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Epigenetic Mechanisms of Escape from BRAF Oncogene Dependency

1
Department of Biomedical Engineering, University of Michigan Medical School, Ann Arbor, MI 48109, USA
2
Program in Cancer Biology, University of Michigan Medical School, Ann Arbor, MI 48109, USA
3
Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI 48109, USA
*
Author to whom correspondence should be addressed.
Cancers 2019, 11(10), 1480; https://doi.org/10.3390/cancers11101480
Received: 13 August 2019 / Revised: 28 September 2019 / Accepted: 29 September 2019 / Published: 1 October 2019
(This article belongs to the Special Issue Oncogenic Forms of BRAF as Cancer Driver Genes)
About eight percent of all human tumors (including 50% of melanomas) carry gain-of-function mutations in the BRAF oncogene. Mutated BRAF and subsequent hyperactivation of the MAPK signaling pathway has motivated the use of MAPK-targeted therapies for these tumors. Despite great promise, however, MAPK-targeted therapies in BRAF-mutant tumors are limited by the emergence of drug resistance. Mechanisms of resistance include genetic, non-genetic and epigenetic alterations. Epigenetic plasticity, often modulated by histone-modifying enzymes and gene regulation, can influence a tumor cell’s BRAF dependency and therefore, response to therapy. In this review, focusing primarily on class 1 BRAF-mutant cells, we will highlight recent work on the contribution of epigenetic mechanisms to inter- and intratumor cell heterogeneity in MAPK-targeted therapy response. View Full-Text
Keywords: oncogene addiction; BRAF-mutant tumors; BRAF and MEK-targeted therapies; phenotype switching; tumor heterogeneity; epigenetic regulation; adaptive drug resistance; histone-modifying enzymes; chromatin regulation; DNA methylation oncogene addiction; BRAF-mutant tumors; BRAF and MEK-targeted therapies; phenotype switching; tumor heterogeneity; epigenetic regulation; adaptive drug resistance; histone-modifying enzymes; chromatin regulation; DNA methylation
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Khaliq, M.; Fallahi-Sichani, M. Epigenetic Mechanisms of Escape from BRAF Oncogene Dependency. Cancers 2019, 11, 1480.

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