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Obesity, metabolic factors and risk of different histological types of lung cancer: A Mendelian randomization study
R. Carreras-Torres, M. Johansson, PC. Haycock, KH. Wade, CL. Relton, RM. Martin, G. Davey Smith, D. Albanes, MC. Aldrich, A. Andrew, SM. Arnold, H. Bickeböller, SE. Bojesen, H. Brunnström, J. Manjer, I. Brüske, NE. Caporaso, C. Chen, DC....
Language English Country United States
Document type Journal Article
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- MeSH
- Phenotype MeSH
- Body Mass Index MeSH
- Insulin blood MeSH
- Insulin Resistance MeSH
- Polymorphism, Single Nucleotide MeSH
- Humans MeSH
- Lipids blood MeSH
- Mendelian Randomization Analysis * MeSH
- Lung Neoplasms blood complications metabolism pathology MeSH
- Obesity blood complications MeSH
- Fasting MeSH
- Likelihood Functions MeSH
- Risk Factors MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
BACKGROUND: Assessing the relationship between lung cancer and metabolic conditions is challenging because of the confounding effect of tobacco. Mendelian randomization (MR), or the use of genetic instrumental variables to assess causality, may help to identify the metabolic drivers of lung cancer. METHODS AND FINDINGS: We identified genetic instruments for potential metabolic risk factors and evaluated these in relation to risk using 29,266 lung cancer cases (including 11,273 adenocarcinomas, 7,426 squamous cell and 2,664 small cell cases) and 56,450 controls. The MR risk analysis suggested a causal effect of body mass index (BMI) on lung cancer risk for two of the three major histological subtypes, with evidence of a risk increase for squamous cell carcinoma (odds ratio (OR) [95% confidence interval (CI)] = 1.20 [1.01-1.43] and for small cell lung cancer (OR [95%CI] = 1.52 [1.15-2.00]) for each standard deviation (SD) increase in BMI [4.6 kg/m2]), but not for adenocarcinoma (OR [95%CI] = 0.93 [0.79-1.08]) (Pheterogeneity = 4.3x10-3). Additional analysis using a genetic instrument for BMI showed that each SD increase in BMI increased cigarette consumption by 1.27 cigarettes per day (P = 2.1x10-3), providing novel evidence that a genetic susceptibility to obesity influences smoking patterns. There was also evidence that low-density lipoprotein cholesterol was inversely associated with lung cancer overall risk (OR [95%CI] = 0.90 [0.84-0.97] per SD of 38 mg/dl), while fasting insulin was positively associated (OR [95%CI] = 1.63 [1.25-2.13] per SD of 44.4 pmol/l). Sensitivity analyses including a weighted-median approach and MR-Egger test did not detect other pleiotropic effects biasing the main results. CONCLUSIONS: Our results are consistent with a causal role of fasting insulin and low-density lipoprotein cholesterol in lung cancer etiology, as well as for BMI in squamous cell and small cell carcinoma. The latter relation may be mediated by a previously unrecognized effect of obesity on smoking behavior.
British Columbia Cancer Agency Vancouver British Columbia Canada
Department of Medical Biosciences Umeå University Umeå Sweden
Department of Preventive Medicine Seoul National University College of Medicine Seoul Korea
Department of Thoracic Surgery Clinical Center of Serbia Belgrade Serbia
Division of Cancer Control and Population Science University of Pittsburgh Cancer Institute
Epidemiology Program University of Hawaii Cancer Center Honolulu Hawaii United States of America
Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark
Fred Hutchinson Cancer Research Center Seattle Washington United States of America
Helmholtz Zentrum München Munich Germany
Laboratory Medicine Region Skåne Department of Clinical Sciences Lund Lund University Lund Sweden
Lunenfeld Tanenbaum Research Institute of Mount Sinai Hospital Toronto Canada
National Institute of Occupational Health Oslo Norway
National Institute of Public Health Bucharest Romania
Nofer Institute of Occupational Medicine Department of Environmental Epidemiology Lodz Poland
Norris Cotton Cancer Center Lebanon New Hampshire United States of America
Ontario Cancer Institute Princess Margaret Cancer Center Toronto Ontario Canada
Princess Margaret Cancer Center Toronto Canada
Radboud University Medical Center Nijmegen The Nederlands
Russian N N Blokhin Cancer Research Centre Moscow The Russian Federation
Section of Genetics International Agency for Research on Cancer Lyon France
The University of Texas MD Anderson Cancer Center Houston Texas United States of America
University Medical Center Göettingen Göttingen Germany
University of Kentucky Markey Cancer Center Lexington Kentucky United States of America
University of Salzburg and Cancer Cluster Salzburg Salzburg Austria
University of Sheffield Sheffield United Kingdom
Washington State University College of Pharmacy Spokane Washington United States of America
References provided by Crossref.org
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- $a Obesity, metabolic factors and risk of different histological types of lung cancer: A Mendelian randomization study / $c R. Carreras-Torres, M. Johansson, PC. Haycock, KH. Wade, CL. Relton, RM. Martin, G. Davey Smith, D. Albanes, MC. Aldrich, A. Andrew, SM. Arnold, H. Bickeböller, SE. Bojesen, H. Brunnström, J. Manjer, I. Brüske, NE. Caporaso, C. Chen, DC. Christiani, WJ. Christian, JA. Doherty, EJ. Duell, JK. Field, MPA. Davies, MW. Marcus, GE. Goodman, K. Grankvist, A. Haugen, YC. Hong, LA. Kiemeney, EHFM. van der Heijden, P. Kraft, MB. Johansson, S. Lam, MT. Landi, P. Lazarus, L. Le Marchand, G. Liu, O. Melander, SL. Park, G. Rennert, A. Risch, EB. Haura, G. Scelo, D. Zaridze, A. Mukeriya, M. Savić, J. Lissowska, B. Swiatkowska, V. Janout, I. Holcatova, D. Mates, MB. Schabath, H. Shen, A. Tardon, MD. Teare, P. Woll, MS. Tsao, X. Wu, JM. Yuan, RJ. Hung, CI. Amos, J. McKay, P. Brennan,
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- $a BACKGROUND: Assessing the relationship between lung cancer and metabolic conditions is challenging because of the confounding effect of tobacco. Mendelian randomization (MR), or the use of genetic instrumental variables to assess causality, may help to identify the metabolic drivers of lung cancer. METHODS AND FINDINGS: We identified genetic instruments for potential metabolic risk factors and evaluated these in relation to risk using 29,266 lung cancer cases (including 11,273 adenocarcinomas, 7,426 squamous cell and 2,664 small cell cases) and 56,450 controls. The MR risk analysis suggested a causal effect of body mass index (BMI) on lung cancer risk for two of the three major histological subtypes, with evidence of a risk increase for squamous cell carcinoma (odds ratio (OR) [95% confidence interval (CI)] = 1.20 [1.01-1.43] and for small cell lung cancer (OR [95%CI] = 1.52 [1.15-2.00]) for each standard deviation (SD) increase in BMI [4.6 kg/m2]), but not for adenocarcinoma (OR [95%CI] = 0.93 [0.79-1.08]) (Pheterogeneity = 4.3x10-3). Additional analysis using a genetic instrument for BMI showed that each SD increase in BMI increased cigarette consumption by 1.27 cigarettes per day (P = 2.1x10-3), providing novel evidence that a genetic susceptibility to obesity influences smoking patterns. There was also evidence that low-density lipoprotein cholesterol was inversely associated with lung cancer overall risk (OR [95%CI] = 0.90 [0.84-0.97] per SD of 38 mg/dl), while fasting insulin was positively associated (OR [95%CI] = 1.63 [1.25-2.13] per SD of 44.4 pmol/l). Sensitivity analyses including a weighted-median approach and MR-Egger test did not detect other pleiotropic effects biasing the main results. CONCLUSIONS: Our results are consistent with a causal role of fasting insulin and low-density lipoprotein cholesterol in lung cancer etiology, as well as for BMI in squamous cell and small cell carcinoma. The latter relation may be mediated by a previously unrecognized effect of obesity on smoking behavior.
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