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- W1019048771 abstract "AbstractFor half of the advanced melanoma population, selective BRAF inhibitor therapy has transformed the natural history of disease and provided a platform for developing molecularly targeted therapy combinations. The clinical utility of vemurafenib, FDA approved BRAF inhibitor, has been validated by another potent and selective agent, dabrafenib. However, two clinical limitations of BRAF inhibitor therapy frame the problem for the melanoma field: de novo and acquired resistance. Insights into the mechanisms underlying both of these phenomena have set the stage for clinical investigation of several novel BRAF inhibitor based combination therapies. Foremost among them is the combination of a MEK inhibitor with BRAF inhibitor. Preliminary clinical evidence suggests that this combination may supplant single agent BRAF inhibitor therapy in the near future as the standard approach for metastatic patients. Yet resistance remains a challenge and strategies to target non-MAP kinase pathway dependent mechanisms are needed. This chapter will outline the preclinical evidence that supports the categorization of resistance mechanisms and the framework for clinical investigation of novel combination therapies.KeywordsMelanomaBRAFResistanceReceptor tyrosine kinasesPI3K pathwayCyclin dependent kinasesApoptosis" @default.
- W1019048771 created "2016-06-24" @default.
- W1019048771 creator A5023174631 @default.
- W1019048771 date "2014-11-25" @default.
- W1019048771 modified "2023-09-24" @default.
- W1019048771 title "Moving Forward: Making BRAF-Targeted Therapy Better" @default.
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- W1019048771 doi "https://doi.org/10.1007/978-1-4939-2143-0_9" @default.
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