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[Cancer Research 47, 281-286, January 1, 1987]
© 1987 American Association for Cancer Research

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Cytokeratin Characterization of Human Prostatic Carcinoma and Its Derived Cell Lines1

Raymond B. Nagle2, Frederick R. Ahmann, Kathleen M. McDaniel, Maria L. Paquin, Virginia A. Clark and Abbie Celniker

Department of Pathology [R. B. N., K. M. M., V. A. C.], University of Arizona School of Medicine, and Section of Hematology and Oncology [F. R. A., A. C.] and Department of Pathology [M. L. P.], Tucson Veterans Administration Medical Center, Tucson, Arizona 85724

Two murine monoclonal anti-cytokeratin antibodies with defined specificity were shown to distinguish between basal cells and luminal cells in human prostate tissue. Forty-one biopsies or transurethral resection specimens were characterized using these two antibodies. In cases of benign prostatic hyperplasia, focal loss of the basal cell layer was noted in areas of glandular proliferation. Ten cases of adenocarcinoma of the prostate, varying in Gleason's histological grade from 2 to 4, were also studied. In each case the carcinoma was shown to represent the luminal cell phenotype with no evidence of involvement of the basal cell phenotype. An analysis of three established metastatic prostatic carcinoma cell lines (DU-145, PC-3, and LNCaP) using two-dimensional electrophoresis showed that the cytokeratin complement of each cell line was slightly different but retained the phenotype of the luminal cell. It was concluded that during both hyperplasia and neoplastic transformation of the prostate, the luminal cell phenotype is primarily involved and that the basal cell phenotype does not appear to contribute to either intraluminal proliferation or invasive cell populations.

1 Supported in part by a V.A. Merit Review Grant and a University of Arizona Cancer Center Institutional Grant.

2 To whom requests for reprints should be addressed, at Department of Pathology, College of Medicine, Arizona Health Sciences Center, 1501 North Campbell Avenue, Tucson, AZ 85724.

Received 6/ 4/86. Revised 9/ 8/86. Accepted 9/11/86.




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Copyright © 1987 by the American Association for Cancer Research.