Matthew G Varga1,2, Hui Cai3, Tim Waterboer4, Gwen Murphy5, Taichi Shimazu6, Phil R Taylor5, You-Lin Qiao7, Sue K Park8, Keun-Young Yoo9, Sun Ha Jee10, Eo Rin Cho10, Jeongseon Kim11, Christian C Abnet5, Shoichiro Tsugane6, Qiuyin Cai3, Wei Zheng3, Michael Pawlita4, Xiao-Ou Shu3, Meira Epplein3,12. 1. Department of Epidemiology, Gillings School of Global Public Health and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, 3207B Michael Hooker Research Center, Chapel Hill, NC, 27599, USA. matthew.varga@med.unc.edu. 2. Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN, 37203, USA. matthew.varga@med.unc.edu. 3. Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN, 37203, USA. 4. Division of Molecular Diagnostics of Oncogenic Infections, Research Program in Infection, Inflammation, and Cancer, German Cancer Research Center (DFKZ), 69120, Heidelberg, Germany. 5. Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, 20892, USA. 6. Epidemiology and Prevention Group, National Cancer Center, Tokyo, 104-0045, Japan. 7. Department of Cancer Epidemiology, Chinese Academy of Medical Sciences and Peking Union Medial College, Beijing, 100021, China. 8. Department of Biomedical Sciences, Cancer Research Institute, Seoul National University College of Medicine, Seoul, 110-799, Korea. 9. Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, 110-799, Korea. 10. Department of Epidemiology and Health Promotion, Institute for Health Promotion, Yonsei University, Seoul, 120-752, Korea. 11. Division of Cancer Epidemiology and Prevention, Research Institute, National Cancer Center, Goyang, 410-769, Korea. 12. Department of Population Health Sciences, Duke University and Cancer Control and Population Sciences Program, Duke Cancer Institute, Durham, NC, 27705, USA.
Abstract
BACKGROUND: Epstein-Barr virus (EBV)-positive gastric cancers represent a distinct subtype of gastric cancers and account for nearly 10% of the gastric cancer burden, yet risk detection strategies for this cancer subtype are lacking. METHODS: We conducted a nested case-control study where we assayed 4 EBV antigens [viral capsid antigen (VCA), early antigen (EA), Epstein-Barr nuclear antigen (EBNA), and BZLF1-encoded replication activator protein (ZEBRA)] in either sera or plasma from 1447 gastric cancer cases and 1797 controls obtained from seven prospective cohorts representing individuals from the high gastric cancer-risk countries of China, Japan, and Korea. RESULTS: The prevalence of EBV sero-positivity was universal with the exception of one sero-negative individual, and the highest titers of the EBV antigens VCA (OR 0.95, 95% CI 0.78-1.17), EBNA (OR 0.88, 95% CI 0.72-1.08), EA (OR 0.97, 95% CI 0.79-1.19), and ZEBRA (OR 0.87, 95% CI 0.71-1.07) were not associated with risk of incident gastric cancer. When we stratified these data by H. pylori status, there was no change in the association. CONCLUSIONS: Multiplex serology of the aforementioned EBV antigens in serum may not be a suitable biomarker for predicting gastric cancer risk in East Asian populations.
BACKGROUND:Epstein-Barr virus (EBV)-positive gastric cancers represent a distinct subtype of gastric cancers and account for nearly 10% of the gastric cancer burden, yet risk detection strategies for this cancer subtype are lacking. METHODS: We conducted a nested case-control study where we assayed 4 EBV antigens [viral capsid antigen (VCA), early antigen (EA), Epstein-Barr nuclear antigen (EBNA), and BZLF1-encoded replication activator protein (ZEBRA)] in either sera or plasma from 1447 gastric cancer cases and 1797 controls obtained from seven prospective cohorts representing individuals from the high gastric cancer-risk countries of China, Japan, and Korea. RESULTS: The prevalence of EBV sero-positivity was universal with the exception of one sero-negative individual, and the highest titers of the EBV antigens VCA (OR 0.95, 95% CI 0.78-1.17), EBNA (OR 0.88, 95% CI 0.72-1.08), EA (OR 0.97, 95% CI 0.79-1.19), and ZEBRA (OR 0.87, 95% CI 0.71-1.07) were not associated with risk of incident gastric cancer. When we stratified these data by H. pylori status, there was no change in the association. CONCLUSIONS: Multiplex serology of the aforementioned EBV antigens in serum may not be a suitable biomarker for predicting gastric cancer risk in East Asian populations.
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