Linked Life Data

18243134

Source:http://linkedlifedata.com/resource/pubmed/id/18243134

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-2-25
pubmed:abstractText
Tumor necrosis factor (TNF) and the TNF receptor (TNFR) superfamily play very important roles for cell death as well as normal immune regulation. Dysregulation of TNF-TNFR superfamily gene expression will influence many biological processes, and contributes to human diseases, including cancer. We investigated the genetic alterations of the TNF-TNFR superfamily genes in hepatocellular carcinoma (HCC). Several genetic alterations were detected in the 44 TNF-TNFR superfamily genes by sequencing hepatocellular carcinoma DNA samples. In particular, we found that the TNFR1 promoter -329G/T polymorphism was strongly associated with primary HCC (odds ratio [OR]=5.22, p=0.0007). We also observed frequent loss of heterozygosity at the polymorphic TNFR1 -329G/T site in the primary tumor tissues, indicating that the polymorphic TNFR1 -329G/T site is very susceptible to genetic alterations in HCC. Furthermore, in the polymorphic TNFR1 -329G/T site, the T allele resulted in the repression of TNFR1 expression. Therefore, our results suggest that TNFR1 -329G/T polymorphism may play an important role in the development of HCC.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1090-2104
pubmed:author
pubmed:issnType
Electronic
pubmed:day
4
pubmed:volume
368
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
395-401
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
TNFR1 promoter -329G/T polymorphism results in allele-specific repression of TNFR1 expression.
pubmed:affiliation
Asan Institute for Life Sciences, University of Ulsan College of Medicine, Laboratory of Genome Research, 388-1 Pungnap-2-Dong, Songpa-Gu, Seoul 138-736, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't