The PROGENSA PCA3 assay can aid in guiding biopsy decisions. It is superior to total prostate specific antigen, prostate specific antigen density and %free prostate specific antigen in predicting initial biopsy outcome, and may be indicative of prostate cancer aggressiveness.

BACKGROUND.We assessed the frequency and molecular basis of p53 mutations in clinically localized prostatic adenocarcinoma. METHODS. Prostate specimens were examined from 100 patients with clinically localized prostatic adenocarcinoma and 13 patients with benign prostatic hyperplasia (BPH). Mutations producing nuclear accumulation of p53 were detected immunohistochemically. Exonspecific mutations were analyzed by polymerase chain reaction amplification and single strand conformation polymorphism (PCR-SSCP) and sequenced. RESULTS. p53 accumulation was detected in 5 tumors using antibody DO-1, and in 4 of these using antibody PAb 1801, but not in BPH. PCR-SSCP detected mutations in all 5 tumors, with alterations in exon 5 for 1 tumor, exon 6 for 3 tumors, and exon 7 for 1 tumor. An exon 6 mutation was also found in a tumor with no anti-p53 staining. CONCLUSIONS. p53 mutations are uncommon in clinically localized prostatic adenocarcinoma and absent from BPH. 5 of the 6 mutations were derived from locally invasive, prostate carcinomas, supporting the hypothesis that mutation of p53 is a late event in prostate carcinoma progression.

No abstract

BACKGROUND We assessed the frequency and molecular basis of p53 mutations in clinically localized prostatic adenocarcinoma. METHODS Prostate specimens were examined from 100 patients with clinically localized prostatic adenocarcinoma and 13 patients with benign prostatic hyperplasia (BPH). Mutations producing nuclear accumulation of p53 were detected immunohistochemically. Exon‐specific mutations were analyzed by polymerase chain reaction amplification and single strand conformation polymorphism (PCR‐SSCP) and sequenced. RESULTS p53 accumulation was detected in 5 tumors using antibody DO‐1, and in 4 of these using antibody PAb 1801, but not in BPH. PCR‐SSCP detected mutations in all 5 tumors, with alterations in exon 5 for 1 tumor, exon 6 for 3 tumors, and exon 7 for 1 tumor. An exon 6 mutation was also found in a tumor with no anti‐p53 staining. CONCLUSIONS p53 mutations are uncommon in clinically localized prostatic adenocarcinoma and absent from BPH. 5 of the 6 mutations were derived from locally invasive, prostate carcinomas, supporting the hypothesis that mutation of p53 is a late event in prostate carcinoma progression. Prostate 31:209–215, 1997.© Wiley‐Liss, Inc.

BACKGROUND We investigated the role of the transforming growth factor beta (TGF‐β) family in the neoplastic progression of the human prostate. METHODS Expression of TGF‐β mRNA was measured by Northern blot analysis of tissue extracts, and TGF‐β protein by immunohistochemical analysis of tissue sections. Proliferating cells were detected by their expression of Ki‐67 antigen. RESULTS The level of TGF‐β1 mRNA was equal among normal prostate, benign prostatic hyperplasia (BPH), and prostate carcinoma. TGF‐β2 mRNA was not detectable, and TGF‐β3 mRNA was expressed 20‐fold lesion in carcinoma compared to BPH and normal prostate. TGF‐β1 protein was expressed in the stromal cells in all three tissues and TGF‐β3 protein in the basal layer of epithelial cells, but not in carcinoma. Proliferating epithelial cells fail to express TGF‐β3. CONCLUSIONS TGF‐β1 and TGF‐β3 are independently regulated, and carcinoma of the prostate is characterized by the loss of basal epithelial cells expressing TGF‐β3. Prostate 31:103–109, 1997. © 1997 Wiley‐Liss, Inc.