Expression and mutational analysis of the MADR2/smad2 gene in human prostate cancer

BACKGROUND, Loss of heterozygosity (LOH) on chromosome arm 18q is common in sporadic prostate cancer and may be involved in cancer development through inactivation of tumor-suppressor genes (TSG). Recent identification, at 18 q21.1, of MADX2/Smad2, a key component in transforming growth factor beta ( TGF beta)-family signaling pathways, led us to investigate the role of this gene in prostate tumorigenesis. METHODS. Sporadic primary prostate tumors from 25 patients with clinically localized tumors and 7 with metastatic forms were examined for MADX2/Smad2 mutations by using polymerase chain reaction-single-strand conformational p olymorphism (PCR-SSCP) analysis of cDNA, and for gene expression by quantit ative reverse transcription-polymerase chain reaction (RT-PCR). RESULTS. We detected no mutation in MADX2/Smad2 and no abnormal mRNA expres sion. CONCLUSIONS. Despite recent evidence indicating that MADR2/Smad2 acts as a tumor-suppressor gene, our findings suggest a limited role of this gene in prostate tumorigenesis, at least in the early stages. Another key tumor-sup pressor gene may therefore be the main target of the observed LOH at 18q21. 1. (C) 1999 Wiley-Liss, Inc.