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BRAF mutation predicts sensitivity to MEK inhibition

Author

Listed:
  • David B. Solit

    (Department of Medicine
    Memorial Sloan-Kettering Cancer Center)

  • Levi A. Garraway

    (Department of Medical Oncology
    Broad Institute of Harvard and MIT)

  • Christine A. Pratilas

    (Department of Pediatrics
    Memorial Sloan-Kettering Cancer Center)

  • Ayana Sawai

    (Memorial Sloan-Kettering Cancer Center)

  • Gad Getz

    (Broad Institute of Harvard and MIT)

  • Andrea Basso

    (Memorial Sloan-Kettering Cancer Center
    Schering-Plough)

  • 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
    Broad Institute of Harvard and MIT)

  • Judith Sebolt-Leopold

    (Pfizer Global Research and Development)

  • William R. Sellers

    (Department of Medical Oncology
    Broad Institute of Harvard and MIT)

  • Neal Rosen

    (Department of Medicine
    Memorial Sloan-Kettering Cancer Center)

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.

Suggested Citation

  • 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, 2006. "BRAF mutation predicts sensitivity to MEK inhibition," Nature, Nature, vol. 439(7074), pages 358-362, January.
    • Handle: RePEc:nat:nature:v:439:y:2006:i:7074:d:10.1038_nature04304
    DOI: 10.1038/nature04304
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    Cited by:

    1. Alison E. Smith & Emanuela Ferraro & Anton Safonov & Cristina Bernado Morales & Enrique J. Arenas Lahuerta & Qing Li & Amanda Kulick & Dara Ross & David B. Solit & Elisa Stanchina & Jorge Reis-Filho &, 2021. "HER2 + breast cancers evade anti-HER2 therapy via a switch in driver pathway," Nature Communications, Nature, vol. 12(1), pages 1-10, December.

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