Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation

Ramin Nazarian, Hubing Shi, Qi Wang, Xiangju Kong, Richard C. Koya, Hane Lee, Zugen Chen, Mi-Kyung Lee, Narsis Attar, Hooman Sazegar, Thinle Chodon, Stanley F. Nelson, Grant McArthur, Jeffrey A. Sosman, Antoni Ribas and Roger S. Lo ()
Additional contact information
Ramin Nazarian: UCLA’s Jonsson Comprehensive Cancer Center, 52-121 CHS, Los Angeles, California 90095-1750, USA
Hubing Shi: UCLA’s Jonsson Comprehensive Cancer Center, 52-121 CHS, Los Angeles, California 90095-1750, USA
Qi Wang: UCLA’s Jonsson Comprehensive Cancer Center, 52-121 CHS, Los Angeles, California 90095-1750, USA
Xiangju Kong: UCLA’s Jonsson Comprehensive Cancer Center, 52-121 CHS, Los Angeles, California 90095-1750, USA
Richard C. Koya: David Geffen School of Medicine, University of California
Hane Lee: David Geffen School of Medicine, University of California
Zugen Chen: David Geffen School of Medicine, University of California
Mi-Kyung Lee: UCLA’s Jonsson Comprehensive Cancer Center, 52-121 CHS, Los Angeles, California 90095-1750, USA
Narsis Attar: David Geffen School of Medicine, University of California
Hooman Sazegar: David Geffen School of Medicine, University of California
Thinle Chodon: David Geffen School of Medicine, University of California
Stanley F. Nelson: David Geffen School of Medicine, University of California
Grant McArthur: Peter MacCallum Cancer Center
Jeffrey A. Sosman: Vanderbilt-Ingram Cancer Center, 777 Preston Research Building, Nashville, Tennessee 37232-6838, USA
Antoni Ribas: David Geffen School of Medicine, University of California
Roger S. Lo: UCLA’s Jonsson Comprehensive Cancer Center, 52-121 CHS, Los Angeles, California 90095-1750, USA

Nature, 2010, vol. 468, issue 7326, 973-977

Abstract: Drug-resistance mechanism in melanoma Clinical trials in melanoma patients carrying B-RAF gene mutations have shown promising results with the B-RAF kinase inhibitor PLX4032, but many patients go on to become resistant. Two papers now uncover possible mechanisms for this resistance. Nazarian et al. report that melanomas can acquire resistance due to mutations of N-RAS or increased expression of PDGFRβ, and Johannessen et al. report resistance due to upregulation of MAP3K8/COT. Each of these mechanisms seems to apply to some patients in the recent PLX4032 trial, yet surprisingly, no secondary B-RAF mutations were observed.

Date: 2010
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DOI: 10.1038/nature09626

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