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Tumor suppressor gene P53 mutations in human prostate cancer
Author(s) -
Kubota Yoshinobu,
Shuin Taro,
Uemura Hiroji,
Fujinami Kiyoshi,
Miyamoto Hiroshi,
Torigoe Soichiro,
Dobashi Yasushi,
Kitamura Hitoshi,
Iwasaki Yoshiko,
Danenberg Kathleen,
Danenberg Peter V.
Publication year - 1995
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.2990270105
Subject(s) - missense mutation , point mutation , exon , carcinogenesis , tumor suppressor gene , biology , cancer research , gene , mutation , prostate cancer , adenocarcinoma , prostate , polymerase chain reaction , genetics , microbiology and biotechnology , cancer
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. © 1995 Wiley‐Liss, Inc.