Journal Article

Targets of Raf in tumorigenesis

Théodora S. Niault and Manuela Baccarini

in Carcinogenesis

Volume 31, issue 7, pages 1165-1174
Published in print July 2010 | ISSN: 0143-3334
Published online January 2010 | e-ISSN: 1460-2180 | DOI:
Targets of Raf in tumorigenesis

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Some 25 years ago, Raf was discovered as the transforming principle shared by a murine sarcoma and an avian carcinoma virus. Thus, Raf and tumorigenesis have been connected from the very beginning. Ten years later, the work of many groups instated Raf as the link between Ras, the oncogene most frequently mutated in human cancers, and the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK/ERK) module, which with its manifold substrates can contribute to different aspects of carcinogenesis. Finally, the discovery of activating B-Raf mutations in a subset of human cancers, notably melanomas, conclusively established Raf as a major player in tumor development. Recent studies in animal models now show that endogenous C-Raf is essential for the development and maintenance of Ras-induced epidermal tumors. Surprisingly, the role of C-Raf in this case is not that of an mitogen-activated protein kinase activator, but rather that of an endogenous inhibitor of Rho signaling, expanding the range of tumor-related Raf targets. This review focuses on old and new targets of Raf in tumorigenesis.

Journal Article.  8266 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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