Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-6-8
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0910-5050
pubmed:author
pubmed:issnType
Print
pubmed:volume
86
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
57-63
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
p53 mutations occur in clinical, but not latent, human prostate carcinoma.
pubmed:affiliation
Second Department of Pathology, Nara Medical University.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't