Linked Life Data

12142524

Source:http://linkedlifedata.com/resource/pubmed/id/12142524

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5581
pubmed:dateCreated
2002-7-26
pubmed:abstractText
Most human cancer cells show signs of genome instability, ranging from elevated mutation rates to gross chromosomal rearrangements and alterations in chromosome number. Little is known about the molecular mechanisms that generate this instability or how it is suppressed in normal cells. Recent studies of the yeast Saccharomyces cerevisiae have begun to uncover the extensive and redundant pathways that keep the rate of genome rearrangements at very low levels. These studies, which we review here, have implicated more than 50 genes in the suppression of genome instability, including genes that function in S-phase checkpoints, recombination pathways, and telomere maintenance. Human homologs of several of these genes have well-established roles as tumor suppressors, consistent with the hypothesis that the mechanisms preserving genome stability in yeast are the same mechanisms that go awry in cancer.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1095-9203
pubmed:author
pubmed:issnType
Electronic
pubmed:day
26
pubmed:volume
297
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
552-7
pubmed:dateRevised
2007-3-19
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Maintenance of genome stability in Saccharomyces cerevisiae.
pubmed:affiliation
Ludwig Institute for Cancer Research, Cancer Center and Department of Medicine, CMME3058, 9500 Gilman Drive, University of California-San Diego School of Medicine, La Jolla, CA 92093, USA. rkolodner@ucsd.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't