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Radiation and the Apo2L/TRAIL Apoptotic Pathway Preferentially Inhibit the Colonization of Premalignant Human Breast Cells Overexpressing Cyclin D1

Women’s Cancers Section [Q. Z., P. S. S.] and Flow Cytometry Unit [P. F., M. S-S.], Laboratory of Pathology and Radiation Biology Branch [W. D., J. B. M.], Division of Clinical Sciences, National Cancer Institute, Bethesda, Maryland 20892, and Department of Molecular Oncology, Genentech, Inc., South San Francisco, California 94080 [A. A.]

The role of cyclin D1 overexpression in human breast premalignancy was investigated using immortal, nontumorigenic MCF-10A cells. Previous work documented that cyclin D1 overexpression promoted in vitro anchorage-independent colonization. We now report that the colonization of MCF-10A cyclin D1 transfectants was preferentially inhibited by -radiation and specific classes of apoptosis inducers [Apo-2 ligand (Apo-2L), but not tumor necrosis factor ]. Antibody inhibition studies and semiquantitative PCR indicated that radiation inhibition of colonization was partially mediated via the Apo2L/TRAIL pathway. The apoptotic removal of cyclin D1-overexpressing, colonization-competent premalignant breast cells by Apo2L/TRAIL or other biologicals may represent a novel approach to the prevention of breast cancer.

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