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Wang X, Su YR, Petersen PS, et al. Exploratory Genome-Wide Interaction Analysis of Nonsteroidal Anti-inflammatory Drugs and Predicted Gene Expression on Colorectal Cancer Risk. Cancer Epidemiol Biomarkers Prev. 2020;29(9):1800-1808doi: 10.1158/1055-9965.EPI-19-1018.
Wang, X., Su, Y. R., Petersen, P. S., Bien, S., Schmit, S. L., Drew, D. A., Albanes, D., Berndt, S. I., Brenner, H., Campbell, P. T., Casey, G., Chang-Claude, J., Gallinger, S. J., Gruber, S. B., Haile, R. W., Harrison, T. A., Hoffmeister, M., Jacobs, E. J., Jenkins, M. A., Joshi, A. D., Li, L., Lin, Y., Lindor, N. M., Marchand, L. L., Martin, V., Milne, R., Maclnnis, R., Moreno, V., Nan, H., Newcomb, P. A., Potter, J. D., Rennert, G., Rennert, H., Slattery, M. L., Thibodeau, S. N., Weinstein, S. J., Woods, M. O., Chan, A. T., White, E., Hsu, L., & Peters, U. (2020). Exploratory Genome-Wide Interaction Analysis of Nonsteroidal Anti-inflammatory Drugs and Predicted Gene Expression on Colorectal Cancer Risk. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 29(9), 1800-1808. https://doi.org/10.1158/1055-9965.EPI-19-1018
Wang, Xiaoliang, et al. "Exploratory Genome-Wide Interaction Analysis of Nonsteroidal Anti-inflammatory Drugs and Predicted Gene Expression on Colorectal Cancer Risk." Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology vol. 29,9 (2020): 1800-1808. doi: https://doi.org/10.1158/1055-9965.EPI-19-1018
Wang X, Su YR, Petersen PS, Bien S, Schmit SL, Drew DA, Albanes D, Berndt SI, Brenner H, Campbell PT, Casey G, Chang-Claude J, Gallinger SJ, Gruber SB, Haile RW, Harrison TA, Hoffmeister M, Jacobs EJ, Jenkins MA, Joshi AD, Li L, Lin Y, Lindor NM, Marchand LL, Martin V, Milne R, Maclnnis R, Moreno V, Nan H, Newcomb PA, Potter JD, Rennert G, Rennert H, Slattery ML, Thibodeau SN, Weinstein SJ, Woods MO, Chan AT, White E, Hsu L, Peters U. Exploratory Genome-Wide Interaction Analysis of Nonsteroidal Anti-inflammatory Drugs and Predicted Gene Expression on Colorectal Cancer Risk. Cancer Epidemiol Biomarkers Prev. 2020 Sep;29(9):1800-1808. doi: 10.1158/1055-9965.EPI-19-1018. Epub 2020 Jul 10. PMID: 32651213; PMCID: PMC7556991.
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Cancer Epidemiol Biomarkers Prev. 2020 Sep;29(9):1800-1808. doi: 10.1158/1055-9965.EPI-19-1018. Epub 2020 Jul 10.

Exploratory Genome-Wide Interaction Analysis of Nonsteroidal Anti-inflammatory Drugs and Predicted Gene Expression on Colorectal Cancer Risk.

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

Xiaoliang Wang, Yu-Ru Su, Paneen S Petersen, Stephanie Bien, Stephanie L Schmit, David A Drew, Demetrius Albanes, Sonja I Berndt, Hermann Brenner, Peter T Campbell, Graham Casey, Jenny Chang-Claude, Steven J Gallinger, Stephen B Gruber, Robert W Haile, Tabitha A Harrison, Michael Hoffmeister, Eric J Jacobs, Mark A Jenkins, Amit D Joshi, Li Li, Yi Lin, Noralane M Lindor, Loïc Le Marchand, Vicente Martin, Roger Milne, Robert Maclnnis, Victor Moreno, Hongmei Nan, Polly A Newcomb, John D Potter, Gad Rennert, Hedy Rennert, Martha L Slattery, Steve N Thibodeau, Stephanie J Weinstein, Michael O Woods, Andrew T Chan, Emily White, Li Hsu, Ulrike Peters

Affiliations

  1. Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington. [email protected].
  2. Department of Epidemiology, University of Washington School of Public Health, Seattle, Washington.
  3. Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington.
  4. Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.
  5. Division of Gastroenterology, Massachusetts General Hospital, Boston, Massachusetts.
  6. Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston, Massachusetts.
  7. Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
  8. Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  9. Division of Preventive Oncology, German Cancer Research Center (DKFZ) and National Center for Tumor Diseases (NCT), Heidelberg, Germany.
  10. German Cancer Consortium (DKTK), Heidelberg, Germany.
  11. Behavioral and Epidemiology Research Group, American Cancer Society, Atlanta, Georgia.
  12. Public Health Sciences, University of Virginia, Charlottesville, Virginia.
  13. Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  14. University Cancer Center Hamburg, University Hospital Hamburg-Eppendorf, Hamburg, Germany.
  15. Department of Pathology and Laboratory Medicine, Lunenfeld-Tanenbaum Research Institute, Toronto, Ontario, Canada.
  16. Division of General Surgery, Toronto General Hospital, Toronto, Ontario, Canada.
  17. Department of Preventive Medicine, USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, California.
  18. Department of Health Research and Policy (Epidemiology), Stanford University School of Medicine, Palo Alto, California.
  19. Department of Medicine (Oncology), Stanford Cancer Institute, Palo Alto, California.
  20. Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Parkville, Victoria, Australia.
  21. Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts.
  22. Department of Family Medicine, University of Virginia, Charlottesville, Virginia.
  23. Department of Health Sciences Research, Mayo Clinic, Scottsdale, Arizona.
  24. Epidemiology Program, University of Hawaii Cancer Center, Honolulu, Hawaii.
  25. CIBER Epidemiología y Salud Pública (CIBERESP), Madrid, Spain.
  26. Biomedicine Institute (IBIOMED), University of León, León, Spain.
  27. Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Victoria, Australia.
  28. Cancer Prevention and Control Program, Catalan Institute of Oncology-IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain.
  29. Department of Clinical Sciences, Faculty of Medicine, University of Barcelona, Barcelona, Spain.
  30. Department of Epidemiology, Richard M. Fairbanks School of Public Health, Indiana University, Indianapolis, Indiana.
  31. Melvin and Bren Simon Cancer Center, Indiana University, Indianapolis, Indiana.
  32. Centre for Public Health Research, Massey University, Wellington, New Zealand.
  33. Department of Community Medicine and Epidemiology, Lady Davis Carmel Medical Center, Haifa, Israel.
  34. Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
  35. Clalit National Cancer Control Center, Haifa, Israel.
  36. Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, Utah.
  37. Department of Laboratory Medicine & Pathology, Mayo Clinic, Rochester, Minnesota.
  38. Discipline of Genetics, Memorial University of Newfoundland, St. John's, Canada.
  39. Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.

PMID: 32651213 PMCID: PMC7556991 DOI: 10.1158/1055-9965.EPI-19-1018

Abstract

BACKGROUND: Regular use of nonsteroidal anti-inflammatory drugs (NSAID) is associated with lower risk of colorectal cancer. Genome-wide interaction analysis on single variants (G × E) has identified several SNPs that may interact with NSAIDs to confer colorectal cancer risk, but variations in gene expression levels may also modify the effect of NSAID use. Therefore, we tested interactions between NSAID use and predicted gene expression levels in relation to colorectal cancer risk.

METHODS: Genetically predicted gene expressions were tested for interaction with NSAID use on colorectal cancer risk among 19,258 colorectal cancer cases and 18,597 controls from 21 observational studies. A Mixed Score Test for Interactions (MiSTi) approach was used to jointly assess G × E effects which are modeled via fixed interaction effects of the weighted burden within each gene set (burden) and residual G × E effects (variance). A false discovery rate (FDR) at 0.2 was applied to correct for multiple testing.

RESULTS: Among the 4,840 genes tested, genetically predicted expression levels of four genes modified the effect of any NSAID use on colorectal cancer risk, including

CONCLUSIONS: By incorporating functional information, we discovered several novel genes that interacted with NSAID use.

IMPACT: These findings provide preliminary support that could help understand the chemopreventive mechanisms of NSAIDs on colorectal cancer.

©2020 American Association for Cancer Research.

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