학술논문
Helicobacter pylori Seropositivity, ABO Blood Type, and Pancreatic Cancer Risk From 5 Prospective Cohorts.
Document Type
Academic Journal
Author
Lee AA; Division of Gastroenterology, Hepatology, and Endoscopy, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.; Wang QL; Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA.; Kim J; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.; Babic A; Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA.; Zhang X; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.; Perez K; Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA.; Ng K; Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA.; Nowak J; Program in Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.; Rifai N; Departments of Pathology and Laboratory Medicine, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts, USA.; Sesso HD; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.; Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.; Division of Aging, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.; Buring JE; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.; Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.; Anderson GL; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.; Wactawski-Wende J; Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University of Buffalo, Buffalo, New York, USA.; Wallace R; Departments of Epidemiology and Medicine, University of Iowa, Iowa City, Iowa, USA.; Manson JE; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.; Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.; Giovannucci EL; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.; Stampfer MJ; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.; Kraft P; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.; Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.; Fuchs CS; Hematology and Oncology Product Development, Genentech & Roche, South San Francisco, California, USA.; Yale Cancer Center and Smillow Cancer Hospital, Yale School of Medicine, New Haven, Connecticut, USA.; Yuan C; Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA.; Wolpin BM; Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA.
Source
Publisher: Wolters Kluwer Health Country of Publication: United States NLM ID: 101532142 Publication Model: Electronic Cited Medium: Internet ISSN: 2155-384X (Electronic) Linking ISSN: 2155384X NLM ISO Abbreviation: Clin Transl Gastroenterol Subsets: MEDLINE
Subject
Language
English
Abstract
Background: Helicobacter pylori infection may be a risk factor for pancreatic cancer, particularly infection by strains without the cytotoxin-associated gene A (CagA) virulence factor. Non-O blood type is a known risk factor for pancreatic cancer, and H. pylori gastric colonization occurs largely from bacterial adhesins binding to blood group antigens on gastric mucosa.
Methods: We included 485 pancreatic cancer cases and 1,122 matched controls from 5 U.S. prospective cohorts. Prediagnostic plasma samples were assessed for H. pylori and CagA antibody titers. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for pancreatic cancer. ABO blood type was assessed using genetic polymorphisms at the ABO gene locus or self-report.
Results: Compared with H. pylori -seronegative participants, those who were seropositive did not demonstrate an increased risk of pancreatic cancer (OR 0.83, 95% CI 0.65-1.06). This lack of association was similar among CagA-seropositive (OR 0.75, 95% CI 0.53-1.04) and -seronegative (OR 0.89, 95% CI 0.65-1.20) participants. The association was also similar when stratified by time between blood collection and cancer diagnosis ( P -interaction = 0.80). Consistent with previous studies, non-O blood type was associated with increased pancreatic cancer risk, but this increase in risk was similar regardless of H. pylori seropositivity ( P -interaction = 0.51).
Discussion: In this nested case-control study, history of H. pylori infection as determined by H. pylori antibody serology was not associated with pancreatic cancer risk, regardless of CagA virulence factor status. The elevated risk associated with non-O blood type was consistent in those with or without H. pylori seropositivity.
(Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.)
Methods: We included 485 pancreatic cancer cases and 1,122 matched controls from 5 U.S. prospective cohorts. Prediagnostic plasma samples were assessed for H. pylori and CagA antibody titers. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for pancreatic cancer. ABO blood type was assessed using genetic polymorphisms at the ABO gene locus or self-report.
Results: Compared with H. pylori -seronegative participants, those who were seropositive did not demonstrate an increased risk of pancreatic cancer (OR 0.83, 95% CI 0.65-1.06). This lack of association was similar among CagA-seropositive (OR 0.75, 95% CI 0.53-1.04) and -seronegative (OR 0.89, 95% CI 0.65-1.20) participants. The association was also similar when stratified by time between blood collection and cancer diagnosis ( P -interaction = 0.80). Consistent with previous studies, non-O blood type was associated with increased pancreatic cancer risk, but this increase in risk was similar regardless of H. pylori seropositivity ( P -interaction = 0.51).
Discussion: In this nested case-control study, history of H. pylori infection as determined by H. pylori antibody serology was not associated with pancreatic cancer risk, regardless of CagA virulence factor status. The elevated risk associated with non-O blood type was consistent in those with or without H. pylori seropositivity.
(Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.)