Effects of hepatitis B virus, alcohol drinking, cigarette smoking and familial tendency on hepatocellular carcinoma

Chen, Chien‐Jen ‐J; Liang, Kung‐Yee; Chang, Ah-Seng; Chang, Yo‐Chi ‐C; Lu, Sheng–Nan; Liaw, Yun–Fan; Chang, Wen‐Yu; Sheen, Maw-Chang; Lin, Tsung‐Hsien

doi:10.1002/hep.1840130303

Cited by 207 publications

(106 citation statements)

References 21 publications

(2 reference statements)

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“…This result is consistent with those reported previously in China,14 Hong Kong,23 and Taiwan 24. Cigarette smoking and chronic hepatitis B virus carrier status were also reported to act synergistically in the development of hepatocellular carcinoma 25.…”

Section: Discussionsupporting

confidence: 92%

Mortality attributable to cigarette smoking in Taiwan: a 12-year follow-up study

Liaw

Chen

1998

Tobacco Control

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Background-Assessment of the impact of cigarette smoking on mortality helps to indicate the importance of tobacco control in a given country. Objectives-To examine the relative risk of dying from various diseases for cigarette smoking and to estimate annual mortality attributable to cigarette smoking in Taiwan. Design-Prospective cohort study. Subjects and setting-A cohort of 14 397 male and female residents aged 40 years or older recruited from 12 townships and precincts in Taiwan from 1982 to 1986. Information on cigarette smoking was collected from each subject at local health centres through a standardised personal interview based on a structured questionnaire. They were followed up regularly to determine their vital status until 1994. Main outcome measures-Cox's proportional hazards regression models were used to derive relative risks of causespecific mortality for current cigarette smokers compared with never-smokers, and to examine dose-response relationships between mortality from various causes and several measures of cigarette smoking (daily consumption, duration, age of initiation, and cumulative smoking in pack-years). Results-A total of 2552 persons died during the study period. Among men, cigarette smoking was significantly associated with an increased risk of dying from all causes combined (relative risk (RR) = 1.3); cancer of all sites combined (RR = 1.5); cancers of the stomach (RR = 1.9), liver (RR = 2.2), and lung (RR = 3.7); ischaemic heart disease (RR = 1.8); other heart diseases (RR = 1.4); and chronic obstructive pulmonary disease (RR = 1.9). Among women, cigarette smoking was significantly associated with an increased risk of dying from all causes combined (RR = 1.8), cancer of the lung (RR = 3.6), and peptic ulcer (RR = 17.8). The estimated number of deaths attributable to cigarette smoking in Taiwan in 1994 was 8161 (13.9% of total deaths) for men and 1216 (3.3% of total deaths) for women. In the same year cigarette smoking caused 21.3% and 2.9% of cancer deaths in men and women, respectively, in Taiwan. Conclusions-Cigarette smoking has a striking impact on overall mortality and deaths from various causes in the Taiwanese population. Tobacco control should be established as the top priority in public health programmes in Taiwan.

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Section: Discussionsupporting

confidence: 92%

Mortality attributable to cigarette smoking in Taiwan: a 12-year follow-up study

Liaw

Chen

1998

Tobacco Control

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“…The main risk factors for liver cancer are hepatitis B infection, hepatitis C infection, and chronic hepatitis and cirrhosis due to alcohol and other causes. 51-56 In 2013, of the 818 000 deaths in men and women, 300 000 (37%) were estimated to be due to hepatitis B infection, 343 000 (42%) due to hepatitis C infection, 92 000 (11%) due to alcohol abuse, and 83 000 (10%) due to other causes. 1 Hepatitis B vaccination has proven cost-effective in preventing liver cancer due to hepatitis B, and treatment for hepatitis C, although expensive, has recently shown success.…”

Section: Discussionmentioning

confidence: 99%

The Global Burden of Cancer 2013

et al. 2015

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IMPORTANCE Cancer is among the leading causes of death worldwide. Current estimates of cancer burden in individual countries and regions are necessary to inform local cancer control strategies. OBJECTIVE To estimate mortality, incidence, years lived with disability (YLDs), years of life lost (YLLs), and disability-adjusted life-years (DALYs) for 28 cancers in 188 countries by sex from 1990 to 2013. EVIDENCE REVIEW The general methodology of the Global Burden of Disease (GBD) 2013 study was used. Cancer registries were the source for cancer incidence data as well as mortality incidence (MI) ratios. Sources for cause of death data include vital registration system data, verbal autopsy studies, and other sources. The MI ratios were used to transform incidence data to mortality estimates and cause of death estimates to incidence estimates. Cancer prevalence was estimated using MI ratios as surrogates for survival data; YLDs were calculated by multiplying prevalence estimates with disability weights, which were derived from population-based surveys; YLLs were computed by multiplying the number of estimated cancer deaths at each age with a reference life expectancy; and DALYs were calculated as the sum of YLDs and YLLs. FINDINGS In 2013 there were 14.9 million incident cancer cases, 8.2 million deaths, and 196.3 million DALYs. Prostate cancer was the leading cause for cancer incidence (1.4 million) for men and breast cancer for women (1.8 million). Tracheal, bronchus, and lung (TBL) cancer was the leading cause for cancer death in men and women, with 1.6 million deaths. For men, TBL cancer was the leading cause of DALYs (24.9 million). For women, breast cancer was the leading cause of DALYs (13.1 million). Age-standardized incidence rates (ASIRs) per 100 000 and age-standardized death rates (ASDRs) per 100 000 for both sexes in 2013 were higher in developing vs developed countries for stomach cancer (ASIR, 17 vs 14; ASDR, 15 vs 11), liver cancer (ASIR, 15 vs 7; ASDR, 16 vs 7), esophageal cancer (ASIR, 9 vs 4; ASDR, 9 vs 4), cervical cancer (ASIR, 8 vs 5; ASDR, 4 vs 2), lip and oral cavity cancer (ASIR, 7 vs 6; ASDR, 2 vs 2), and nasopharyngeal cancer (ASIR, 1.5 vs 0.4; ASDR, 1.2 vs 0.3). Between 1990 and 2013, ASIRs for all cancers combined (except nonmelanoma skin cancer and Kaposi sarcoma) increased by more than 10% in 113 countries and decreased by more than 10% in 12 of 188 countries. CONCLUSIONS AND RELEVANCE Cancer poses a major threat to public health worldwide, and incidence rates have increased in most countries since 1990. The trend is a particular threat to developing nations with health systems that are ill-equipped to deal with complex and expensive cancer treatments. The annual update on the Global Burden of Cancer will provide all stakeholders with timely estimates to guide policy efforts in cancer prevention, screening, treatment, and palliation.

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“…The authors also reported increased risk (2-fold) in patients with HCV/HBV infections or diabetes mellitus combined with chronic alcohol consumption. Additionally, the synergistic effect between HCV/HBV infection and chronic alcohol abuse has also been reported in other countries where hepatitis infections are more prevalent (4;5). …”

Section: Introductionmentioning

confidence: 60%

Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway

Mercer

Hennings

Sharma

et al. 2014

Cancer Prevention Research

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Although alcohol effects within the liver have been extensively studied, the complex mechanisms by which alcohol causes liver cancer are not well understood. It has been suggested that ethanol (EtOH) metabolism promotes tumor growth by increasing hepatocyte proliferation. In this study, we developed a mouse model of tumor promotion by chronic EtOH consumption in which EtOH feeding began 46 days post-injection of the chemical carcinogen diethylnitrosamine (DEN) and continued for 16 weeks. With a final EtOH concentration of 28% of total calories, we observed a significant increase in the total number of preneoplastic foci and liver tumors per mouse in the EtOH+DEN group compared to corresponding pair-fed (PF)+DEN and chow+DEN control groups. We also observed a 4-fold increase in hepatocyte proliferation (p<0.05) and increased cytoplasmic staining of active-β-catenin in non-tumor liver sections from EtOH+DEN mice compared to PF+DEN controls. In a rat model of alcohol-induced liver disease, we found increased hepatocyte proliferation (p<0.05); depletion of retinol and retinoic acid stores (p<0.05); increased expression of cytosolic and nuclear expression of β-catenin (p<0.05) and phosphorylated-glycogen synthase kinase 3 β (p-GSK3β, p<0.05; significant up-regulation in Wnt7a mRNA expression; and increased expression of several β-catenin targets, including, glutamine synthetase (GS), cyclin D1, Wnt1 inducible signaling pathway protein (WISP1), and matrix metalloproteinase-7 (MMP7), p<0.05. These data suggest that chronic EtOH consumption activates the Wnt/β-catenin signaling pathways to increase hepatocyte proliferation, thus promoting tumorigenesis following an initiating insult to the liver.

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Effects of hepatitis B virus, alcohol drinking, cigarette smoking and familial tendency on hepatocellular carcinoma

Cited by 207 publications

References 21 publications

Mortality attributable to cigarette smoking in Taiwan: a 12-year follow-up study

Mortality attributable to cigarette smoking in Taiwan: a 12-year follow-up study

The Global Burden of Cancer 2013

Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway

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