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-p21(CIP1) pathway in Ras-driven skin tumorigenesis are discussed.
Trumpp
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Genetics and Stem Cell Laboratory, Swiss Institute for Experimental Cancer Research (ISREC), Ch. des Boveresses 155, CH-1066 Epalinges, Switzerland. Andreas.Trumpp@isrec.ch
D002471:Cell Transformation, Neoplastic; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism*; D006801:Humans; D016271:Proto-Oncogene Proteins c-myc / Q000378:metabolism* / Q000502:physiology; D012867:Skin / Q000378:metabolism / Q000503:physiopathology; D012878:Skin Neoplasms / Q000378:metabolism* / Q000473:pathology; D013234:Stem Cells / Q000166:cytology*
C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016271:Proto-Oncogene Proteins c-myc