Source:http://linkedlifedata.com/resource/pubmed/id/14504198
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2003-9-23
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pubmed:abstractText |
Genetic polymorphism in HPC2/ELAC2 was recently associated with risk of sporadic prostate cancer. To determine the contribution of two HPC2/ELAC2 missense variants (Ser217Leu and Ala541Thr) to the risk of developing prostate cancer, we conducted a population-based case-control study of middle-aged men (40-64 years). Cases (n=591) were ascertained from the Seattle-Puget Sound Surveillance, Epidemiology, and End Results Cancer Registry and Controls (n=538) from the same general population were identified through random-digit dialing. Subjects were residents of King County, Washington, and were frequency matched on age. Cases (32%) had a slightly higher frequency of the Leu217 variant compared with controls (29%), but there were no differences in the frequency of the Thr541 allele (4%). When considering joint genotypes, white men homozygous for the Leu217 variant on an Ala541/Ala541 background had an increased risk of prostate cancer [odds ratio (OR)=1.84; 95% confidence interval (CI), 1.11-3.06]. Different risk profiles were also observed when cases were stratified by disease aggressiveness. Men with at least one Leu217 allele had an elevated risk (OR=1.34; 95% CI, 1.02-1.76) of less aggressive prostate cancer (localized stage and Gleason score < or = 7), with a stronger association among men with two Leu217 alleles (OR=1.73; 95% CI, 1.08-2.77). The Ala541Thr polymorphism was not associated with risk, and neither variant was associated with more aggressive prostate cancer phenotypes. We estimate that the Ser217Leu genotype may account for approximately 14% of less aggressive prostate cancer cases and 9% of all sporadic cases in the general United States population of white men <age 65 years.
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pubmed:grant | |
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 |
1055-9965
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
876-81
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:14504198-Adenocarcinoma,
pubmed-meshheading:14504198-Adult,
pubmed-meshheading:14504198-Alleles,
pubmed-meshheading:14504198-Case-Control Studies,
pubmed-meshheading:14504198-European Continental Ancestry Group,
pubmed-meshheading:14504198-Gene Frequency,
pubmed-meshheading:14504198-Genetic Variation,
pubmed-meshheading:14504198-Homozygote,
pubmed-meshheading:14504198-Humans,
pubmed-meshheading:14504198-Leucine,
pubmed-meshheading:14504198-Male,
pubmed-meshheading:14504198-Middle Aged,
pubmed-meshheading:14504198-Mutation, Missense,
pubmed-meshheading:14504198-Neoplasm Proteins,
pubmed-meshheading:14504198-Neoplasm Staging,
pubmed-meshheading:14504198-Polymorphism, Genetic,
pubmed-meshheading:14504198-Prostatic Neoplasms,
pubmed-meshheading:14504198-Risk Factors
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pubmed:year |
2003
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pubmed:articleTitle |
Association of HPC2/ELAC2 polymorphisms with risk of prostate cancer in a population-based study.
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pubmed:affiliation |
Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA. jstanfor@fhcrc.org
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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