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Chen et al. Hepatoma Res 2018;4:4 I http://dx.doi.org/10.20517/2394-5079.2017.50 Page 5 of 10

Table 1. Key variables of structure questionnaires
Baseline questionnaires (1998) Updated questionnaires (2012)
Unique code Occupation
Name Family size
Gender Family income
ID code (containing birth date and gender) Temporary place
Occupation Staple food
Home address Drinking water
Employer Alcohol drinking
Phone call Tea drinking
Birth place Smoking
Education Medical history
Marital status Family history of cancer
Financial condition Family history of HCC
Staple food Diabetes history
Drinking water High blood pressure history
Tobacco consumption
Alcohol drinking
Tea drinking
Medical history
Menstrual and reproductive history (if female)
Vaccination history
Prophylactic intervention
HCC: hepatocellular carcinoma

antibody to hepatitis B surface antigen, hepatitis B e antigen, antibody to hepatitis B e antigen, and antibody to
hepatitis B core antigen, as well as urine glucose, and fasting blood glucose were also measured. In particular,
baseline HBV DNA load, a well acknowledged viral parameter, was surveyed by using cryopreserved plasma
samples between 2014 and 2015.

Other parameters based on nested case-control design
Several nested case-control studies have been carried out by using samples collected in the QBC. Exposure
biomarkers and genetic variation markers measured were determined for some of the study participants,
including aflatoxin metabolism , aflatoxin-albumin adducts , polymorphism of Glutathione S-Transferase
[10]
[11]
[14]
[13]
T1 and M1 , epoxide hydrolase , xeroderma pigmentosum group D , codon 249 mutation of p53, loss of
[12]
heterozygosity at chromosome 4q , HBV genotype and versatile HBV mutations in X gene [16-20] , S gene , C
[15]
[21]
gene [22,23] , and P gene [24-27] of HBV genome.
WHAT HAS BEEN FOUND?
HBV infection and PLC endemic in Qidong
By the end of February 2017, after a median follow-up duration of 24.83 years, a total of 201 incident PLC cases
were identified in the QBC. PLC was the most common cancer type, comprising more than 65% (201/304) of
all cancer cases. PLC incidence in the HBV exposed sub-cohort was significantly higher than that of the HBV non-
exposed sub-cohort with an incidence rate ratio (IRR) of 12.32 (95% CI: 7.16-21.21, P < 0.0001). No other statistically
significant IRR were observed on any other cancers including lung, gastric, colorectal etc. [Table 2]. These findings,
in addition to our previous publications on the QBC, define HBV infection as the most important etiologic
factor for explaining the PLC epidemic in Qidong [28-30] .

Furthermore, we have explored the association between HBeAg status, HBV DNA load and PLC risk in the
HBV exposed sub-cohort. We found that the relative risk of PLC was 13.25 (95% 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 [31,32] . Those with levels of HBV DNA more than 250
-
-
copies/mL had a 4.78-fold risk of PLC compared to those without detectable HBV DNA. The HBsAg carriers
with serum HBV DNA between 10 and 10 copies/mL had the greatest PLC risk, that is to say, greater than
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