<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Koutros S</submitter><funding>Intramural NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>2389-96</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2840184</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>70(6)</volume><pubmed_abstract>The phosphatidylinositol 3-kinase (PI3K) pathway regulates various cellular processes, including cellular proliferation and intracellular trafficking, and may affect prostate carcinogenesis. Thus, we explored the association between single-nucleotide polymorphisms (SNP) in PI3K genes and prostate cancer. Pooled data from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium were examined for associations between 89 SNPs in PI3K genes (PIK3C2B, PIK3AP1, PIK3C2A, PIK3CD, and PIK3R3) and prostate cancer risk in 8,309 cases and 9,286 controls. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using logistic regression. SNP rs7556371 in PIK3C2B was significantly associated with prostate cancer risk [OR(per allele), 1.08 (95% CI, 1.03-1.14); P(trend) = 0.</pubmed_abstract><journal>Cancer research</journal><pubmed_title>Pooled analysis of phosphatidylinositol 3-kinase pathway variants and risk of prostate cancer.</pubmed_title><pmcid>PMC2840184</pmcid><funding_grant_id>U01 CA098758</funding_grant_id><funding_grant_id>UO1CA98758</funding_grant_id><funding_grant_id>UO1 CA98710</funding_grant_id><funding_grant_id>UO1 CA98216</funding_grant_id><funding_grant_id>U01 CA098216</funding_grant_id><funding_grant_id>Z01 CP010152</funding_grant_id><funding_grant_id>U01 CA098233</funding_grant_id><funding_grant_id>UO1CA98233</funding_grant_id><funding_grant_id>Z99 CA999999</funding_grant_id><funding_grant_id>U01 CA098710</funding_grant_id><pubmed_authors>Diver WR</pubmed_authors><pubmed_authors>Huang WY</pubmed_authors><pubmed_authors>Feigelson HS</pubmed_authors><pubmed_authors>Kaaks R</pubmed_authors><pubmed_authors>Schumacher FR</pubmed_authors><pubmed_authors>Thomas G</pubmed_authors><pubmed_authors>Berndt SI</pubmed_authors><pubmed_authors>Kolonel LN</pubmed_authors><pubmed_authors>Hunter DJ</pubmed_authors><pubmed_authors>Le Marchand L</pubmed_authors><pubmed_authors>Koutros S</pubmed_authors><pubmed_authors>Giovanucci E</pubmed_authors><pubmed_authors>Yeager M</pubmed_authors><pubmed_authors>Thun MJ</pubmed_authors><pubmed_authors>Haiman CA</pubmed_authors><pubmed_authors>Riboli E</pubmed_authors><pubmed_authors>Chanock SJ</pubmed_authors><pubmed_authors>Stampfer MJ</pubmed_authors><pubmed_authors>Stram DO</pubmed_authors><pubmed_authors>Hayes RB</pubmed_authors><pubmed_authors>Albanes D</pubmed_authors><pubmed_authors>Henderson BE</pubmed_authors><pubmed_authors>Siddiq A</pubmed_authors><pubmed_authors>Ma J</pubmed_authors><pubmed_authors>Kraft P</pubmed_authors><pubmed_authors>Travis RC</pubmed_authors><pubmed_authors>Crawford ED</pubmed_authors><pubmed_authors>Canzian F</pubmed_authors></additional><is_claimable>false</is_claimable><name>Pooled analysis of phosphatidylinositol 3-kinase pathway variants and risk of prostate cancer.</name><description>The phosphatidylinositol 3-kinase (PI3K) pathway regulates various cellular processes, including cellular proliferation and intracellular trafficking, and may affect prostate carcinogenesis. Thus, we explored the association between single-nucleotide polymorphisms (SNP) in PI3K genes and prostate cancer. Pooled data from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium were examined for associations between 89 SNPs in PI3K genes (PIK3C2B, PIK3AP1, PIK3C2A, PIK3CD, and PIK3R3) and prostate cancer risk in 8,309 cases and 9,286 controls. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using logistic regression. SNP rs7556371 in PIK3C2B was significantly associated with prostate cancer risk [OR(per allele), 1.08 (95% CI, 1.03-1.14); P(trend) = 0.</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Mar</publication><modification>2026-05-05T00:33:52.863Z</modification><creation>2026-04-07T21:09:00.752Z</creation></dates><accession>S-EPMC2840184</accession><cross_references><pubmed>20197460</pubmed><doi>10.1158/0008-5472.CAN-09-3575</doi><doi>10.1158/0008-5472.can-09-3575</doi></cross_references></HashMap>