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Cyclin D1 in Breast Cancer Pathogenesis

From the Center for Molecular Medicine, University of Connecticut School of Medicine, Farmington, CT

Address reprint requests to Andrew Arnold, MD, Center for Molecular Medicine, University of Connecticut School of Medicine, 263 Farmington Ave, Farmington, CT 06030-3101; e-mail: molecularmedicine{at}uchc.edu

Taking a perspective on available evidence that emphasizes relevance to human disease, cyclin D1 is solidly established as an oncogene with an important pathogenetic role in breast cancer and other human tumors. However, the precise cellular mechanisms through which aberrant cyclin D1 expression drives human neoplasia are less well established. Indeed, emerging evidence suggests that cyclin D1 might act, predominantly or at least in part, through pathways that do not involve its widely accepted function as a cell cycle regulator. Although therapeutic exploitation of the role of cyclin D1 as a molecular driver of breast cancer carries great promise, it is also suggested that direct targeting of the cyclin D1 gene or gene products may prove more successful than approaches that rely on arguably incomplete knowledge of the oncogenic mechanisms of cyclin D1.

Supported by a grant CA55909 (to A.A.) from the National Institutes of Health and a postdoctoral fellowship from the Susan G. Komen Breast Cancer Foundation (to A.P).

Authors' disclosures of potential conflicts of interest are found at the end of this article.

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