RAF/RAS oncogenes and mismatch-repair status

Harith Rajagopalan, Alberto Bardelli, Christoph Lengauer, Kenneth W. Kinzler, Bert Vogelstein and Victor E. Velculescu ()
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Harith Rajagopalan: Sidney Kimmel Comprehensive Cancer Center, Howard Hughes Medical Institute, and Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine
Alberto Bardelli: Sidney Kimmel Comprehensive Cancer Center, Howard Hughes Medical Institute, and Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine
Christoph Lengauer: Sidney Kimmel Comprehensive Cancer Center, Howard Hughes Medical Institute, and Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine
Kenneth W. Kinzler: Sidney Kimmel Comprehensive Cancer Center, Howard Hughes Medical Institute, and Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine
Bert Vogelstein: Sidney Kimmel Comprehensive Cancer Center, Howard Hughes Medical Institute, and Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine
Victor E. Velculescu: Sidney Kimmel Comprehensive Cancer Center, Howard Hughes Medical Institute, and Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine

Nature, 2002, vol. 418, issue 6901, 934-934

Abstract: Abstract Genes of the RAF family encode kinases that are regulated by Ras and mediate cellular responses to growth signals. Activating mutations in one RAF gene, BRAF, have been found in a high proportion of melanomas and in a small fraction of other cancers1. Here we show that BRAF mutations in colorectal cancers occur only in tumours that do not carry mutations in a RAS gene known as KRAS, and that BRAF mutation is linked to the proficiency of these tumours in repairing mismatched bases in DNA. Our results not only provide genetic support for the idea that mutations in BRAF and KRAS exert equivalent effects in tumorigenesis2, but also emphasize the role of repair processes in establishing the mutation spectra that underpin human cancer.

Date: 2002
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DOI: 10.1038/418934a

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