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Abnormal p53 expression is rare in clinically localized human prostate cancer: Comparison between immunohistochemical and molecular detection of p53 mutations
Author(s) -
Mottaz Alain E.,
Markwalder Regula,
Fey Martin F.,
Klima Irena,
Merz Vincent W.,
Thalmann George N.,
Ball Roland K.,
Studer Urs E.
Publication year - 1997
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/(sici)1097-0045(19970601)31:4<209::aid-pros1>3.0.co;2-f
Subject(s) - immunohistochemistry , prostate , prostate cancer , pathology , cancer , medicine , p53 protein , cancer research , p53 expression , pca3 , biology , oncology
BACKGROUND We assessed the frequency and molecular basis of p53 mutations in clinically localized prostatic adenocarcinoma. METHODS Prostate specimens were examined from 100 patients with clinically localized prostatic adenocarcinoma and 13 patients with benign prostatic hyperplasia (BPH). Mutations producing nuclear accumulation of p53 were detected immunohistochemically. Exon‐specific mutations were analyzed by polymerase chain reaction amplification and single strand conformation polymorphism (PCR‐SSCP) and sequenced. RESULTS p53 accumulation was detected in 5 tumors using antibody DO‐1, and in 4 of these using antibody PAb 1801, but not in BPH. PCR‐SSCP detected mutations in all 5 tumors, with alterations in exon 5 for 1 tumor, exon 6 for 3 tumors, and exon 7 for 1 tumor. An exon 6 mutation was also found in a tumor with no anti‐p53 staining. CONCLUSIONS p53 mutations are uncommon in clinically localized prostatic adenocarcinoma and absent from BPH. 5 of the 6 mutations were derived from locally invasive, prostate carcinomas, supporting the hypothesis that mutation of p53 is a late event in prostate carcinoma progression. Prostate 31:209–215, 1997. © Wiley‐Liss, Inc.