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- Aubhishek Zaman
- Department of Medicine, University of California, San Francisco, CA 94143, USA
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- Wei Wu
- Department of Medicine, University of California, San Francisco, CA 94143, USA
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- Trever G. Bivona
- Department of Medicine, University of California, San Francisco, CA 94143, USA
書誌事項
- 公開日
- 2019-08-16
- 権利情報
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- https://creativecommons.org/licenses/by/4.0/
- DOI
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- 10.3390/cancers11081197
- 公開者
- MDPI AG
説明
<jats:p>Identifying recurrent somatic genetic alterations of, and dependency on, the kinase BRAF has enabled a “precision medicine” paradigm to diagnose and treat BRAF-driven tumors. Although targeted kinase inhibitors against BRAF are effective in a subset of mutant BRAF tumors, resistance to the therapy inevitably emerges. In this review, we discuss BRAF biology, both in wild-type and mutant settings. We discuss the predominant BRAF mutations and we outline therapeutic strategies to block mutant BRAF and cancer growth. We highlight common mechanistic themes that underpin different classes of resistance mechanisms against BRAF-targeted therapies and discuss tumor heterogeneity and co-occurring molecular alterations as a potential source of therapy resistance. We outline promising therapy approaches to overcome these barriers to the long-term control of BRAF-driven tumors and emphasize how an extensive understanding of these themes can offer more pre-emptive, improved therapeutic strategies.</jats:p>
収録刊行物
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- Cancers
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Cancers 11 (8), 1197-, 2019-08-16
MDPI AG
