c-Myc and Activated Ras During Skin Tumorigenesis: Cooperation at the Cancer Stem Cell Level?
Mutations leading to overexpression and activation of the oncogenes Myc and Ras are among the most frequent lesions known to occur in human and murine cancers. These genes are also the pioneering example for oncogene cooperation during tumorigenesis, whereby the anticancer effects of Myc deregulation (apoptosis) and oncogenic Ras (senescence) are antagonized and therefore canceled out by each other. Here I review the role of endogenous and overexpressed c-Myc in murine skin, focusing primarily on epidermal stem cells. In addition, recent data suggesting an essential role for the endogenous c-Myc-p21CIP1 pathway in Ras-driven skin tumorigenesis are discussed.
KeywordsHair Follicle Epidermal Stem Cell Bulge Region Interfollicular Epidermis Skin Tumorigenesis
The author would like to thank Drs. Thordur Oskarsson, Christelle Adolphe and Anne Wilson for critical comments on the manuscript. This work was supported by grants to A.T. from the Swiss National Science Foundation, the Swiss Cancer League, and the EU-FP6 Program “INTACT”.
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