COMPARISON OF ANDROGEN-INDEPENDENT GROWTH AND ANDROGEN-DEPENDENT GROWTH IN BPH AND CANCER-TISSUE FROM THE SAME RADICAL PROSTATECTOMIES IN SPONGE-GEL MATRIX HISTOCULTURE

BACKGROUND. In order to determine androgen sensitivities of prostate c ancer and benign prostatic hypertrophy (BPH) tissues from the same pat ient in vitro, we used a histoculture technique to measure androgen-in dependent and androgen-dependent growth and compared them in paired sp ecimens of BPH and prostate cancer from 23 radical prostatectomies. Bo th androgen-independent growth and androgen-dependent growth are measu res of important biological characteristics of benign and malignant pr ostate tissue. METHODS. The effect of hydroxyflutamide and antiandroge ns on dihydrotestosterone (DHT)-stimulated incorporation of H-3-thymid ine into both paired specimens of BPH and cancer was utilized to measu re androgen-independent and androgen-dependent growth. The percentage decrease in H-3-thymidine incorporation/mu g protein in the flutamide- treated specimen compared to the DHT-treated specimen represented andr ogen-dependent growth. Residual H-3-thymidine incorporation/mu g prote in during hydroxyflutamide administration represented androgen-indepen dent growth. RESULTS. Androgen-independent growth was significantly gr eater (P = 0.015) in the BPH compared to the cancer paired tissue. And rogen-dependent growth was significantly higher in 23 paired specimens of cancer compared to BPH (P < 0.03). CONCLUSIONS. Ln paired specimen s of BPH and prostate cancer from the same radical prostatectomy speci men, androgen-independent growth appeared greater in BPH compared to c ancer specimens; androgen-dependent growth, however, was greater in pr ostate cancer than in BPH. There was no correlation of either growth p arameter with Gleason tumor grade. Future clinical correlations will i ndicate whether either growth parameter represents an important progno stic factor for prostate cancer aggressiveness stimulated H-3-thymidin e incorporation into DNA. (C) 1997 Wiley-Liss, Inc.