Linked Life Data

9865715

Source:http://linkedlifedata.com/resource/pubmed/id/9865715

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
24
pubmed:dateCreated
1999-1-25
pubmed:abstractText
Genome recombination is essential for life; however, its dysfunction causes cancer. Here we report the formation of a chimera structure of the p53 gene due to homologous recombination with the p53 pseudogene in tumors produced by repeated local beta-irradiation of the backs of mice. The recombination occurred near the 5' end of exon 5. Because this tumor carried a 5-bp deletion in exon 6 of the expressed p53 allele, and the defect in p53 is reported to elevate the cellular recombination activity, this chimera formation is thought to be initiated by a radiation-induced DNA double strand break in the p53-mutated cell with enhanced recombination. The abundance of this chimera structure was estimated to be 8% of the total of tumor p53, and the functional p53 side of this chimera had no deletion in exon 6. The indication is that the recombination occurred before the loss of heterozygosity of the mutated p53 allele took place but after a few divisions of the original heterozygous p53-mutated cell toward monoclonal expansion. A novel mechanism of cancer induction is suggested.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
58
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5649-51
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Homologous recombination between p53 and its pseudogene in a radiation-induced mouse tumor.
pubmed:affiliation
Genetics Division, National Cancer Center Research Institute, Tokyo, Japan. htanooka@ncc.go.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't