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Alfatoxin B1-Dna Adducts and Hepatitis B Virus Antigens in Hepatocellular Carcinoma and Non-Tumorous Liver Tissue Publisher Pubmed



Zhang YJ1, 2 ; Chen CJ1, 2 ; Lee CS1, 2, 3 ; Haghighi B1, 2, 4 ; Yang GY1, 2 ; Wang LW1, 2 ; Feitelson M1, 2, 5 ; Santella R1, 2
Authors
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Authors Affiliations
  1. 1. Comprehensive Cancer Center, Division of Environmental Science, United States
  2. 2. School of Public Health, Columbia University, New York, NY 10032, United States
  3. 3. Department of Surgery, National Taiwan University, College of Medicine, Taipei 10018, Taiwan
  4. 4. Fox Chase Cancer Center, Philadelphia, PA 19111, United States
  5. 5. Department of Biochemistry, Isfahan University of Medical Sciences, Isfahan, Iran

Source: Carcinogenesis Published:1991


Abstract

Studies were carried out to test the hypothesis that exposure to aflation B1 (AFB1) is comman among individuals with hepatocellular carcinoma (HCC) who are also chronically infected with hapititis B virus (HBV). Experiments were also carried out to determine whether there is a close association between the presence of AFB1-DNA adducts and the expression of one or more HBV antigens in the tumor or non-tumor regions of the liver. Twently-seven paired tumor and non-tumor liver tissues of HCC patients from Taiwan were analyzed. Monoclonal antibody 6A10, generated against the imidazole ring-opened persistent form of the major N-7 guanine adduct of AFB1, was used for adduct detection by both indirect immunofluorescence and competitive enzymelinked immunosorbent assay. An avidin-biotin complex staining method was used for the detection of HBsAg and HBxAg in Liver sections. A total of 8 (30%) HCC samples and 7 (26%) adjacent non-tumor liver tissue samples from Taiwan were positive for AFB1-DNA adducts. For HBsAg, 10 (37%) HCC samples and 22 (81%) adjacent non-tumorous liver samples were positive while 9 (33%) HCC samples and 11 (41%) adjacent non-tumor liver samples were HBxAgpositive. No association with AFB1-DNA adducts was observed for HBsAg and HBxAg. These results suggest that both AFB, exposure and carrier status of HBsAg/HBxAg may be involved in the induction of HCC in Taiwan. © 1991 Oxford University Press.