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Associations Between Glycemic Traits and Colorectal Cancer: A Mendelian Randomization Analysis
N. Murphy, M. Song, N. Papadimitriou, R. Carreras-Torres, C. Langenberg, RM. Martin, KK. Tsilidis, I. Barroso, J. Chen, TM. Frayling, CJ. Bull, EE. Vincent, M. Cotterchio, SB. Gruber, RK. Pai, PA. Newcomb, A. Perez-Cornago, FJB. van Duijnhoven,...
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
MC_UU_00006/1
Medical Research Council - United Kingdom
C18281/A29019
Cancer Research UK - United Kingdom
NLK
Free Medical Journals
od 1996 do Před 1 rokem
Open Access Digital Library
od 1996-01-01
PubMed
35048991
DOI
10.1093/jnci/djac011
Knihovny.cz E-zdroje
- MeSH
- celogenomová asociační studie MeSH
- diabetes mellitus 2. typu * komplikace epidemiologie genetika MeSH
- glykovaný hemoglobin analýza MeSH
- hyperinzulinismus * komplikace genetika MeSH
- inzulin MeSH
- jednonukleotidový polymorfismus MeSH
- kolorektální nádory * komplikace epidemiologie genetika MeSH
- krevní glukóza analýza genetika MeSH
- lidé MeSH
- mendelovská randomizace MeSH
- rizikové faktory MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
BACKGROUND: Glycemic traits-such as hyperinsulinemia, hyperglycemia, and type 2 diabetes-have been associated with higher colorectal cancer risk in observational studies; however, causality of these associations is uncertain. We used Mendelian randomization (MR) to estimate the causal effects of fasting insulin, 2-hour glucose, fasting glucose, glycated hemoglobin (HbA1c), and type 2 diabetes with colorectal cancer. METHODS: Genome-wide association study summary data were used to identify genetic variants associated with circulating levels of fasting insulin (n = 34), 2-hour glucose (n = 13), fasting glucose (n = 70), HbA1c (n = 221), and type 2 diabetes (n = 268). Using 2-sample MR, we examined these variants in relation to colorectal cancer risk (48 214 case patient and 64 159 control patients). RESULTS: In inverse-variance models, higher fasting insulin levels increased colorectal cancer risk (odds ratio [OR] per 1-SD = 1.65, 95% confidence interval [CI] = 1.15 to 2.36). We found no evidence of any effect of 2-hour glucose (OR per 1-SD = 1.02, 95% CI = 0.86 to 1.21) or fasting glucose (OR per 1-SD = 1.04, 95% CI = 0.88 to 1.23) concentrations on colorectal cancer risk. Genetic liability to type 2 diabetes (OR per 1-unit increase in log odds = 1.04, 95% CI = 1.01 to 1.07) and higher HbA1c levels (OR per 1-SD = 1.09, 95% CI = 1.00 to 1.19) increased colorectal cancer risk, although these findings may have been biased by pleiotropy. Higher HbA1c concentrations increased rectal cancer risk in men (OR per 1-SD = 1.21, 95% CI = 1.05 to 1.40), but not in women. CONCLUSIONS: Our results support a causal effect of higher fasting insulin, but not glucose traits or type 2 diabetes, on increased colorectal cancer risk. This suggests that pharmacological or lifestyle interventions that lower circulating insulin levels may be beneficial in preventing colorectal tumorigenesis.
Bristol Medical School Department of Population Health Sciences University of Bristol Bristol UK
Cancer Epidemiology Unit Nuffield Department of Population Health University of Oxford Oxford UK
Computational Medicine Berlin Institute of Health Charité University Medicine Berlin Germany
Department of Epidemiology Harvard T H Chan School of Public Health Harvard University Boston MA USA
Department of Epidemiology University of Washington Seattle WA USA
Department of Hygiene and Epidemiology University of Ioannina School of Medicine Ioannina Greece
Department of Nutrition Harvard T H Chan School of Public Health Boston MA USA
Department of Pathology and Laboratory Medicine Mayo Clinic Arizona Scottsdale AZ USA
Department of Preventive Medicine USC Norris Comprehensive Cancer Center CA USA
Department of Radiation Sciences Oncology Umeå University Umeå Sweden
Division of Gastroenterology Massachusetts General Hospital and Harvard Medical School Boston MA USA
Division of Human Nutrition and Health Wageningen University and Research Wageningen the Netherlands
Exeter Centre of Excellence in Diabetes Exeter Medical School University of Exeter Exeter UK
Faculty of Medicine and Biomedical Center in Pilsen Charles University Pilsen Czech Republic
Health Data Research UK Wellcome Genome Campus and University of Cambridge Cambridge UK
Institute of Environmental Medicine Karolinska Institutet Stockholm Sweden
Keck School of Medicine University of Southern California Los Angeles CA USA
MRC Epidemiology Unit University of Cambridge Cambridge UK
Nutrition and Metabolism Branch International Agency for Research on Cancer Lyon France
Prevention and Cancer Control Clinical Institutes and Quality Programs Ontario Health Ontario Canada
Public Health Sciences Division Fred Hutchinson Cancer Research Center Seattle WA USA
School of Cellular and Molecular Medicine University of Bristol Bristol UK
University of Southern California Preventative Medicine Los Angeles CA USA
Wallenberg Centre for Molecular Medicine Umeå University Umeå Sweden
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