotherapy (P=0.03).
CONCLUSIONS: Dabrafenib and trametinib were safely combined at full monotherapy doses. The rate of pyrexia was increased with combination therapy, whereas the rate of proliferative skin lesions was nonsignificantly reduced. Progression-free survival was significantly improved. (Funded by GlaxoSmithKline; ClinicalTrials.gov number, NCT01072175.).

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Year:  2012        PMID: 23020132      PMCID: PMC3549295          DOI: 10.1056/NEJMoa1210093

Source DB:  PubMed          Journal:  N Engl J Med        ISSN: 0028-4793            Impact factor:   91.245


  26 in total

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Authors:  Gerald S Falchook; Karl D Lewis; Jeffrey R Infante; Michael S Gordon; Nicholas J Vogelzang; Douglas J DeMarini; Peng Sun; Christopher Moy; Stephen A Szabo; Lori T Roadcap; Vijay G R Peddareddigari; Peter F Lebowitz; Ngocdiep T Le; Howard A Burris; Wells A Messersmith; Peter J O'Dwyer; Kevin B Kim; Keith Flaherty; Johanna C Bendell; Rene Gonzalez; Razelle Kurzrock; Leslie A Fecher
Journal:  Lancet Oncol       Date:  2012-07-16       Impact factor: 41.316

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9.  MEK1 mutations confer resistance to MEK and B-RAF inhibition.

Authors:  Caroline M Emery; Krishna G Vijayendran; Marie C Zipser; Allison M Sawyer; Lili Niu; Jessica J Kim; Charles Hatton; Rajiv Chopra; Patrick A Oberholzer; Maria B Karpova; Laura E MacConaill; Jianming Zhang; Nathanael S Gray; William R Sellers; Reinhard Dummer; Levi A Garraway
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10.  RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF.

Authors:  Poulikos I Poulikakos; Chao Zhang; Gideon Bollag; Kevan M Shokat; Neal Rosen
Journal:  Nature       Date:  2010-03-18       Impact factor: 49.962

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