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Salicylic Acid and Risk of Colorectal Cancer: A Two-Sample Mendelian Randomization Study
A. Nounu, RC. Richmond, ID. Stewart, P. Surendran, NJ. Wareham, A. Butterworth, SJ. Weinstein, D. Albanes, JA. Baron, JL. Hopper, JC. Figueiredo, PA. Newcomb, NM. Lindor, G. Casey, EA. Platz, LL. Marchand, CM. Ulrich, CI. Li, FJB. van Dujinhoven,...
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články
NLK
Free Medical Journals
od 2009
PubMed Central
od 2009
Europe PubMed Central
od 2009
ProQuest Central
od 2009-01-01
Open Access Digital Library
od 2009-01-01
Open Access Digital Library
od 2009-01-01
Health & Medicine (ProQuest)
od 2009-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2009
PubMed
34836419
DOI
10.3390/nu13114164
Knihovny.cz E-zdroje
- MeSH
- Aspirin terapeutické užití MeSH
- celogenomová asociační studie MeSH
- dieta MeSH
- genotypizační techniky MeSH
- jednonukleotidový polymorfismus MeSH
- kolorektální nádory krev epidemiologie genetika prevence a kontrola MeSH
- kyselina salicylová aplikace a dávkování krev MeSH
- lidé MeSH
- mendelovská randomizace MeSH
- rizikové faktory MeSH
- studie případů a kontrol MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
Salicylic acid (SA) has observationally been shown to decrease colorectal cancer (CRC) risk. Aspirin (acetylsalicylic acid, that rapidly deacetylates to SA) is an effective primary and secondary chemopreventive agent. Through a Mendelian randomization (MR) approach, we aimed to address whether levels of SA affected CRC risk, stratifying by aspirin use. A two-sample MR analysis was performed using GWAS summary statistics of SA (INTERVAL and EPIC-Norfolk, N = 14,149) and CRC (CCFR, CORECT, GECCO and UK Biobank, 55,168 cases and 65,160 controls). The DACHS study (4410 cases and 3441 controls) was used for replication and stratification of aspirin-use. SNPs proxying SA were selected via three methods: (1) functional SNPs that influence the activity of aspirin-metabolising enzymes; (2) pathway SNPs present in enzymes' coding regions; and (3) genome-wide significant SNPs. We found no association between functional SNPs and SA levels. The pathway and genome-wide SNPs showed no association between SA and CRC risk (OR: 1.03, 95% CI: 0.84-1.27 and OR: 1.08, 95% CI: 0.86-1.34, respectively). Results remained unchanged upon aspirin use stratification. We found little evidence to suggest that an SD increase in genetically predicted SA protects against CRC risk in the general population and upon stratification by aspirin use.
Broad Institute of Harvard and MIT Cambridge MA 02142 USA
Cancer Epidemiology Division Cancer Council Victoria Melbourne VIC 3004 Australia
Cancer Epidemiology Program University of Hawaii Cancer Center Honolulu HI 96813 USA
CIBER Epidemiología y Salud Pública 28029 Madrid Spain
Clalit National Cancer Control Center Haifa 3436212 Israel
Department of Clinical Genetics Karolinska University Hospital 171 64 Solna Sweden
Department of Clinical Sciences Faculty of Medicine University of Barcelona 08007 Barcelona Spain
Department of Epidemiology Johns Hopkins Bloomberg School of Public Health Baltimore MD 21205 USA
Department of Epidemiology University of Washington School of Public Health Seattle WA 98195 USA
Department of Family Medicine University of Virginia Charlottesville VA 22903 USA
Department of General Surgery University Hospital Rostock 18057 Rostock Germany
Department of Health Science Research Mayo Clinic Scottsdale AZ 85259 USA
Department of Internal Medicine University of Utah Salt Lake City UT 84112 USA
Department of Medicine School of Medicine University of North Carolina Chapel Hill NC 27516 USA
Department of Molecular Medicine and Surgery Karolinska Institutet 171 64 Solna Sweden
Department of Population Science American Cancer Society Atlanta GA 30303 USA
Department of Preventive Medicine Chonnam National University Medical School Gwangju 61186 Korea
Department of Public Health and Primary Care University of Cambridge Cambridge CB1 8RN UK
Department of Radiation Sciences Oncology Unit Umeå University 901 87 Umeå Sweden
Department of Surgical Sciences Uppsala University 751 85 Uppsala Sweden
Division of Cancer Epidemiology German Cancer Research Center 69120 Heidelberg Germany
Division of Preventive Oncology German Cancer Research Center 69120 Heidelberg Germany
Division of Research Kaiser Permanente Northern California Oakland CA 94612 USA
Faculty of Medicine and Biomedical Center in Pilsen Charles University 323 00 Pilsen Czech Republic
Genetic Medicine and Family Cancer Clinic The Royal Melbourne Hospital Parkville VIC 3000 Australia
German Cancer Consortium 69120 Heidelberg Germany
Institute of Cancer Research Department of Medicine 1 Medical University Vienna 1090 Vienna Austria
Institute of Environmental Medicine Karolinska Institutet 171 64 Solna Sweden
Jeonnam Regional Cancer Center Chonnam National University Hwasun Hospital Hwasun 58128 Korea
Leeds Institute of Cancer and Pathology School of Medicine University of Leeds Leeds LS2 9JT UK
Memorial Sloan Kettering Cancer Center Department of Medicine New York NY 10065 USA
MRC Epidemiology Unit School of Clinical Medicine University of Cambridge Cambridge CB2 0SL UK
ONCOBEL Program Bellvitge Biomedical Research Institute 08908 Barcelona Spain
Oncology Data Analytics Program Catalan Institute of Oncology IDIBELL 08908 Barcelona Spain
Public Health Sciences Division Fred Hutchinson Cancer Research Center Seattle WA 98109 1024 USA
School of Cellular and Molecular Medicine University of Bristol Bristol BS8 1TD UK
School of Public Health University of Washington Seattle WA 98195 USA
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