Tunable-Combinatorial Mechanisms of Acquired Resistance Limit the Efficacy of BRAF/MEK Cotargeting but Result in Melanoma Drug Addiction
Open Access
- 15 January 2015
- journal article
- research article
- Published by Elsevier BV in Cancer Cell
- Vol. 27 (2), 240-256
- https://doi.org/10.1016/j.ccell.2014.11.018
Abstract
No abstract availableThis publication has 22 references indexed in Scilit:
- Acquired Resistance and Clonal Evolution in Melanoma during BRAF Inhibitor TherapyCancer Discovery, 2014
- The Genetic Landscape of Clinical Resistance to RAF Inhibition in Metastatic MelanomaCancer Discovery, 2014
- Single-molecule superresolution imaging allows quantitative analysis of RAF multimer formation and signalingProceedings of the National Academy of Sciences of the United States of America, 2013
- Concurrent MEK2 Mutation and BRAF Amplification Confer Resistance to BRAF and MEK Inhibitors in MelanomaCell Reports, 2013
- Modelling vemurafenib resistance in melanoma reveals a strategy to forestall drug resistanceNature, 2013
- Exome sequencing identifies recurrent somatic RAC1 mutations in melanomaNature Genetics, 2012
- A Landscape of Driver Mutations in MelanomaCell, 2012
- Preexisting MEK1 Exon 3 Mutations in V600E/K BRAF Melanomas Do Not Confer Resistance to BRAF InhibitorsCancer Discovery, 2012
- Melanoma whole-exome sequencing identifies V600EB-RAF amplification-mediated acquired B-RAF inhibitor resistanceNature Communications, 2012
- MEK1 mutations confer resistance to MEK and B-RAF inhibitionProceedings of the National Academy of Sciences of the United States of America, 2009