Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1994-9-16
pubmed:abstractText
The tumor suppressor gene p53 is the most frequently mutated gene in human cancer. We have used polymerase chain reaction-single-strand conformation polymorphism analysis and sequencing to examine the status of the p53 gene in human testicular cancers of various histologies. We were unable to find in 40 samples and four cell lines any mutations in the regions of this gene (exons 5 through 8) that are usually mutated in other cancers. Northern blot analysis showed expression of this gene in most of the samples analyzed, as well as in four human testicular tumor cell lines. The MDM-2 gene is amplified and overexpressed in sarcomas; it binds and functionally inactivates p53. The 44 testicular tumor samples and cell lines were examined for amplification of MDM-2 by dot-blot analysis; none was found. The proto-oncogene c-kit probably plays an important role in normal testicular development. Mutation of the tyrosine phosphorylation site of a closely related member of this family of tyrosine kinase receptors (c-fms) is associated with cellular transformation and cancer. Codon 936 is the analogous tyrosine of c-kit; using polymerase chain reaction-single-strand conformation polymorphism analyses, we were unable to detect mutations at this site in our 44 testicular cancer samples. We conclude from our studies that mutations in the most conserved region of the p53 gene, as well as at codon 936 of the c-kit gene and amplification of MDM-2, are extremely rare in human testicular cancers.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0893-3952
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:geneSymbol
c-kit
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
435-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Mutations of the p53 gene are not detectable in human testicular tumors.
pubmed:affiliation
Division of Hematology-Oncology, Cedars-Sinai Medical Center, Los Angeles, California.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't