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Chen et al. Hepatoma Res 2018;4:4 Hepatoma Research
DOI: 10.20517/2394-5079.2017.50

Cohort Profile Open Access

Qidong hepatitis B virus infection cohort: a 25-year
prospective study in high risk area of primary liver

cancer

Tao-Yang Chen , Geng-Sun Qian , Chun-Sun Fan , Yan Sun , Jin-Bing Wang , Pei-Xin Lu , Xue-Feng
1
2#
1
1
1#
1,2
Xue , Yan Wu , Qi-Nan Zhang , Yan Jin , Yi-Qian Wu , Yu Gan , Jian-Quan Lu , Thomas W. Kensler , John
1
1
2
2
1
2
3
1
D. Groopman , Hong Tu 2
3
1 Department of Etiology, Qidong Liver Cancer Institute, Qidong People’s Hospital, Qidong 226200, Jiangsu, China.
2 State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University
School of Medicine, Shanghai 200032, China.
3 Environmental Health and Engineering, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA.
# Contribute equally to this work.
Correspondence to: Dr. Hong Tu, State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji
Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200032, China. E-mail: tuhong@shsci.org
How to cite this article: Chen TY, Qian GS, Fan CS, Sun Y, Wang JB, Lu PX, Xue XF, Wu Y, Zhang QN, Jin Y, Wu YQ, Gan Y, Lu
JQ, Kensler TW, Groopman JD, Tu H. Qidong hepatitis B virus infection cohort: a 25-year prospective study in high risk area of
primary liver cancer. Hepatoma Res 2018;4:4. http://dx.doi.org/10.20517/2394-5079.2017.50
Received: 30 Nov 2017 First Decision: 21 Dec 2017 Revised: 18 Jan 2018 Accepted: 19 Jan 2018 Published: 26 Jan 2018
Science Editor: Guang-Wen Cao Copy Editor: Jun-Yao Li Production Editor: Cai-Hong Wang
Abstract
Qidong hepatitis B virus (HBV) infection cohort (QBC) is a prospective community-based study designed to investigate
causative factors of primary liver cancer (PLC) in Qidong, China, where both PLC and HBV infection are highly endemic.
Residents aged 20-65 years, living in seven townships of Qidong, were surveyed using hepatitis B surface antigen (HBsAg)
serum test and invited to participate in QBC from June 1991 to December 1991. A total of 852 and 786 participants were
enrolled in HBsAg-positive and HBsAg-negative sub-cohorts in May 1992, respectively. All participants were actively
followed up in person, received HBsAg, alanine aminotransferase, alpha-fetoprotein tests and upper abdominal ultrasonic
examination, and donated blood and urine samples once or twice a year. The total response rate was 99.6%, and the number
of incident PLC was 201 till the end of February 2017. The ratio of incidence rates was 12.32 [95% confidence interval (CI):
7.16-21.21, P < 0.0001] in HBsAg-positive arm compared with HBsAg-negative arm. The relative risk of PLC was 13.25 (95%
+
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CI: 6.67-26.33, P < 0.0001) and 28.05 (95% CI: 13.87-56.73, P < 0.0001) in the HBsAg /HBeAg group and the HBsAg /
HBeAg group, respectively, as compared to the HBsAg /HBeAg group. A series of novel PLC-related mutations including
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A2159G, A2189C and G2203W at the C gene, A799G, A987G and T1055A at the P gene of HBV genome were identified
by using samples from the cohort. The mutation in HBV basal core promoter region of HBV genome has an accumulative
effect on the occurrence of PLC. In addition, the tripartite relationship of aflatoxin exposure, P53 mutation and PLC was also
© The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
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