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Mammary Gland Development, Reproductive History, and Breast Cancer Risk¹

Departments of Molecular and Cellular Engineering [L. A. C., C. M. D., H. P. G., S. I H., S. T. M., J. V. R., D. B. S., J. Y. W., M. W.], and Department of Medicine, Division of Endocrinology, Diabetes and Metabolism [L. A. C.], Stellar-Chance Laboratories, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6100

^* To whom requests for reprints should be addressed, at Department of Molecular and Cellular Engineering, Stellar-Chance Laboratories, Room 309A, University of Pennsylvania School of Medicine, 422 Curie Boulevard, Philadelphia, PA 19104-6100. Phone: (215) 898-1321; Fax: (215) 573-8590; E-mail: chodosh{at}mail.med.upenn.edu.

The observation that normal pathways of differentiation and development are invariably altered during the process of carcinogenesis implies an intrinsic relationship between these processes. This relationship is particularly evident in the breast, as exemplified by the existence of endocrine risk factors for breast cancer that are related to the timing of normal developmental events. Understanding the mechanisms by which normal developmental events alter breast cancer risk is a central focus of our laboratory. Herein, we describe three approaches being taken in our laboratory toward defining the molecular basis of this relationship. These include: determining the roles played by the tumor suppressor genes, BRCA1 and BRCA2, in the normal differentiation and development of the breast; studying the function of three novel protein kinases identified in our laboratory in mammary epithelial development; and defining the molecular and cellular changes that occur in the breast as a result of reproductive events known to influence breast cancer risk.

¹ Presented at the "General Motors Cancer Research Foundation Twentieth Annual Scientific Conference: Developmental Biology and Cancer," June 9–10, 1998, Bethesda, MD. This work was supported by: NIH Grants CA71513 (to L. A. C.) and CA78410 (to L. A. C.) from the National Cancer Institute and the National Institute of Diabetes and Digestive and Kidney Diseases; American Cancer Society Grant RPG-97-097-01-CCG (to L. A. C.); United States Army Breast Cancer Research Program Grants DAMD17-96-1-6113 (to L. A. C.), DAMD17-96-1-6112 (to H. P. G.), DAMD17-98-1-8227 (to C. M. D.), DAMD17-98-1-8235 (to D. B. S.), and DAMD17-98-2-8226 (to L. A. C.); and the Charles E. Culpeper Foundation (to L. A. C.). L. A. C. is a Charles E. Culpeper Medical Scholar.

Received 11/11/98. Accepted 2/ 4/99.

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