<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Toth R</submitter><funding>Intramural NIH HHS</funding><funding>Cancer Research UK</funding><funding>NHGRI NIH HHS</funding><funding>National Institute for Health Research (NIHR)</funding><funding>NCI NIH HHS</funding><funding>Wellcome Trust</funding><pagination>816-825</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6054308</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>26(6)</volume><pubmed_abstract>&lt;b>Background:&lt;/b> Epigenetic disturbances are crucial in cancer initiation, potentially with pleiotropic effects, and may be influenced by the genetic background.&lt;b>Methods:&lt;/b> In a subsets (ASSET) meta-analytic approach, we investigated associations of genetic variants related to epigenetic mechanisms with risks of breast, lung, colorectal, ovarian and prostate carcinomas using 51,724 cases and 52,001 controls. False discovery rate-corrected &lt;i>P&lt;/i> values (q values &lt; 0.05) were considered statistically significant.&lt;b>Results:&lt;/b> Among 162,887 imputed or genotyped variants in 555 candidate genes, SNPs in eight genes were associated with risk of more than one cancer type. For example, variants in &lt;i>BABAM1&lt;/i> were confirmed as a susceptibility locus for squamous cell lung, overall bre</pubmed_abstract><journal>Cancer epidemiology, biomarkers &amp; prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology</journal><pubmed_title>Genetic Variants in Epigenetic Pathways and Risks of Multiple Cancers in the GAME-ON Consortium.</pubmed_title><pmcid>PMC6054308</pmcid><funding_grant_id>R35 CA197735</funding_grant_id><funding_grant_id>U01 HG004446</funding_grant_id><funding_grant_id>U19 CA148537</funding_grant_id><funding_grant_id>P01 CA087969</funding_grant_id><funding_grant_id>U01 CA098233</funding_grant_id><funding_grant_id>U01 CA167551</funding_grant_id><funding_grant_id>U01 CA098710</funding_grant_id><funding_grant_id>U01 CA098758</funding_grant_id><funding_grant_id>Z01 CP010200</funding_grant_id><funding_grant_id>P30 CA014089</funding_grant_id><funding_grant_id>UM1 CA167551</funding_grant_id><funding_grant_id>R01 CA122443</funding_grant_id><funding_grant_id>U01 CA098216</funding_grant_id><funding_grant_id>15007</funding_grant_id><funding_grant_id>17528</funding_grant_id><funding_grant_id>R01 CA151993</funding_grant_id><funding_grant_id>U19 CA148065</funding_grant_id><funding_grant_id>R01 CA076366</funding_grant_id><funding_grant_id>U19 CA148127</funding_grant_id><funding_grant_id>U01 HG004438</funding_grant_id><funding_grant_id>U19 CA148107</funding_grant_id><funding_grant_id>U01 CA122839</funding_grant_id><funding_grant_id>C5047/A7357</funding_grant_id><funding_grant_id>U01 CA181770</funding_grant_id><funding_grant_id>R01 CA081488</funding_grant_id><funding_grant_id>R01 CA143237</funding_grant_id><funding_grant_id>076113</funding_grant_id><funding_grant_id>NF-SI-0510-10096</funding_grant_id><funding_grant_id>P50 CA136393</funding_grant_id><funding_grant_id>P30 CA015083</funding_grant_id><funding_grant_id>P50 CA127003</funding_grant_id><funding_grant_id>U19 CA148112</funding_grant_id><funding_grant_id>R01 CA136726</funding_grant_id><funding_grant_id>R01 CA144040</funding_grant_id><funding_grant_id>UM1 CA186107</funding_grant_id><pubmed_authors>Eeles RA</pubmed_authors><pubmed_authors>Hazra A</pubmed_authors><pubmed_authors>Toth R</pubmed_authors><pubmed_authors>Kelemen LE</pubmed_authors><pubmed_authors>Risch A</pubmed_authors><pubmed_authors>Ye Y</pubmed_authors><pubmed_authors>Scherer D</pubmed_authors><pubmed_authors>Issa JJ</pubmed_authors><pubmed_authors>Ogino S</pubmed_authors><pubmed_authors>OCAC, CORECT, TRICL, ELLIPSE, DRIVE, and GAME-ON consortia</pubmed_authors><pubmed_authors>Moreno V</pubmed_authors><pubmed_authors>Hung RJ</pubmed_authors><pubmed_authors>Ulrich CM</pubmed_authors><pubmed_authors>Balavarca Y</pubmed_authors><pubmed_authors>Wu X</pubmed_authors><pubmed_authors>Goode EL</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genetic Variants in Epigenetic Pathways and Risks of Multiple Cancers in the GAME-ON Consortium.</name><description>&lt;b>Background:&lt;/b> Epigenetic disturbances are crucial in cancer initiation, potentially with pleiotropic effects, and may be influenced by the genetic background.&lt;b>Methods:&lt;/b> In a subsets (ASSET) meta-analytic approach, we investigated associations of genetic variants related to epigenetic mechanisms with risks of breast, lung, colorectal, ovarian and prostate carcinomas using 51,724 cases and 52,001 controls. False discovery rate-corrected &lt;i>P&lt;/i> values (q values &lt; 0.05) were considered statistically significant.&lt;b>Results:&lt;/b> Among 162,887 imputed or genotyped variants in 555 candidate genes, SNPs in eight genes were associated with risk of more than one cancer type. For example, variants in &lt;i>BABAM1&lt;/i> were confirmed as a susceptibility locus for squamous cell lung, overall bre</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Jun</publication><modification>2026-05-02T19:51:44.196Z</modification><creation>2019-03-26T23:47:17Z</creation></dates><accession>S-EPMC6054308</accession><cross_references><pubmed>28115406</pubmed><doi>10.1158/1055-9965.EPI-16-0728</doi><doi>10.1158/1055-9965.epi-16-0728</doi></cross_references></HashMap>