<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Deshmukh HA</submitter><funding>Medical Research Council</funding><funding>National Institute for Health Research (NIHR)</funding><funding>European Commission FP7</funding><pagination>1000-1011</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3329377</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>53(5)</volume><pubmed_abstract>We carried out a genome-wide association study (GWAS) of LDL-c response to statin using data from participants in the Collaborative Atorvastatin Diabetes Study (CARDS; n = 1,156), the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT; n = 895), and the observational phase of ASCOT (n = 651), all of whom were prescribed atorvastatin 10 mg. Following genome-wide imputation, we combined data from the three studies in a meta-analysis. We found associations of LDL-c response to atorvastatin that reached genome-wide significance at rs10455872 (P = 6.13 × 10(-9)) within the LPA gene and at two single nucleotide polymorphisms (SNP) within the APOE region (rs445925; P = 2.22 × 10(-16) and rs4420638; P = 1.01 × 10(-11)) that are proxies for the ε2 and ε4 variants, respectively, in APOE. The novel ass</pubmed_abstract><journal>Journal of lipid research</journal><pubmed_title>Genome-wide association study of genetic determinants of LDL-c response to atorvastatin therapy: importance of Lp(a).</pubmed_title><pmcid>PMC3329377</pmcid><funding_grant_id>FP7_223004</funding_grant_id><funding_grant_id>G9521010</funding_grant_id><funding_grant_id>NF-SI-0508-10116</funding_grant_id><pubmed_authors>Ford I</pubmed_authors><pubmed_authors>Neil A</pubmed_authors><pubmed_authors>Hyde C</pubmed_authors><pubmed_authors>Poulter N</pubmed_authors><pubmed_authors>Stanton AV</pubmed_authors><pubmed_authors>Durrington PN</pubmed_authors><pubmed_authors>Hitman GA</pubmed_authors><pubmed_authors>Betteridge DJ</pubmed_authors><pubmed_authors>Jukema JW</pubmed_authors><pubmed_authors>Chatterjee A</pubmed_authors><pubmed_authors>Johnson T</pubmed_authors><pubmed_authors>DeMicco DA</pubmed_authors><pubmed_authors>Charlton-Menys V</pubmed_authors><pubmed_authors>Sever P</pubmed_authors><pubmed_authors>Caulfield M</pubmed_authors><pubmed_authors>Deshmukh HA</pubmed_authors><pubmed_authors>Fuller JH</pubmed_authors><pubmed_authors>Postmus I</pubmed_authors><pubmed_authors>Livingstone S</pubmed_authors><pubmed_authors>McKeigue PM</pubmed_authors><pubmed_authors>Shields DC</pubmed_authors><pubmed_authors>Colhoun HM</pubmed_authors><pubmed_authors>Calle RA</pubmed_authors><pubmed_authors>Trompet S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genome-wide association study of genetic determinants of LDL-c response to atorvastatin therapy: importance of Lp(a).</name><description>We carried out a genome-wide association study (GWAS) of LDL-c response to statin using data from participants in the Collaborative Atorvastatin Diabetes Study (CARDS; n = 1,156), the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT; n = 895), and the observational phase of ASCOT (n = 651), all of whom were prescribed atorvastatin 10 mg. Following genome-wide imputation, we combined data from the three studies in a meta-analysis. We found associations of LDL-c response to atorvastatin that reached genome-wide significance at rs10455872 (P = 6.13 × 10(-9)) within the LPA gene and at two single nucleotide polymorphisms (SNP) within the APOE region (rs445925; P = 2.22 × 10(-16) and rs4420638; P = 1.01 × 10(-11)) that are proxies for the ε2 and ε4 variants, respectively, in APOE. The novel ass</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 May</publication><modification>2025-04-18T14:46:39.403Z</modification><creation>2019-03-27T00:52:27Z</creation></dates><accession>S-EPMC3329377</accession><cross_references><pubmed>22368281</pubmed><doi>10.1194/jlr.P021113</doi></cross_references></HashMap>