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Expression and mutational analysis of theMADR2/smad2 gene in human prostate cancer

✍ Scribed by Latil, Alain; Pesche, Sandrine; Val�ri, Antoine; Fournier, Georges; Cussenot, Olivier; Lidereau, Rosette

Publisher
John Wiley and Sons
Year
1999
Tongue
English
Weight
229 KB
Volume
40
Category
Article
ISSN
0270-4137

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✦ Synopsis

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 18q21.1, of MADR2/Smad2, a key component in transforming growth factor ␤ (TGF␤)-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 MADR2/Smad2 mutations by using polymerase chain reaction-single-strand conformational polymorphism (PCR-SSCP) analysis of cDNA, and for gene expression by quantitative reverse transcription-polymerase chain reaction (RT-PCR). RESULTS. We detected no mutation in MADR2/Smad2 and no abnormal mRNA expression. CONCLUSIONS. Despite recent evidence indicating that MADR2/Smad2 acts as a tumorsuppressor gene, our findings suggest a limited role of this gene in prostate tumorigenesis, at least in the early stages. Another key tumor-suppressor gene may therefore be the main target of the observed LOH at 18q21.1.

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