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Hey F, Pritchard C. A new mode of RAF autoregulation: a further complication in the inhibitor paradox. Cancer Cell. 2013;23(5):561-3doi: 10.1016/j.ccr.2013.04.021.
Hey, F., & Pritchard, C. (2013). A new mode of RAF autoregulation: a further complication in the inhibitor paradox. Cancer cell, 23(5), 561-3. https://doi.org/10.1016/j.ccr.2013.04.021
Hey, Fiona, and Pritchard, Catrin. "A new mode of RAF autoregulation: a further complication in the inhibitor paradox." Cancer cell vol. 23,5 (2013): 561-3. doi: https://doi.org/10.1016/j.ccr.2013.04.021
Hey F, Pritchard C. A new mode of RAF autoregulation: a further complication in the inhibitor paradox. Cancer Cell. 2013 May 13;23(5):561-3. doi: 10.1016/j.ccr.2013.04.021. PMID: 23680140.
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Cancer Cell. 2013 May 13;23(5):561-3. doi: 10.1016/j.ccr.2013.04.021.

A new mode of RAF autoregulation: a further complication in the inhibitor paradox.

Cancer cell

Fiona Hey, Catrin Pritchard

Affiliations

  1. Department of Biochemistry, University of Leicester, Lancaster Road, Leicester LE1 9HN, UK.

PMID: 23680140 DOI: 10.1016/j.ccr.2013.04.021

Abstract

ERK pathway activation in cells expressing wild-type BRAF is a well-reported, clinically-relevant adverse effect of the otherwise impressive response of BRAF(V600E)-mutated melanomas to RAF inhibitors. In this issue of Cancer Cell, Holderfield and colleagues show that RAF autoinhibition underpins this paradox, further complicating therapeutic strategies centered around RAF.

Copyright © 2013 Elsevier Inc. All rights reserved.

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