Charles V. Clevenger,
Priscilla A. Furth,
Susan E. Hankinson and
Linda A. Schuler
Department of Pathology and Laboratory Medicine (C.V.C), University of Pennsylvania, Philadelphia, Pennsylvania 19104; Lombardi Cancer Center (P.A.F.), Department of Oncology, Georgetown University, Washington, D.C. 20057; Channing Laboratories, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, and Department of Epidemiology (S.E.H.), Harvard School of Public Health, Cambridge, Massachusetts 02115; and Department of Comparative Bioscience (L.A.S.), University of Wisconsin, Madison, Wisconsin 53706
Correspondence: Address all correspondence and requests for reprints to: Charles V. Clevenger, M.D., Ph.D., Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104. E-mail: clevengc{at}mail.med.upenn.edu
The contribution of prolactin (PRL) to the pathogenesis andprogression of human breast cancer at the cellular, transgenic,and epidemiological levels is increasingly appreciated. Actingat the endocrine and autocrine/paracrine levels, PRL functionsto stimulate the growth and motility of human breast cancercells. The actions of this ligand are mediated by at least sixrecognized PRL receptor isoforms found on, or secreted by, humanbreast epithelium. The PRL/PRL receptor complex associates withand activates several signaling networks that are shared withother members of the cytokine receptor superfamily. Coupledwith the recently identified intranuclear function of PRL, thesenetworks are integrated into the in vitro and in vivo actionsinduced by ligand. These findings indicate that antagonistsof PRL/PRL receptor interaction or PRL receptor-associated signaltransduction may be of considerable utility in the treatmentof human breast cancer.
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