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Journal of Clinical Oncology, Vol 26, No 28 (October 1), 2008: pp. 4557-4562 © 2008 American Society of Clinical Oncology. DOI: 10.1200/JCO.2008.17.3526 Association Between Hepatitis B Virus and Pancreatic Cancer
From the Departments of Gastrointestinal Medical Oncology, Epidemiology, and Gastroenterology, Hepatology, and Nutrition, The University of Texas M. D. Anderson Cancer Center, Houston, TX Corresponding author: James L. Abbruzzese, MD, Department of Gastrointestinal Medical Oncology, Unit 426, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030; e-mail: jabbruzz{at}mdanderson.org Purpose Hepatitis B virus (HBV) and hepatitis C virus (HCV) are considered to be hepatotropic and are a major cause of hepatocellular carcinoma. However, little is known about the role of HBV and HCV infection in other malignancies. This study aimed to determine whether HBV and HCV infections increase the risk for pancreatic cancer development. Patients and Methods At The University of Texas M. D. Anderson Cancer Center, Houston, TX, we recruited 476 patients with pathologically confirmed adenocarcinoma of the pancreas and 879 age-, sex-, and race-matched healthy controls. Blood samples were tested for the presence of HCV antibodies (anti-HCV), HBV surface antigen (HBsAg), antibodies against HBV core antigen (anti-HBc), and antibodies against HBsAg (anti-HBs). The positive samples were retested by two confirmatory tests. An unconditional multivariable logistic regression analysis was used to estimate adjusted odds ratios (AORs). Results Anti-HCV was positive in seven cases (1.5%) and nine controls (1%). Anti-HBc was positive in 36 cases (7.6%) and 28 controls (3.2%). The estimated AORs and 95% CIs were as follows: anti-HCV–positive, 0.9 (95% CI, 0.3 to 2.8), anti-HBc–positive, 2.5 (95% CI, 1.5 to 4.2), anti-HBc–positive/anti-HBs–positive, 2.3 (95% CI, 1.2 to 4.2), and anti-HBc–positive/anti-HBs–negative, 4 (95% CI, 1.4 to 11.1). Risk modification by past exposure to HBV was observed among diabetics (AOR, 7.1; 95% CI, 1.7 to 28.7). Conclusion Past exposure to HBV may be associated with pancreatic cancer development. Should such findings be confirmed by other studies, it may offer important insights into the etiology of pancreatic cancer and may suggest the need to consider prevention of HBV reactivation among patients with HBV-related pancreatic cancer during chemotherapy. Supported by National Institutes of Health (NIH) RO1 Grant No. CA098380 (D.L.), Specialized Programs of Research Excellence P20 Grant No. CA101936 (J.L.A.), National Institute of Environmental Health Sciences Grant No. ES07784, a research grant from the Lockton Research Funds (D.L.), NIH RO3 Grant No. ES11481 (M.M.H.), and Grant No. CA106458-01 (M.M.H.). Authors disclosures of potential conflicts of interest and author contributions are found at the end of this article.
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Copyright © 2008 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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