Linked Life Data

11166582

Source:http://linkedlifedata.com/resource/pubmed/id/11166582

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-2-22
pubmed:abstractText
Deficient repair of DNA double-strand breaks, resulting in an abnormally high frequency of chromatid breaks after G(2) exposure of cells to radiation, appears to be associated with cancer predisposition. Unrepaired DNA strand breaks contribute to genomic instability. Unrepaired chromatid breaks representing DNA strand breaks can result in chromosome deletions, translocations and gene amplifications seen in human cancers. This cytogenetic response of cells to radiation may be useful as a marker of cancer susceptibility and in identifying individuals at risk of developing cancer in cancer families.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1040-8428
pubmed:author
pubmed:issnType
Print
pubmed:volume
37
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
87-96
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Radiation-induced chromatid breaks and deficient DNA repair in cancer predisposition.
pubmed:affiliation
Department of Pathology, Howard University College of Medicine, 520 West Street, Washington, DC 20059, USA. rparshad@fac.howard.edu
pubmed:publicationType
Journal Article, Review