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ER and PR in Renomedullary Interstitial Cells During Syrian Hamster Estrogen-Induced Tumorigenesis: Evidence for Receptor-Mediated Oncogenesis

Hormonal Carcinogenesis Laboratory, Division of Etiology and Prevention of Hormonal Cancers, Kansas Cancer Institute, and Departments of Pharmacology, Toxicology, and Therapeutics (J.J.L., S.J.W., S.A.L.); Preventive Medicine (J.J.L.); and Pathology and Laboratory Medicine (O.T., M.F.D.), University of Kansas Medical Center, Kansas City, Kansas 66160-7312; and Department of Hematology/Oncology, University of Alabama (X.H.), Birmingham, Alabama 35294

Address all correspondence and requests for reprints to: Dr. Jonathan J. Li, Division of Etiology and Prevention of Hormonal Cancers, Kansas Cancer Institute, University of Kansas Medical Center, 1043 Lied Biomedical Research Facility, 3901 Rainbow Boulevard, Kansas City, Kansas 66160-7312. E-mail: jlil{at}kumc.edu

The estrogen-induced and -dependent Syrian hamster renal tumor is the most intensively studied model in estrogen carcinogenesis. Yet, it remains confounding that the kidney of this species behaves as an estrogen target tissue. As both reproductive and urinary systems arise from the same germinal ridge, we propose that some of the germinal cells, normally destined for the uterus, migrate and establish themselves in the renal corticomedullary region in this hamster strain. These ectopically located germinal cells remain dormant unless exposed to estrogen. Supporting this contention, a subset of renal interstitial cells, primarily located in the corticomedullary region, express PR after only 2 wk and ER after 1.5–3.0 months of estrogen treatment. As treatment continues, groups of cells of the renal interstitium and small and large renal tumors show ER⁺ and PR⁺ staining. Although ER and PR isoform profiles in estrogen-treated hamster kidneys are distinctly different from corresponding uterine patterns, both receptor isoform profiles in primary renal tumors closely resemble those seen in hamster uteri. Renal ER protein and mRNA expression increased after 2.0 and 4.0 months of estrogen treatment and in all renal tumors examined. Using nuclear image cytometry, both early small and large renal tumors were highly aneuploid, indicating that genomic instability is probably a critical early event in estrogen carcinogenesis.

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