Source:http://linkedlifedata.com/resource/pubmed/id/16007211
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
38
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pubmed:dateCreated |
2005-9-2
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pubmed:abstractText |
Hepatocellular carcinoma (HCC) from regions with high dietary exposure to aflatoxins and endemic for hepatitis B virus (HBV) often contain a specific mutation at codon 249 in TP53 (249(ser); AGG to AGT, Arg to Ser). This mutation is also detectable in circulating cell-free DNA from the plasma of HCC patients and healthy subjects in these regions. We have examined the joint effect of plasma 249(ser) and HBV infection in a case-control study design involving 348 control, 98 cirrhotic, and 186 HCC participants from The Gambia, West Africa, an area of high HCC incidence. The 249(ser) mutation was detected in 3.5% of controls, 15.3% of cirrhotics, and 39.8% of HCC cases (adjusted odds ratios (OR): 4.83, (95% confidence interval (CI): 1.71-13.7) for cirrhosis and 20.3 (8.19-50.0) for HCC). HBsAg positivity along with plasma 249(ser) was observed in 45/183 (24.6%) HCC cases compared to only one (0.3%) control. Risk for HCC was associated with markers of HBV alone (OR: 10.0, 95% CI: 5.16-19.6), 249(ser) alone (OR: 13.2, 95% CI: 4.99-35.0), and both markers present (OR: 399, 95% CI: 48.6-3270). These results suggest a multiplicative effect on HCC risk resulting from the mutational effect of aflatoxin on TP53, as monitored by detection of plasma 249(ser), with concomitant chronic infection with HBV.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0950-9232
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
24
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5858-67
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:16007211-Aflatoxins,
pubmed-meshheading:16007211-Carcinoma, Hepatocellular,
pubmed-meshheading:16007211-Case-Control Studies,
pubmed-meshheading:16007211-DNA,
pubmed-meshheading:16007211-Female,
pubmed-meshheading:16007211-Genes, p53,
pubmed-meshheading:16007211-Hepatitis B,
pubmed-meshheading:16007211-Hepatitis B virus,
pubmed-meshheading:16007211-Humans,
pubmed-meshheading:16007211-Liver Neoplasms,
pubmed-meshheading:16007211-Male,
pubmed-meshheading:16007211-Middle Aged,
pubmed-meshheading:16007211-Mutation,
pubmed-meshheading:16007211-Polymerase Chain Reaction,
pubmed-meshheading:16007211-Polymorphism, Restriction Fragment Length,
pubmed-meshheading:16007211-Risk Factors
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pubmed:year |
2005
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pubmed:articleTitle |
249(ser) TP53 mutation in plasma DNA, hepatitis B viral infection, and risk of hepatocellular carcinoma.
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pubmed:affiliation |
Gambia Hepatitis Intervention Study, Banjul. gkirk@jhsph.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, N.I.H., Extramural
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