{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yarmolinsky J"],"funding":["Programa FORTALECE del Ministerio de Ciencia e Innovación","World Health Organization","National Institute for Health and Care Research Imperial Biomedical Research Centre","Instituto de Salud Carlos III","A*STAR (UIBR), the Academy of Medical Sciences Professorship","Biomedical Research in Epidemiology and Public Health","Spanish Association Against Cancer","Engineering and Physical Sciences Research Council"],"pagination":["1836-1847"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12415964"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["117(9)"],"pubmed_abstract":["<h4>Background</h4>The role of lipid-perturbing medications in cancer risk is unclear.<h4>Methods</h4>We employed cis-Mendelian randomization and colocalization to evaluate the role of 5 lipid-perturbing drug targets (ANGPTL3, ANGPTL4, APOC3, CETP, and PCSK9) in risk of 5 cancers (breast, colorectal, head and neck, ovarian, and prostate). We triangulated findings using pre-diagnostic protein measures in prospective analyses in EPIC (977 colorectal cancer cases, 4080 sub-cohort members) and the UK Biobank (860 colorectal cancer cases, 50 177 controls). To gain mechanistic insight into the role of ANGPTL4 in carcinogenesis, we examined the impact of the ANGPTL4 p. E40K loss-of-function variant on differential gene expression in normal colon tissue in BarcUVa-Seq. Finally, we evaluated the as"],"journal":["Journal of the National Cancer Institute"],"pubmed_title":["Proteogenomic and observational evidence implicate ANGPTL4 as a potential therapeutic target for colorectal cancer prevention."],"pmcid":["PMC12415964"],"funding_grant_id":["001","CIBERESP","ISCIII","FORT23/00032","APR7_1002","GCTRA18022MORE","EP/V029045/1"],"pubmed_authors":["Woods MO","Wang D","Yarmolinsky J","Willems van Dijk K","Smith AG","Le Marchand L","Sieri S","Li-Gao R","Sangphukieo A","Papier K","Visvanathan K","Virani S","Vincent EE","Gunter MJ","Ebrahimi E","Dudding T","Dehghan A","Masala G","Lee MA","Hampe J","Tzoulaki I","Tsilidis KK","van Duijnhoven FJB","Moreno V","Rensen PCN","Lau E","Moratalla-Navarro F","Guevara M"],"additional_accession":[]},"is_claimable":false,"name":"Proteogenomic and observational evidence implicate ANGPTL4 as a potential therapeutic target for colorectal cancer prevention.","description":"<h4>Background</h4>The role of lipid-perturbing medications in cancer risk is unclear.<h4>Methods</h4>We employed cis-Mendelian randomization and colocalization to evaluate the role of 5 lipid-perturbing drug targets (ANGPTL3, ANGPTL4, APOC3, CETP, and PCSK9) in risk of 5 cancers (breast, colorectal, head and neck, ovarian, and prostate). We triangulated findings using pre-diagnostic protein measures in prospective analyses in EPIC (977 colorectal cancer cases, 4080 sub-cohort members) and the UK Biobank (860 colorectal cancer cases, 50 177 controls). To gain mechanistic insight into the role of ANGPTL4 in carcinogenesis, we examined the impact of the ANGPTL4 p. E40K loss-of-function variant on differential gene expression in normal colon tissue in BarcUVa-Seq. Finally, we evaluated the as","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-04-13T03:23:22.405Z","creation":"2026-04-13T03:12:34.832Z"},"accession":"S-EPMC12415964","cross_references":{"pubmed":["40511612"],"doi":["10.1093/jnci/djaf137"]}}