Linked Life Data

18640857

Source:http://linkedlifedata.com/resource/pubmed/id/18640857

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2008-9-8
pubmed:abstractText
Deletions at 8p are frequent in many human cancers and represent a genetic marker associated with a more aggressive tumor phenotype. Previous mutational analysis of DBC2 (deleted in breast cancer 2), a tumor suppressor gene located in the region of loss of heterozygosity (LOH) on 8p21, failed to show a high frequency of mutation linked to low expression in bladder cancer. Promoter hypermethylation may be an alternative mechanism of inactivation of the second allele. We detected the methylation status and expression of the DBC2 gene in 75 bladder cancer samples and 57 corresponding normal tissues. Aberrant methylation and down-regulation of DBC2 were observed preferentially in tumor samples (P < 0.05), and the expression changes were associated with methylation (P < 0.05). These findings, together with the previously mutation reports, suggest that aberrant methylation in DBC2 promoter may be responsible for the expression loss of DBC2 expression in bladder cancer and this hypermethylation event could play a crucial role in the early stage of bladder tumorigenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1078-1439
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
465-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:articleTitle
DBC2 gene is silenced by promoter methylation in bladder cancer.
pubmed:affiliation
Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
pubmed:publicationType
Journal Article