Lack of association between modifiable exposures and glioma risk: A Mendelian randomization analysis
Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
Standard
Lack of association between modifiable exposures and glioma risk : A Mendelian randomization analysis. / Saunders, Charlie N.; Cornish, Alex J.; Kinnersley, Ben; Law, Philip J.; Claus, Elizabeth B.; Il'yasova, Dora; Schildkraut, Joellen; Barnholtz-Sloan, Jill S.; Olson, Sara H.; Bernstein, Jonine L.; Lai, Rose K.; Chanock, Stephen; Rajaraman, Preetha; Johansen, Christoffer; Jenkins, Robert B.; Melin, Beatrice S.; Wrensch, Margaret R.; Sanson, Marc; Bondy, Melissa L.; Houlston, Richard S.
I: Neuro-Oncology, Bind 22, Nr. 2, 2020, s. 207-215.Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - Lack of association between modifiable exposures and glioma risk
T2 - A Mendelian randomization analysis
AU - Saunders, Charlie N.
AU - Cornish, Alex J.
AU - Kinnersley, Ben
AU - Law, Philip J.
AU - Claus, Elizabeth B.
AU - Il'yasova, Dora
AU - Schildkraut, Joellen
AU - Barnholtz-Sloan, Jill S.
AU - Olson, Sara H.
AU - Bernstein, Jonine L.
AU - Lai, Rose K.
AU - Chanock, Stephen
AU - Rajaraman, Preetha
AU - Johansen, Christoffer
AU - Jenkins, Robert B.
AU - Melin, Beatrice S.
AU - Wrensch, Margaret R.
AU - Sanson, Marc
AU - Bondy, Melissa L.
AU - Houlston, Richard S.
PY - 2020
Y1 - 2020
N2 - Background: The etiological basis of glioma is poorly understood. We have used genetic markers in a Mendelian randomization (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 insulin-like growth factor 1, blood carnitine, blood methionine, blood selenium, blood zinc, circulating adiponectin, circulating carotenoids, iron status, serum calcium, vitamins (A1, B12, B6, E, and 25-hydroxyvitamin D), fatty acid levels (monounsaturated, omega-3, and omega-6) and circulating fetuin-A; Cardiometabolic factors - birth weight, high density lipoprotein cholesterol, low density lipoprotein cholesterol, total cholesterol, total triglycerides, basal metabolic rate, body fat percentage, body mass index, fasting glucose, fasting proinsulin, glycated hemoglobin levels, diastolic and systolic blood pressure, waist circumference, waist-to-hip ratio; and Inflammatory factors - C-reactive protein, plasma interleukin-6 receptor subunit alpha and serum immunoglobulin E. Results: After correction for the testing of multiple potential risk factors and excluding associations driven by one single nucleotide polymorphism, no significant association with glioma risk was observed (ie, 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.
AB - Background: The etiological basis of glioma is poorly understood. We have used genetic markers in a Mendelian randomization (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 insulin-like growth factor 1, blood carnitine, blood methionine, blood selenium, blood zinc, circulating adiponectin, circulating carotenoids, iron status, serum calcium, vitamins (A1, B12, B6, E, and 25-hydroxyvitamin D), fatty acid levels (monounsaturated, omega-3, and omega-6) and circulating fetuin-A; Cardiometabolic factors - birth weight, high density lipoprotein cholesterol, low density lipoprotein cholesterol, total cholesterol, total triglycerides, basal metabolic rate, body fat percentage, body mass index, fasting glucose, fasting proinsulin, glycated hemoglobin levels, diastolic and systolic blood pressure, waist circumference, waist-to-hip ratio; and Inflammatory factors - C-reactive protein, plasma interleukin-6 receptor subunit alpha and serum immunoglobulin E. Results: After correction for the testing of multiple potential risk factors and excluding associations driven by one single nucleotide polymorphism, no significant association with glioma risk was observed (ie, 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.
KW - cancer
KW - glioma
KW - Mendelian randomization
KW - risk
U2 - 10.1093/neuonc/noz209
DO - 10.1093/neuonc/noz209
M3 - Review
C2 - 31665421
AN - SCOPUS:85081141216
VL - 22
SP - 207
EP - 215
JO - Neuro-Oncology
JF - Neuro-Oncology
SN - 1522-8517
IS - 2
ER -
ID: 261614625