Hepatitis B virus (HBV) and hepatitis C virus (HCV) are the major causes of chronic hepatitis infection (CHI). This longitudinal cohort study investigated the association of CHI with hepatic and extrahepatic cancer development in Taiwan. Patients with HBV infection and HCV infection were identified from the Taiwan National Health Insurance Research Database. A Cox proportional hazard model was used to calculate hazard ratios (HRs) and 95 % confidence intervals (CIs) for determining the association between CHI and cancer development. The patients with HBV infection exhibited an increased risk of colorectal cancer (HR: 1.36, 95 % CI: 1.09–1.70), liver cancer (HR: 21.47, 95 % CI: 18.0–25.6), gallbladder and extrahepatic bile duct cancer (HR: 2.05, 95 % CI: 1.07–3.91), pancreatic cancer (HR: 2.61, 95 % CI: 1.47–4.61), kidney cancer (HR: 1.72, 95 % CI: 1.10–2.68), ovarian cancer (HR: 2.31, 95 % CI: 1.21–4.39), and non-Hodgkin’s lymphoma (HR: 2.10, 95 % CI: 1.25–3.52). The patients with HCV infection exhibited an increased risk of liver cancer (HR: 25.10, 95 % CI: 20.9–30.2), gallbladder and extrahepatic bile duct cancer (HR: 2.60, 95 % CI: 1.42–4.73), ovarian cancer (HR: 5.15, 95 % CI: 1.98–13.4), and non-Hodgkin’s lymphoma (HR: 2.30, 95 % CI: 1.34–3.96). The present population-based study revealed that in addition to its association with primary liver cancer, CHI is associated with an increased risk of extrahepatic cancer.

We investigate whether cigarette smoking is associated with survival in patients with colorectal cancer (CRC) through a nationwide population-based cohort study in Taiwan. The Taiwan Cancer Registry and National Health Insurance Research Database were used to identify data from patients with CRC from 2011 to 2017. Tobacco use was evaluated based on the smoking status, intensity, and duration before cancer diagnosis. A total of 18,816 patients was included. A Kaplan–Meier survival analysis indicated smoking to be significantly associated with the CRC mortality risk (log-rank p = 0.0001). A multivariable Cox model indicated that smoking patients had a 1.11-fold higher mortality risk (HR = 1.11, 95% CI = 1.05–1.19) than nonsmoking patients did. This increased risk was also present in patients with CRC who smoked 11–20 cigarettes per day (HR = 1.16; 95% CI = 1.07–1.26) or smoked for >30 years (HR = 1.14; 95% CI = 1.04–1.25). Stratified analyses of sex and cancer subsites indicated that the effects of smoking were higher in male patients and in those with colon cancer. Our results indicate that cigarette smoking is significantly associated with poor survival in patients with CRC. An integrated smoking cessation campaign is warranted to prevent CRC mortality.

Background: In Taiwan, there is a high incidence of breast cancer and a high prevalence of viral hepatitis. In this case-control study, we used a population-based insurance dataset to evaluate whether breast cancer in women is associated with chronic viral hepatitis infection.Methods: From the claims data, we identified 1,958 patients with newly diagnosed breast cancer during the period 2000-2008. A randomly selected, age-matched cohort of 7,832 subjects without cancer was selected for comparison. Multivariable logistic regression models were constructed to calculate odds ratios of breast cancer associated with viral hepatitis after adjustment for age, residential area, occupation, urbanization, and income. The age-specific (<50 years and ≥50 years) risk of breast cancer was also evaluated.Results: There were no significant differences in the prevalence of hepatitis C virus (HCV) infection, hepatitis B virus (HBV), or the prevalence of combined HBC/HBV infection between breast cancer patients and control subjects (p= 0.48). Multivariable logistic regression analysis, however, revealed that age <50 years was associated with a 2-fold greater risk of developing breast cancer (OR = 2.03, 95% CI = 1.23-3.34).Conclusions: HCV infection, but not HBV infection, appears to be associated with early onset risk of breast cancer in areas endemic for HCV and HBV. This finding needs to be replicated in further studies.

The association between viral hepatitis (B and C) and oral cavity cancer has been widely debated. This nationwide, population-based cohort study assessed the subsequent risk of oral cavity cancer among patients with chronic viral hepatitis infection. Data were retrieved from insurance claims data of 1,000,000 randomly sampled individuals covered under the Taiwan National Health Insurance system. We identified a total of 21,199 adults with chronic viral hepatitis infection (12,369 with HBV alone, 5,311 with HCV alone, and 3,519 with HBV/HCV dual infections) from 2000–2005. Comparison group comprised 84,796 sex- and age-matched subjects without viral hepatitis during the same study period. Incidence and risk of subsequent oral cavity cancer were measured until 2008. The incidence of oral cavity cancers was 2.28-fold higher among patients with HCV alone than non-viral hepatitis group (6.15 versus 2.69 per 10,000 person-years). After adjusting for sociodemographic covariates, HCV alone was significantly associated with an increased risk for oral cavity cancer (hazard ratio (HR) = 1.90, 95% confidence interval (CI) = 1.20–3.02). This positive association was highest among individuals in the 40–49-year age group (HR = 2.57, 95% CI = 1.21–5.46). However, there were no significant associations between HBV alone or HBV/HCV dual infections and risk for oral cavity cancer. Our data suggest that HCV but not HBV infection is a risk factor for oral cavity cancer. In addition, subjects with HCV infection tend to be at early onset risk for oral cavity cancer. This finding needs to be replicated in further studies.

AIM: To investigate the colorectal cancer risk associated with polymorphic GSTM1, GSTT1 and GSTP1 and the effect of diet and smoking. METHODS: With consents, genotypes of the genes were determined using PCR methods for 727 cases and 736 sex and age-matched healthy controls recruited at a medical center in the Northern Taiwan. Nurses who were blind to the study hypothesis conducted interviews with study participants for the information of socio-demographic variables, diet and smoking. RESULTS: There was no significant association between GSTM1 genotypes and the disease. Men, not women, with GSTT1 null genotype were at significant risk of colorectal cancer, but limited to rectal tumor, and in men aged 60 years and less. The corresponding association with the GSTP1 with G allele compared to GSTP1 A/A genotype was at borderline significance. Compared to men with GSTT1 present and GSTP1 A/A combined, men with both GSTT1 null and GSTP1 with G allele genotypes were at significant risk (odds ratio (OR) = 1.91, 95% confidence interval (CI) = 1.21-3.02), also limited to the rectal tumor and younger men. The beneficial effects of vegetable/fruit intake on colorectal cancer were much higher for men with GSTT1 present (OR = 0.32, 95%CI = 0.20-0.50) or GSTP1 A/A genotypes (OR = 0.40, 95%CI = 0.25-0.64). These effects remained significant for women. But, the greatest protective effect from vegetable/fruit intake for women was observed in those with GSTT1 null or GSTP1 with G allele genotypes. In addition, non-smoking men benefitted significantly from combined effect of higher vegetable/fruit intake and GSTT1 present or GSTP1 A/A genotypes with OR = 0.17 and 0.21 respectively. CONCLUSION: This study suggests that the GSTT1 gene can modulate the colorectal cancer risk and vegetable/fruit-related colorectal cancer risk, particularly in men of no smoking history.