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Genes Dev. 1998 Aug 15;12(16):2469-74.

Reduced skin tumor development in cyclin D1-deficient mice highlights the oncogenic ras pathway in vivo.

Robles AI, Rodriguez-Puebla ML, Glick AB, Trempus C, Hansen L, Sicinski P, Tennant RW, Weinberg RA, Yuspa SH, Conti CJ.

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The University of Texas, M.D. Anderson Cancer Center, Science Park-Research Division (SPRD), Smithville, Texas 78957 USA.

Abstract

Cyclin D1 is part of a cell cycle control node consistently deregulated in most human cancers. However, studies with cyclin D1-null mice indicate that it is dispensable for normal mouse development as well as cell growth in culture. Here, we provide evidence that ras-mediated tumorigenesis depends on signaling pathways that act preferentially through cyclin D1. Cyclin D1 expression and the activity of its associated kinase are up-regulated in keratinocytes in response to oncogenic ras. Furthermore, cyclin D1 deficiency results in up to an 80% decrease in the development of squamous tumors generated through either grafting of retroviral ras-transduced keratinocytes, phorbol ester treatment of ras transgenic mice, or two-stage carcinogenesis.

PMID:: 9716400; [PubMed - indexed for MEDLINE]
PMCID:: PMC317082

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