M Constanza Camargo1, Kyoung-Mee Kim2, Keitaro Matsuo3, Javier Torres4, Linda M Liao1, Douglas R Morgan5, Angelika Michel6, Tim Waterboer6, Jovanny Zabaleta7, Ricardo L Dominguez8, Yasushi Yatabe9, Sung Kim10, Erick R Rocha-Guevara11, Jolanta Lissowska12, Michael Pawlita6, Charles S Rabkin1. 1. Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA. 2. Department of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. 3. Division of Molecular Medicine, Aichi Cancer Center Research Institute, Nagoya, Japan. 4. Unidad de Investigación en Enfermedades Infecciosas, UMAE Pediatría, CMN SXXI, Instituto Mexicano del Seguro Social, México City, México. 5. Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, School of Medicine, Vanderbilt University, Nashville, Tennessee, USA. 6. Division of Genome Modifications and Carcinogenesis, Infection and Cancer Program, German Cancer Research Center (DFKZ), Heidelberg, Germany. 7. Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA. 8. Department of Medicine, Western Regional Hospital, Santa Rosa de Copan, Honduras. 9. Department of Pathology and Molecular Diagnostics, Aichi Cancer Center Hospital, Nagoya, Japan. 10. Department of Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. 11. Hospital de Oncología, CMN SXXI, Instituto Mexicano del Seguro Social, México City, México. 12. Division of Cancer Epidemiology and Prevention, M Sklodowska-Curie Memorial Cancer Centre and Institute of Oncology, Warsaw, Poland.
Abstract
BACKGROUND: Helicobacter pylori is the primary cause of gastric cancer, but about 9% of cases harbor Epstein-Barr virus (EBV) in the tumor cells. There is limited evidence on the possible interaction or antagonism between these infectious agents in gastric carcinogenesis. METHODS: We compared H. pylori serologic profiles of EBV-positive (n = 58) and EBV-negative (n = 111) noncardia gastric cancer patients from the United States National Cancer Institute's International EBV-Gastric Cancer Consortium. EBV positivity of tumors was assessed by in situ hybridization. Serum levels of 15 antibodies to immunogenic proteins of H. pylori (Cad, CagA, Cagδ, CagM, Catalase, GroEL, HcpC, HP0231, HP0305, HpaA, HyuA, NapA, Omp, UreA, VacA) were assessed using bead-based multiplex serology. Logistic regression models were used to adjust odds ratios (OR) for country, age, sex, and year of diagnosis. RESULTS: Seropositivity to individual proteins ranged up to 90% overall. Antibodies to Catalase were borderline associated with tumor EBV positivity (adjusted OR = 3.15, p = .0024, Bonferroni corrected p = .036). Distributions of other antibodies did not vary by tumor EBV status. CONCLUSION: Similarity of host-response indicates the essential etiological role of H. pylori in EBV-positive gastric cancer.
BACKGROUND:Helicobacter pylori is the primary cause of gastric cancer, but about 9% of cases harbor Epstein-Barr virus (EBV) in the tumor cells. There is limited evidence on the possible interaction or antagonism between these infectious agents in gastric carcinogenesis. METHODS: We compared H. pylori serologic profiles of EBV-positive (n = 58) and EBV-negative (n = 111) noncardia gastric cancerpatients from the United States National Cancer Institute's International EBV-Gastric Cancer Consortium. EBV positivity of tumors was assessed by in situ hybridization. Serum levels of 15 antibodies to immunogenic proteins of H. pylori (Cad, CagA, Cagδ, CagM, Catalase, GroEL, HcpC, HP0231, HP0305, HpaA, HyuA, NapA, Omp, UreA, VacA) were assessed using bead-based multiplex serology. Logistic regression models were used to adjust odds ratios (OR) for country, age, sex, and year of diagnosis. RESULTS: Seropositivity to individual proteins ranged up to 90% overall. Antibodies to Catalase were borderline associated with tumorEBV positivity (adjusted OR = 3.15, p = .0024, Bonferroni corrected p = .036). Distributions of other antibodies did not vary by tumorEBV status. CONCLUSION: Similarity of host-response indicates the essential etiological role of H. pylori in EBV-positive gastric cancer.
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