Format

Send to

Choose Destination
Neuro Oncol. 2019 Oct 30. pii: noz209. doi: 10.1093/neuonc/noz209. [Epub ahead of print]

Lack of association between modifiable exposures and glioma risk: A Mendelian randomisation analysis.

Author information

1
Division of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.
2
School of Public Health, Yale University, New Haven, CT, USA.
3
Department of Neurosurgery, Brigham and Women's Hospital, Boston, MA, USA.
4
Department of Epidemiology and Biostatistics, School of Public Health, Georgia State University, Atlanta, GA, USA.
5
Duke Cancer Institute, Duke University Medical Center, Durham, NC,USA.
6
Cancer Control and Prevention Program, Department of Community and Family Medicine, Duke University Medical Center, Durham, NC, USA.
7
Department of Population and Quantitative Health Sciences and the Cleveland Center for Health Outcomes Research, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
8
Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
9
Departments of Neurology and Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
10
Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA.
11
Danish Cancer Society Research Center, Survivorship, Danish Cancer Society, Copenhagen, Denmark.
12
Oncology Clinic, Finsen Centre, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
13
Department of Laboratory Medicine and Pathology, Mayo Clinic Comprehensive Cancer Center, Mayo Clinic, Rochester, MI, USA.
14
Department of Radiation Sciences, Umeå University, Umeå, Sweden.
15
Department of Neurological Surgery, School of Medicine, University of California, San Francisco, CA, USA.
16
Institute of Human Genetics, University of California, San Francisco, CA, USA.
17
Sorbonne Université, Inserm, CNRS, UMR S 1127, Institut du Cerveau et de la Moelle épinière, ICM, Paris.
18
AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Service de Neurologie 2-Mazarin, Paris, France.
19
Section of Epidemiology and Population Sciences, Department of Medicine, Dan L. Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX, USA.
20
Division of Molecular Pathology, The Institute of Cancer Research, London, UK.

Abstract

BACKGROUND:

The etiological basis of glioma is poorly understood. We have used genetic markers in a Mendelian Randomisation (MR) framework to examine if lifestyle, cardiometabolic and inflammatory factors influence the risk of glioma. This methodology reduces bias from confounding and is not affected by reverse causation.

METHODS:

We identified genetic instruments for 37 potentially modifiable risk factors and evaluated their association with glioma risk using data from a genome-wide association study of 12,488 glioma patients and 18,169 controls. We used the estimated odds ratio of glioma associated with each of the genetically defined traits to infer evidence for a causal relationship with the following exposures: lifestyle and dietary factors (height, plasma IGF-1, blood carnitine, blood methionine, blood selenium, blood zinc, circulating adiponectin, circulating carotenoids, iron status, serum calcium, vitamin [A1, B12, B6, E and 25-hydroxyvitamin D], fatty acids levels [mono-unsaturated, omega-3 and omega-6] and circulating fetuin-A); cardiometabolic factors (birth weight, HDL cholesterol, LDL cholesterol, total cholesterol, total triglycerides, basal metabolic rate, body fat percentage, body mass index, fasting glucose, fasting proinsulin, HbA1C levels, diastolic and systolic blood pressure, waist circumference, waist-to-hip ratio) were included; inflammatory factors (C-reactive protein (CRP), plasma IL-6 sRa and serum IgE).

RESULTS:

After correction for the testing of multiple potential risk factors and excluding associations driven by one single nucleotide polymorphism (SNP) no significant association with glioma risk was observed (i.e. PCorrected > 0.05).

CONCLUSIONS:

This study did not provide evidence supporting any of the 37 factors examined as having a significant influence on glioma risk.

PMID:
31665421
DOI:
10.1093/neuonc/noz209

Supplemental Content

Full text links

Icon for Silverchair Information Systems
Loading ...
Support Center