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[Cancer Research 52, 6940-6944, December 15, 1992]
© 1992 American Association for Cancer Research
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Expression of the Protooncogene bcl-2 in the Prostate and Its Association with Emergence of Androgen-independent Prostate Cancer1

Timothy J. McDonnell2, Patricia Troncoso, Shawn M. Brisbay, Christopher Logothetis, Leland W. K. Chung, Jer-Tsong Hsieh, Shi-Ming Tu and Martin L. Campbell

Departments of Molecular Pathology [T. J. M., S. M. B., M. L. C.], Pathology [T. J. M., P. T.], Department of Medical Oncology [C. L., S-M. T.], and Urology [L. W. K. C., J-T. H.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030

2 To whom requests for reprints should be addressed, at The University of Texas M. D. Anderson Cancer Center, Department of Molecular Pathology, Box 89, 1515 Holcombe Boulevard, Houston, TX 77030.

The significance of apoptosis in relation to the development and progression of prostate cancer remains largely undefined, bcl-2 is an oncogene that functions by overriding apoptosis. bcl-2 expression was localized to the basal epithelial cells in the normal human prostate with the use of immunohistochemistry. Androgen-dependent and androgen-independent prostate carcinomas were evaluated immunohistochemically for bcl-2 expression, bcl-2 was undetectable in 13 of 19 cases of androgen-dependent cancers. In contrast, androgen-independent cancers displayed diffuse, high levels of bcl-2 staining (P < 0.01). In rats, steady-state levels of bcl-2 mRNA, assessed by S1 assays, reached maximum levels 10 days following castration. Addition of exogenous testosterone with, or without, flutamide demonstrated that the increased bcl-2 mRNA resulted from androgen ablation. Our findings indicate that bcl-2 expression is augmented following androgen ablation and is correlated with the progression of prostate cancer from androgen dependence to androgen independence.

1 This work was supported in part by NIH Grant DK38649, NIH-NCI Grant CA16672, and by Grant CA56307 from Tenneco, Inc., awarded to L. W. K. C. T. J. M. is a Pen Scholar in the Biomedical Sciences.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Received 9/10/92. Accepted 10/23/92.




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