p53 mutations occur in clinical, but not latent, human prostate carcinoma.
To elucidate the role of the p53 tumor suppressor gene in prostate tumorigenesis, we probed for mutations in latent and clinical prostate cancers using single strand conformation polymorphism (SSCP) and restriction fragment length polymorphism (RFLP) analysis in combination with direct gene sequencing and immunohistochemical methodologies. Fifteen cases of subclinical and 32 cases of clinical carcinoma, the latter graded in stages A through D, were available for study. While p53 point mutations were detected in only 5 of 32 (16%) clinical cancers, no mutations were detected in latent disease. Of the carcinomas in stages B, C and D, 15% (2/13), 29% (2/7) and 9% (1/11) were positive for p53 mutations, respectively. Although no specific mutational patterns were observed, the aberrations found were predominantly single base missense substitutions. The data suggest not only an association of p53 mutation and progression of clinical prostate cancer, but also imply that some other mechanism(s) are at work in latent carcinoma.
Konishi
N
N
Second Department of Pathology, Nara Medical University.
Hiasa
Y
Y
Hayashi
I
I
Matsuda
H
H
Tsuzuki
T
T
Ming
T
T
Kitahori
Y
Y
Shiraishi
T
T
Yatani
R
R
Shimazaki
J
J
D001483:Base Sequence; D004273:DNA, Neoplasm / Q000737:chemistry; D016158:Genes, p53; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008969:Molecular Sequence Data; D009154:Mutation; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D018807:Polymorphism, Single-Stranded Conformational; D011471:Prostatic Neoplasms / Q000235:genetics*; D017422:Sequence Analysis, DNA
D004273:DNA, Neoplasm