Integrative genomic analyses identify MITF as a lineage survival oncogene amplified in malignant melanoma

Levi A. Garraway, Hans R. Widlund, Mark A. Rubin, Gad Getz, Aaron J. Berger, Sridhar Ramaswamy, Rameen Beroukhim, Danny A. Milner, Scott R. Granter, Jinyan Du, Charles Lee, Stephan N. Wagner, Cheng Li, Todd R. Golub, David L. Rimm, Matthew L. Meyerson, David E. Fisher and William R. Sellers ()
Additional contact information
Levi A. Garraway: Dana-Farber Cancer Institute
Hans R. Widlund: Dana-Farber Cancer Institute
Mark A. Rubin: Brigham and Women's Hospital and Harvard Medical School
Gad Getz: The Broad Institute of Harvard and MIT
Aaron J. Berger: Yale University School of Medicine
Sridhar Ramaswamy: The Broad Institute of Harvard and MIT
Rameen Beroukhim: Dana-Farber Cancer Institute
Danny A. Milner: Brigham and Women's Hospital and Harvard Medical School
Scott R. Granter: Brigham and Women's Hospital and Harvard Medical School
Jinyan Du: Dana-Farber Cancer Institute
Stephan N. Wagner: Medical University of Vienna
Cheng Li: Dana-Farber Cancer Institute
Todd R. Golub: Dana-Farber Cancer Institute
David L. Rimm: Yale University School of Medicine
Matthew L. Meyerson: Dana-Farber Cancer Institute
David E. Fisher: Dana-Farber Cancer Institute
William R. Sellers: Dana-Farber Cancer Institute

Nature, 2005, vol. 436, issue 7047, 117-122

Abstract: Melanoma target Analysis of pharmacological and genetic data from the US National Cancer Institute's NCI60 collection of cancer cell lines has identified a novel DNA amplification event in human melanomas. It alters MITF gene expression to promote melanoma formation, probably in cooperation with mutated BRAF, another key melanoma gene. Amplification of MITF may also help melanoma cells resist destruction by drugs. This work identifies MITF itself as a possible drug target in melanoma, and may encourage future genomics efforts to identify genetic alterations in other cancers.

Date: 2005
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DOI: 10.1038/nature03664

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