Journal
JOURNAL OF CLINICAL PATHOLOGY
Volume 58, Issue 11, Pages 1175-1179Publisher
B M J PUBLISHING GROUP
DOI: 10.1136/jcp.2005.026955
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Background: The p73 gene is a p53 homologue that induces apoptosis and inhibits cell proliferation. N-terminal truncated isoforms of p73 (Delta Np73) act as dominant-negative inhibitors of wild-type p53 and TAp73 and result in tumour growth in nude mice. Aims: To detect Delta Np73 expression in 24 benign prostatic hyperplasia samples, 33 prostate carcinomas, and five normal samples and to evaluate the relation between Delta Np73, TAp73 concentrations, and the clinicopathological characteristics of patients with prostate cancer. Methods: TAp73 was determined by real time polymerase chain reaction (PCR); Delta Np73 and Delta N'p73 were assessed using reverse transcription PCR. western blotting was used to analyse protein expression. p53 mutation was determined by immunohistochemistry. Results: A significant increase of Delta Np73 was seen in 20 of 33 carcinomas and 17 of 24 benign prostate hyperplasia tissues, but in none of the normal samples. None of the specimens expressed Delta N'p73. No significant relation was found between TAp73 expression and clinical parameters. The incidence of positive expression of Delta Np73 correlated with the Gleason score in prostate carcinomas. Cancer samples with wild-type p53 had significantly higher expression of Delta Np73 than p53 mutant cancers. Conclusion: These data suggest a potential role for Delta Np73 in prostate cancer progression.
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