Yu-Ju Chu1, Hwai-I Yang2, Hui-Chen Wu3, Mei-Hsuan Lee4, Jessica Liu5, Li-Yu Wang6, Sheng-Nan Lu7, Chin-Lan Jen8, San-Lin You9, Regina M Santella10, Chien-Jen Chen11. 1. Institute of Microbiology and Immunology, National Yang-Ming University, No.155, Sec.2, Linong Street, Taipei, 112, Taiwan; Genomics Research Center, Academia Sinica, 128 Academia Road, Section 2, Nankang, Taipei, 115, Taiwan. Electronic address: lulululuchu@gmail.com. 2. Genomics Research Center, Academia Sinica, 128 Academia Road, Section 2, Nankang, Taipei, 115, Taiwan. Electronic address: hwaii.yang@gmail.com. 3. Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 630 West 168th St, New York, NY, 10032, USA. Electronic address: hw2057@cumc.columbia.edu. 4. Institute of Clinical Medicine, National Yang-Ming University, No.155, Sec.2, Linong Street, Taipei, 112, Taiwan. Electronic address: meihlee@ntu.edu.tw. 5. Genomics Research Center, Academia Sinica, 128 Academia Road, Section 2, Nankang, Taipei, 115, Taiwan. Electronic address: jessica.b.liu@gmail.com. 6. Department of Medicine, Mackay Medical College, No.46, Sec. 3, Zhongzheng Rd., Sanzhi Dist., New Taipei City, 252, Taiwan. Electronic address: yannbo@mmc.edu.tw. 7. Division of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, 123 Ta Pei Road, Niao Sung Dist., Kaohsiung, 833, Taiwan. Electronic address: juten@ms17.hinet.net. 8. Genomics Research Center, Academia Sinica, 128 Academia Road, Section 2, Nankang, Taipei, 115, Taiwan. Electronic address: chinlan.jen@gmail.com. 9. School of Medicine & Big Data Research Center, Fu Jen Catholic University, No.510, Zhongzheng Rd., Xinzhuang Dist., New Taipei City, 242, Taiwan. Electronic address: 087780@mail.fju.edu.tw. 10. Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 630 West 168th St, New York, NY, 10032, USA. Electronic address: rps1@columbia.edu. 11. Genomics Research Center, Academia Sinica, 128 Academia Road, Section 2, Nankang, Taipei, 115, Taiwan. Electronic address: chencj@gate.sinica.edu.tw.
Abstract
BACKGROUND: Hepatocarcinogenicity of aflatoxin B1 (AFB1) has rarely been studied in populations with hepatitis C virus (HCV) infection and those without hepatitis B virus (HBV) and HCV infection (non-B-non-C). This case-control study nested in a community-based cohort aimed to investigate the HCC risk associated with AFB1 in HCV-infected and non-B-non-C participants. METHODS: Baseline serum AFB1-albumin adduct levels were measured in 100 HCC cases and 1767 controls seronegative for anti-HCV and HBsAg (non-B-non-C), and another 103 HCC cases and 176 controls who were anti-HCV-seropositive and HBsAg-seronegative. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated using logistic regression. RESULTS: In 20 years of follow-up, the follow-up time to newly developed HCC was significantly shorter in participants with higher serum AFB1-albumin adduct levels in non-B-non-C (p = 0.0162) and HCV-infected participants (p < 0.0001). Within 8 years of follow-up, HCV infection and AFB1 exposure were independent risk factors for HCC. Elevated serum AFB1-albumin adduct levels were significantly associated with an increased risk of HCC newly developed within 8 years of follow-up in non-B-non-C participants with habitual alcohol consumption [crude OR (95% CI) for high vs. low/undetectable levels, 4.22 (1.16-15.37)] and HCV-infected participants [3.39 (1.31-8.77)], but not in non-B-non-C participants without alcohol drinking habit. AFB1 exposure remained an independent risk predictor for HCV-related HCC after adjustment for other HCC predictors (multivariate-adjusted OR [95% CI], 3.65 [1.32-10.10]). CONCLUSIONS: AFB1 exposure contributes to the development of HCC in participants with significant risk factors for cirrhosis including alcohol and HCV infection.
BACKGROUND: Hepatocarcinogenicity of aflatoxin B1 (AFB1) has rarely been studied in populations with hepatitis C virus (HCV) infection and those without hepatitis B virus (HBV) and HCV infection (non-B-non-C). This case-control study nested in a community-based cohort aimed to investigate the HCC risk associated with AFB1 in HCV-infected and non-B-non-C participants. METHODS: Baseline serum AFB1-albumin adduct levels were measured in 100 HCC cases and 1767 controls seronegative for anti-HCV and HBsAg (non-B-non-C), and another 103 HCC cases and 176 controls who were anti-HCV-seropositive and HBsAg-seronegative. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated using logistic regression. RESULTS: In 20 years of follow-up, the follow-up time to newly developed HCC was significantly shorter in participants with higher serum AFB1-albumin adduct levels in non-B-non-C (p = 0.0162) and HCV-infectedparticipants (p < 0.0001). Within 8 years of follow-up, HCV infection and AFB1 exposure were independent risk factors for HCC. Elevated serum AFB1-albumin adduct levels were significantly associated with an increased risk of HCC newly developed within 8 years of follow-up in non-B-non-C participants with habitual alcohol consumption [crude OR (95% CI) for high vs. low/undetectable levels, 4.22 (1.16-15.37)] and HCV-infectedparticipants [3.39 (1.31-8.77)], but not in non-B-non-C participants without alcohol drinking habit. AFB1 exposure remained an independent risk predictor for HCV-related HCC after adjustment for other HCC predictors (multivariate-adjusted OR [95% CI], 3.65 [1.32-10.10]). CONCLUSIONS:AFB1 exposure contributes to the development of HCC in participants with significant risk factors for cirrhosis including alcohol and HCV infection.
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