Accession Number : ADA331989
Title : Modulation of Cyclin Expression by c-Myc in Malignant and Nonmalignant Mammary Epithelial Cells.
Descriptive Note : Final rept. 1 Sep 94-31 Aug 97,
Corporate Author : GEORGETOWN UNIV WASHINGTON DC
Personal Author(s) : Dickson, Robert B. ; Benaud, Christelle
PDF Url : ADA331989
Report Date : AUG 1997
Pagination or Media Count : 52
Abstract : The purpose of this grant was to support predoctoral training on an experimental model relevant to breast cancer etiology. Specifically, we explored the multifactorial nature of the interaction a growth factor (TGFalpha, which is commonly expressed both in benign and malignant proliferative disease of the human breast) and an oncogene (c-myc, whose gene is amplified and whose protein is inappropriately expressed in 20-30% of human breast tumors. Using a transgenic mouse model we observed that co-expression of these two genes was remarkably synergistic for onset and progression of cell survival and proliferation. While mye induced both p53 and bax death-promoting genes, TCFalpha promoted cell survival by inducing Bc1XL. In terms of the cell cycle, mye shortened G1 by modulating cyc1lin E, p27, and cdc25A, which activated cdk-2 and inactivated Rb. Thus, the interaction of TGFalpha and myc promoted shortened, aberrant cycles resulting in survival of genetically aberrant cells.
Descriptors : *HUMANS, *BREAST CANCER, EPITHELIUM, SURVIVABILITY, GROWTH(GENERAL), NEOPLASMS, GENES, CELLS(BIOLOGY), ABNORMALITIES, MAMMARY GLANDS, DISEASE VECTORS.
Subject Categories : Anatomy and Physiology
Medicine and Medical Research
Distribution Statement : APPROVED FOR PUBLIC RELEASE