Linked Life Data

10701370

Source:http://linkedlifedata.com/resource/pubmed/id/10701370

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-3-21
pubmed:abstractText
Tumorigenesis is known to result from multiple genetic changes. Although endogenous and environmental insults can damage DNA, cellular mechanisms exist to repair various forms of damage or to kill those cells irreparably damaged. Hence, the accumulation of numerous genetic changes that would lead to cancer in normal cells is extremely rare. Nevertheless, disruption of a DNA repair pathway has the potential to expedite tumorigenesis by resulting in a cell that is hypermutable. Multiple pathways exist to repair the various forms of DNA damage that can cause mutagenesis. Recent studies have demonstrated a key role for homologous recombination in DNA repair, in particular in the repair chromosomal double-strand breaks. This review summarizes those studies and discusses how disruption of homologous recombination pathways can create genetic instability.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
0735-7907
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
78-86
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Chromosome breaks and genomic instability.
pubmed:affiliation
Memorial Sloan-Kettering Cancer Center, Cornell University Graduate School of Medical Sciences, New York, New York, USA. m-jasin@ski.mskcc.org
pubmed:publicationType
Journal Article, Review