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A STATement on vemurafenib-resistant melanoma
Journal article   Open access   Peer reviewed

A STATement on vemurafenib-resistant melanoma

Edward J Hartsough and Andrew E Aplin
Journal of investigative dermatology, v 133(8), pp 1928-1929
01 Aug 2013
PMID: 23856932
url
https://doi.org/10.1038/jid.2013.136View
Published, Version of Record (VoR) Open

Abstract

Drug Resistance, Neoplasm - physiology Humans Indoles - pharmacology Keratinocytes - drug effects Male Melanoma - drug therapy Skin Neoplasms - drug therapy STAT3 Transcription Factor - antagonists & inhibitors Sulfonamides - pharmacology
Despite recent advancements in the treatment of late-stage mutant BRAF (V600E/K) melanomas, a major hurdle continues to be acquired resistance to BRAF inhibitors such as vemurafenib. The mechanisms for resistance have proven to be heterogeneous, emphasizing the need to use broad therapeutic approaches. In this issue, the study "Stat3-targeted therapies overcome the acquired resistance to vemurafenib in melanomas" by Liu et al. proposes that signal transducer and activator of transcription 3 (STAT3)-paired box 3 (PAX3) signaling may be a mechanism that is used by melanomas to resist RAF inhibitors.

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Dermatology
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