Mechanisms of prostate cancer recurrence during androgen deprivation are poorly understood. We recently described androgen receptor (AR) gene ampli®-cation in 28% of recurrent prostate carcinomas from hormone-refractory prostate cancer patients. To investigate the hypothesis that ampli®cation of the AR gene promotes the growth of hormone-refractory prostate carcinomas, DNA¯ow cytometric (FCM) studies were carried out to compare matched, primary and hormone-refractory recurrent samples from 31 prostate cancer patients. Recurrent tumours had a higher (P 0.05) S-phase fraction (SPF) (10.6 AE 4.6) than corresponding primary tumours from the same patients (7.0 AE 4.1) and the frequency of aneuploidy also increased from 8±55%. Recurrent tumours with AR gene ampli®cation had a signi®cantly higher (P 0.02) SPF (14.0 AE 6.5) than those with no ampli®cation (9.0 AE 2.9). The results suggest that clinical progression of prostate cancer during androgen withdrawal therapy is often associated with increased cell proliferation rate and formation of DNA aneuploidy. AR ampli®-cation may be an important molecular mechanism underlying the increase in proliferation rate of some recurrent tumours.
Mechanisms of prostate cancer recurrence during androgen deprivation are poorly understood. Recently, the putative role of apolipoprotein E varepsilon 4 allele in the aetiology of prostate cancer was raised. To investigate the hypothesis that varepsilon 4 allele of apolipoprotein E gene predisposes to prostate cancer and is involved in the relapse of hormonal therapy response, 38 hormone-refractory locally recurrent carcinoma samples from 38 prostate cancer patients were screened for apolipoprotein E genotype. The frequency distribution of apolipoprotein E genotypes among tumours did not differ significantly from that among controls. The allele frequency of varepsilon 4 was 19.7% and 19.3% in tumours and controls, respectively. The results suggest that clinical progression of prostate cancer during androgen withdrawal therapy is not associated with apolipoprotein E genotype. Prostate Cancer and Prostatic Diseases (2000) 3, 107-109
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