BRAF mutation predicts sensitivity to MEK inhibition

David B. Solit, Levi A. Garraway, Christine A. Pratilas, Ayana Sawai, Gad Getz, Andrea Basso, Qing Ye, Jose M. Lobo, Yuhong She, Iman Osman, Todd R. Golub, Judith Sebolt-Leopold, William R. Sellers and Neal Rosen ()
Additional contact information
David B. Solit: Department of Medicine
Levi A. Garraway: Department of Medical Oncology
Christine A. Pratilas: Department of Pediatrics
Ayana Sawai: Memorial Sloan-Kettering Cancer Center
Gad Getz: Broad Institute of Harvard and MIT
Andrea Basso: Memorial Sloan-Kettering Cancer Center
Qing Ye: Memorial Sloan-Kettering Cancer Center
Jose M. Lobo: Memorial Sloan-Kettering Cancer Center
Yuhong She: Memorial Sloan-Kettering Cancer Center
Iman Osman: New York University Medical Center
Todd R. Golub: Harvard Medical School
Judith Sebolt-Leopold: Pfizer Global Research and Development
William R. Sellers: Department of Medical Oncology
Neal Rosen: Department of Medicine

Nature, 2006, vol. 439, issue 7074, 358-362

Abstract: Tumour profiling advances Molecular tumour profiling is one way in which effective targeted cancer treatment regimes might be developed. Two groups report significant developments in this direction. Bild et al. studied gene expression patterns that reflect the activation of various oncogenic (cancer-causing) signal transduction pathways. Using combinations of these pathway signatures, they predict which patients with breast, lung or ovarian cancer have a particularly poor prognosis. The ability to identify molecular pathways that are deregulated in a particular cancer in this way might be used to predict its sensitivity to specific therapeutic drugs. Solit et al. studied tumour cells with mutations in the RAS and BRAF genes, thought to cause cancer at least in part by activating the MEK/ERK signalling pathway. They show that tumours with the BRAF mutation, but not RAS, are highly sensitive to PD0325901, an MEK inhibitor that is in early-stage clinical trials in patients with melanoma, colon, breast and lung cancers. So by testing for the presence of BRAF mutations it may be possible to identify those patients most likely to benefit from this type of drug.

Date: 2006
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DOI: 10.1038/nature04304

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