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In vivo MAPK reporting reveals the heterogeneity in tumoral selection of resistance to RAF inhibitors
Journal article   Open access   Peer reviewed

In vivo MAPK reporting reveals the heterogeneity in tumoral selection of resistance to RAF inhibitors

Kevin J. Basile, Ethan V. Abel, Neda Dadpey, Edward J. Hartsough, Paolo Fortina and Andrew E. Aplin
Cancer research (Chicago, Ill.), v 73(23), pp 7101-7110
01 Dec 2013
PMID: 24121492
url
https://doi.org/10.5334/aogh.3963View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open

Abstract

ERK1 luciferase RAF resistance vemurafenib
Activation of the ERK1/2 mitogen-activated protein kinases (MAPKs) confers resistance to the RAF inhibitors vemurafenib and dabrafenib in mutant BRAF-driven melanomas. Methods to understand how resistance develops are important to optimize the clinical utility of RAF inhibitors in patients. Here we report the development of a novel ERK1/2 reporter system that provides a non-invasive, quantitative and temporal analysis of RAF inhibitor efficacy in vivo . Use of this system revealed heterogeneity in the level of ERK1/2 reactivation associated with acquired resistance to RAF inhibition. We identified several distinct novel and known molecular changes in resistant tumors emerging from treatment-naïve cell populations including BRAF V600E variants and HRAS mutation, both of which were required and sufficient for ERK1/2 reactivation and drug resistance. Our work offers an advance in understanding RAF inhibitor resistance and the heterogeneity in resistance mechanisms, which emerge from a malignant cell population.

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Web of Science research areas
Oncology
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