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    Mendelian Randomization of Circulating Polyunsaturated Fatty Acids and Colorectal Cancer Risk

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    Author
    Khankari, NK; Banbury, BL; Borges, MC; Haycock, P; Albanes, D; Arndt, V; Berndt, SI; Bezieau, S; Brenner, H; Campbell, PT; ...
    Date
    2020-04-01
    Source Title
    Cancer Epidemiology, Biomarkers and Prevention
    Publisher
    AMER ASSOC CANCER RESEARCH
    University of Melbourne Author/s
    Jenkins, Mark; English, Dallas; Win, Aung Ko
    Affiliation
    Melbourne School of Population and Global Health
    Metadata
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    Document Type
    Journal Article
    Citations
    Khankari, N. K., Banbury, B. L., Borges, M. C., Haycock, P., Albanes, D., Arndt, V., Berndt, S. I., Bezieau, S., Brenner, H., Campbell, P. T., Casey, G., Chan, A. T., Chang-Claude, J., Conti, D. V., Cotterchio, M., English, D. R., Figueiredo, J. C., Giles, G. G., Giovannucci, E. L. ,... Zheng, W. (2020). Mendelian Randomization of Circulating Polyunsaturated Fatty Acids and Colorectal Cancer Risk. CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION, 29 (4), pp.860-870. https://doi.org/10.1158/1055-9965.EPI-19-0891.
    Access Status
    Access this item via the Open Access location
    URI
    http://hdl.handle.net/11343/254020
    DOI
    10.1158/1055-9965.EPI-19-0891
    Open Access URL
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7125012
    NHMRC Grant code
    NHMRC/1141746
    Abstract
    BACKGROUND: Results from epidemiologic studies examining polyunsaturated fatty acids (PUFA) and colorectal cancer risk are inconsistent. Mendelian randomization may strengthen causal inference from observational studies. Given their shared metabolic pathway, examining the combined effects of aspirin/NSAID use with PUFAs could help elucidate an association between PUFAs and colorectal cancer risk. METHODS: Information was leveraged from genome-wide association studies (GWAS) regarding PUFA-associated SNPs to create weighted genetic scores (wGS) representing genetically predicted circulating blood PUFAs for 11,016 non-Hispanic white colorectal cancer cases and 13,732 controls in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO). Associations per SD increase in the wGS were estimated using unconditional logistic regression. Interactions between PUFA wGSs and aspirin/NSAID use on colorectal cancer risk were also examined. RESULTS: Modest colorectal cancer risk reductions were observed per SD increase in circulating linoleic acid [ORLA = 0.96; 95% confidence interval (CI) = 0.93-0.98; P = 5.2 × 10-4] and α-linolenic acid (ORALA = 0.95; 95% CI = 0.92-0.97; P = 5.4 × 10-5), whereas modest increased risks were observed for arachidonic (ORAA = 1.06; 95% CI = 1.03-1.08; P = 3.3 × 10-5), eicosapentaenoic (OREPA = 1.04; 95% CI = 1.01-1.07; P = 2.5 × 10-3), and docosapentaenoic acids (ORDPA = 1.03; 95% CI = 1.01-1.06; P = 1.2 × 10-2). Each of these effects was stronger among aspirin/NSAID nonusers in the stratified analyses. CONCLUSIONS: Our study suggests that higher circulating shorter-chain PUFAs (i.e., LA and ALA) were associated with reduced colorectal cancer risk, whereas longer-chain PUFAs (i.e., AA, EPA, and DPA) were associated with an increased colorectal cancer risk. IMPACT: The interaction of PUFAs with aspirin/NSAID use indicates a shared colorectal cancer inflammatory pathway. Future research should continue to improve PUFA genetic instruments to elucidate the independent effects of PUFAs on colorectal cancer.

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