Source:http://linkedlifedata.com/resource/pubmed/id/19875696
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2009-12-16
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pubmed:abstractText |
Genetic variations in phosphoinositide-3 kinase (PI3K)-AKT-mammalian target of rapamycin (mTOR) pathway may affect critical cellular functions and increase an individual's cancer risk. We systematically evaluate 231 single-nucleotide polymorphisms (SNPs) in 19 genes in the PI3K-AKT-mTOR signaling pathway as predictors of bladder cancer risk. In individual SNP analysis, four SNPs in regulatory associated protein of mTOR (RAPTOR) remained significant after correcting for multiple testing: rs11653499 [odds ratio (OR): 1.79, 95% confidence interval (CI): 1.24-2.60, P = 0.002], rs7211818 (OR: 2.13, 95% CI: 1.35-3.36, P = 0.001), rs7212142 (OR: 1.57, 95% CI: 1.19-2.07, P = 0.002) and rs9674559 (OR: 2.05, 95% CI: 1.31-3.21, P = 0.002), among which rs7211818 and rs9674559 are within the same haplotype block. In haplotype analysis, compared with the most common haplotypes, haplotype containing the rs7212142 wild-type allele showed a protective effect of bladder cancer (OR: 0.83, 95% CI: 0.70-0.97). In contrast, the haplotype containing the rs7211818 variant allele showed a 1.32-fold elevated bladder cancer risk (95% CI: 1.09-1.60). In combined analysis of three independent significant RAPTOR SNPs (rs11653499, rs7211818 and rs7212142), a significant trend was observed for increased risk with an increase in the number of unfavorable genotypes (P for trend <0.001). Compared with the subjects without any of the unfavorable genotypes, those carrying all three unfavorable genotypes showed a 2.22-fold (95% CI: 1.33-3.71) increased bladder cancer risk. This is the first study to evaluate the role of germ line genetic variations in PI3K-AKT-mTOR pathway as cancer susceptibility factors that will help us identify high-risk individuals for bladder cancer.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/MTOR protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt,
http://linkedlifedata.com/resource/pubmed/chemical/TOR Serine-Threonine Kinases
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1460-2180
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pubmed:author |
pubmed-author:CassidyAdrianA,
pubmed-author:ChamberlainRobert MRM,
pubmed-author:ChenMengM,
pubmed-author:DelclosGeorge LGL,
pubmed-author:DeyD KDK,
pubmed-author:DinneyColin PCP,
pubmed-author:FanZhenZ,
pubmed-author:HaftD ADA,
pubmed-author:HildebrandtMichelle A TMA,
pubmed-author:WuXifengX,
pubmed-author:YangHushanH,
pubmed-author:YeYuanqingY
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pubmed:issnType |
Electronic
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pubmed:volume |
30
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2047-52
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pubmed:dateRevised |
2011-3-3
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pubmed:meshHeading |
pubmed-meshheading:19875696-Aged,
pubmed-meshheading:19875696-Case-Control Studies,
pubmed-meshheading:19875696-Female,
pubmed-meshheading:19875696-Gene Frequency,
pubmed-meshheading:19875696-Genetic Variation,
pubmed-meshheading:19875696-Genotype,
pubmed-meshheading:19875696-Haplotypes,
pubmed-meshheading:19875696-Humans,
pubmed-meshheading:19875696-Male,
pubmed-meshheading:19875696-Middle Aged,
pubmed-meshheading:19875696-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:19875696-Polymorphism, Single Nucleotide,
pubmed-meshheading:19875696-Protein Kinases,
pubmed-meshheading:19875696-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:19875696-Risk,
pubmed-meshheading:19875696-TOR Serine-Threonine Kinases,
pubmed-meshheading:19875696-Urinary Bladder Neoplasms
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pubmed:year |
2009
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pubmed:articleTitle |
Genetic variations in PI3K-AKT-mTOR pathway and bladder cancer risk.
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pubmed:affiliation |
Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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