Tumor suppressor gene P53 mutations in human prostate cancer

Yoshinobu Kubota(Yokohama City University), Taro Shuin(Yokohama City University), Hiroji Uemura(Yokohama City University), Kiyoshi Fujinami(Yokohama City University), Hiroshi Miyamoto(Yokohama City University), Soichiro Torigoe(Yokohama City University), Yasushi Dobashi(Yokohama City University), Hitoshi Kitamura(Yokohama City University), Yoshiko Iwasaki(Kanagawa Dental University), Kathleen D. Danenberg(University of Southern California), Peter V. Danenberg(University of Southern California)
The Prostate
July 1, 1995
Cited by 56

Abstract

The genetic background underlying the growth and development of human prostatic cancer is not yet clear. Here we searched for possible mutations in the entire coding region of tumor suppressor gene p53 in primary human prostatic carcinomas, using polymerase chain reaction and single-strand conformational polymorphism analysis of RNA. We found p53 gene mutations in 4 of 21 cases (19%). DNA sequencing of the polymerase chain reaction products revealed missense point mutations that resulted in amino acid changes in exon 5 or 3 in three cases and single base deletions in exon 7 in two cases. One case contained both a missense point mutation and a single base deletion. Three of these four cases were pathologically diagnosed as poorly differentiated adenocarcinomas, and three of the four cases were clinically localized to stage C or D. None of seven noncancerous prostate tissues nor three well-differentiated adenocarcinoma tissues showed any mutations. The present results suggest that p53 gene mutation is involved in the late progression steps of human prostate carcinogenesis.


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