دورية أكاديمية

Two genome-wide interaction loci modify the association of nonsteroidal anti-inflammatory drugs with colorectal cancer.

التفاصيل البيبلوغرافية
العنوان: Two genome-wide interaction loci modify the association of nonsteroidal anti-inflammatory drugs with colorectal cancer.
المؤلفون: Drew DA; Clinical & Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA., Kim AE; Division of Biostatistics, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA., Lin Y; Public Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, Washington, USA., Qu C; Public Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, Washington, USA., Morrison J; Division of Biostatistics, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA., Lewinger JP; Division of Biostatistics, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA., Kawaguchi E; Division of Biostatistics, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA., Wang J; Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, California, USA., Fu Y; Division of Biostatistics, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA., Zemlianskaia N; Division of Biostatistics, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA., Díez-Obrero V; Colorectal Cancer Group, ONCOBELL Program, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain.; Consortium for Biomedical Research in Epidemiology and Public Health (CIBERESP), Madrid, Spain.; Department of Clinical Sciences, Faculty of Medicine, University of Barcelona, Barcelona, Spain., Bien SA; Public Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, Washington, USA., Dimou N; Nutrition and Metabolism Branch, International Agency for Research on Cancer, World Health Organization, Lyon, France., Albanes D; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA., Baurley JW; Bioinformatics and Data Science Research Center, Bina Nusantara University, Jakarta, Indonesia.; BioRealm LLC, Walnut, CA, USA., Wu AH; Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, California, USA., Buchanan DD; Colorectal Oncogenomics Group, Department of Clinical Pathology, The University of Melbourne, Parkville, Victoria 3010 Australia.; University of Melbourne Centre for Cancer Research, Victorian Comprehensive Cancer Centre, Parkville, Victoria 3010 Australia.; Genomic Medicine and Family Cancer Clinic, The Royal Melbourne Hospital, Parkville, Victoria, Australia., Potter JD; Public Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, Washington, USA.; Research Centre for Hauora and Health, Massey University, Wellington, New Zealand., Prentice RL; Public Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, Washington, USA., Harlid S; Department of Radiation Sciences, Oncology Unit, Umeå University, Umeå, Sweden., Arndt V; Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany., Barry EL; Department of Epidemiology, Geisel School of Medicine at Dartmouth, Hanover, NH, USA., Berndt SI; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA., Bouras E; Laboratory of Hygiene, Social & Preventive Medicine and Medical Statistics, Department of Medicine, School of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece., Brenner H; Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.; Division of Preventive Oncology, German Cancer Research Center (DKFZ) and National Center for Tumor Diseases (NCT), Heidelberg, Germany.; German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany., Budiarto A; 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Public Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, Washington, USA., Hoffmeister M; Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany., Huyghe JR; Public Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, Washington, USA., Jenkins MA; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Victoria, Australia., Jordahl KM; Public Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, Washington, USA.; Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, USA., Kundaje A; Department of Genetics, Stanford University, Stanford, CA, USA.; Department of Computer Science, Stanford University, Stanford, CA, USA., Le Marchand L; University of Hawaii Cancer Center, Honolulu, HI, USA., Li L; Department of Family Medicine, University of Virginia, Charlottesville, VA, USA.; UVA Comprehensive Cancer Center, Charlottesville, VA, USA., Lynch BM; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Victoria, Australia.; Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Victoria, Australia., Murphy N; Nutrition and Metabolism Branch, International Agency for Research on Cancer, World Health Organization, Lyon, France., Nassir R; Department of Pathology, School of Medicine, Umm Al-Qura'a University, Mecca, Saudi Arabia., Newcomb PA; Public Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, Washington, USA.; School of Public Health, University of Washington, Seattle, WA, USA., Newton CC; Department of Population Science, American Cancer Society, Atlanta, GA, USA., Obón-Santacana M; Colorectal Cancer Group, ONCOBELL Program, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain.; Unit of Biomarkers and Susceptibility (UBS), Oncology Data Analytics Program (ODAP), Catalan Institute of Oncology (ICO), L'Hospitalet del Llobregat, 08908 Barcelona, Spain.; 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المصدر: Science advances [Sci Adv] 2024 May 31; Vol. 10 (22), pp. eadk3121. Date of Electronic Publication: 2024 May 29.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: American Association for the Advancement of Science Country of Publication: United States NLM ID: 101653440 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2375-2548 (Electronic) Linking ISSN: 23752548 NLM ISO Abbreviation: Sci Adv Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Washington, DC : American Association for the Advancement of Science, [2015]-
مواضيع طبية MeSH: Colorectal Neoplasms*/genetics , Colorectal Neoplasms*/drug therapy , Anti-Inflammatory Agents, Non-Steroidal*/pharmacology , Genome-Wide Association Study* , Polymorphism, Single Nucleotide*, Humans ; Aspirin/pharmacology ; Receptors, Prostaglandin E, EP4 Subtype/genetics ; Receptors, Prostaglandin E, EP4 Subtype/metabolism ; Male ; Genetic Predisposition to Disease ; Female ; Case-Control Studies ; Middle Aged ; Genetic Loci ; Aged
مستخلص: Regular, long-term aspirin use may act synergistically with genetic variants, particularly those in mechanistically relevant pathways, to confer a protective effect on colorectal cancer (CRC) risk. We leveraged pooled data from 52 clinical trial, cohort, and case-control studies that included 30,806 CRC cases and 41,861 controls of European ancestry to conduct a genome-wide interaction scan between regular aspirin/nonsteroidal anti-inflammatory drug (NSAID) use and imputed genetic variants. After adjusting for multiple comparisons, we identified statistically significant interactions between regular aspirin/NSAID use and variants in 6q24.1 (top hit rs72833769 ), which has evidence of influencing expression of TBC1D7 (a subunit of the TSC1-TSC2 complex, a key regulator of MTOR activity), and variants in 5p13.1 (top hit rs350047 ), which is associated with expression of PTGER4 (codes a cell surface receptor directly involved in the mode of action of aspirin). Genetic variants with functional impact may modulate the chemopreventive effect of regular aspirin use, and our study identifies putative previously unidentified targets for additional mechanistic interrogation.
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معلومات مُعتمدة: 001 International WHO_ World Health Organization; K01 DK120742 United States DK NIDDK NIH HHS
المشرفين على المادة: 0 (Anti-Inflammatory Agents, Non-Steroidal)
R16CO5Y76E (Aspirin)
0 (Receptors, Prostaglandin E, EP4 Subtype)
0 (PTGER4 protein, human)
تواريخ الأحداث: Date Created: 20240529 Date Completed: 20240529 Latest Revision: 20240712
رمز التحديث: 20240712
مُعرف محوري في PubMed: PMC11135391
DOI: 10.1126/sciadv.adk3121
PMID: 38809988
قاعدة البيانات: MEDLINE
الوصف
تدمد:2375-2548
DOI:10.1126/sciadv.adk3121