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1
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Yue T, Xu M, Cai T, Zhu H, Pourkarim MR, De Clercq E, Li G. Gender disparity and temporal trend of liver cancer in China from 1990 to 2019 and predictions in a 25-year period. Front Public Health 2022; 10:956712. [PMID: 36091549 PMCID: PMC9459158 DOI: 10.3389/fpubh.2022.956712] [Citation(s) in RCA: 9] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/30/2022] [Accepted: 07/25/2022] [Indexed: 01/24/2023] Open
Abstract
Objective This study aims to reveal epidemiological features and trends of liver cancer (LC) in China. Methods We retrieved data from the Global Burden of Disease database 2019. Joinpoint regression was used to examine the temporal trend of LC. Future trends of LC were estimated using the Nordpred. Results The incidence, mortality, and disability-standardized life year (DALY) rate of LC declined in China from 1990 to 2019. Among >210,000 LC cases in 2019, the LC incidences were nearly 3.15 times higher in males than in females. LC cases and LC-associated deaths were mostly found among patients aged 65 to 69 years. The proportion of LC attributable to hepatitis B decreased over time, whereas the proportions of LC attributable to hepatitis C, alcohol use, and non-alcoholic steatohepatitis increased modestly from 1990 to 2019. The majority of LC-associated deaths could be traced to four risk factors: smoking (20%), drug use (13.6%), alcohol use (11.7%), and high body mass index (10.1%). Based on the Nordpred prediction, there will be a steady decline in the incidence (39.0%) and mortality (38.3%) of liver cancer over a 25-year period from 2020 to 2044. Conclusion The disease burden of liver cancer in China has declined over the past 30 years. However, it remains important to control liver cancer among high-risk populations, especially elderly males with obesity, alcohol use, tobacco use, and/or drug abuse.
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Affiliation(s)
- Tingting Yue
- Hunan Provincial Key Laboratory of Clinical Epidemiology, Xiangya School of Public Health, Central South University, Changsha, China
| | - Ming Xu
- Hunan Provincial Key Laboratory of Clinical Epidemiology, Xiangya School of Public Health, Central South University, Changsha, China
| | - Ting Cai
- Hunan Provincial Key Laboratory of Clinical Epidemiology, Xiangya School of Public Health, Central South University, Changsha, China
| | - Haizhen Zhu
- Institute of Pathogen Biology and Immunology of College of Biology, Hunan Provincial Key Laboratory of Medical Virology, State Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha, China
| | - Mahmoud Reza Pourkarim
- Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, KU Leuven, Leuven, Belgium,Health Policy Research Center, Institute of Health, Shiraz University of Medical Sciences, Shiraz, Iran,Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran
| | - Erik De Clercq
- Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, KU Leuven, Leuven, Belgium
| | - Guangdi Li
- Hunan Provincial Key Laboratory of Clinical Epidemiology, Xiangya School of Public Health, Central South University, Changsha, China,Hunan Children's Hospital, Changsha, China,*Correspondence: Guangdi Li
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Premkumar M, Anand AC. Tobacco, Cigarettes, and the Liver: The Smoking Gun. J Clin Exp Hepatol 2021; 11:700-712. [PMID: 34866849 PMCID: PMC8617531 DOI: 10.1016/j.jceh.2021.07.016] [Citation(s) in RCA: 14] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/13/2021] [Accepted: 07/29/2021] [Indexed: 12/12/2022] Open
Abstract
The association between alcohol and liver disease, including alcoholic hepatitis, cirrhosis, acute-on-chronic liver failure, and hepatocellular carcinoma, has been well described, but the same cannot be said for the association between smoking, water pipe or tobacco chewing. A review of cumulative evidence suggests that smoking is independently a risk factor for liver fibrosis and contributes to carcinogenesis in HCC. Smoking-related fibrosis has been reported in patients with nonalcoholic fatty liver disease, primary biliary cholangitis, alcoholic liver disease and chronic viral hepatitis. Heavy smoking leads to systemic inflammation, oxidative stress, insulin resistance, and results in tissue hypoxia, as well as free radical damage. Other than damaging the liver, patients also suffer from the systemic effects of the 4000 chemicals associated with tobacco, which include nitrosamines, aromatic hydrocarbons, nicotine, nornicotine, and other alkaloids. These include respiratory ailments, cancer of the lungs, oral cavity, esophagus, pancreas and colon, atherosclerotic vascular disease, and stroke.
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Key Words
- ALP, alkaline phosphatase
- BMI, body mass index
- CLD, chronic liver disease
- GGT, gamma-glutamyl transpeptidase
- HBV, hepatitis B virus
- HCC, hepatocellular carcinoma
- HCV, hepatitis C virus
- HR, hazard ratio
- MetS, metabolic syndrome
- NAFLD, nonalcoholic fatty liver disease
- NASH, nonalcoholic steatohepatitis
- OR, odds ratio
- RR, relative risk
- ST, smokeless tobacco
- WHO, World Health Organization
- cirrhosis
- hepatocellular carcinoma
- inflammation
- smoking
- tobacco
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Affiliation(s)
- Madhumita Premkumar
- Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India
| | - Anil C Anand
- Department of Hepatology, Kalinga Institute of Medical Sciences, Bhubaneshwar, Odisha, India
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3
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Shen Y, Risch H, Lu L, Ma X, Irwin ML, Lim JK, Taddei T, Pawlish K, Stroup A, Brown R, Wang Z, Jia W, Wong L, Mayne ST, Yu H. Risk factors for hepatocellular carcinoma (HCC) in the northeast of the United States: results of a case-control study. Cancer Causes Control 2020; 31:321-332. [PMID: 32060838 PMCID: PMC7136513 DOI: 10.1007/s10552-020-01277-1] [Citation(s) in RCA: 23] [Impact Index Per Article: 4.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/19/2019] [Accepted: 02/10/2020] [Indexed: 12/13/2022]
Abstract
PURPOSE HCC incidence has been continuously rising in the US for the past 30 years. To understand the increase in HCC risk, we conducted a case-control study in Connecticut, New Jersey and part of New York City. METHODS Through rapid case ascertainment and random digit dialing, we recruited 673 incident HCC patients and 1,166 controls. Information on demographic and anthropometric characteristics, lifestyle factors, medical and family cancer histories, were ascertained through telephone interviews using a structured questionnaire. Saliva specimens were collected for testing hepatitis C virus (HCV) antibodies. Unconditional logistic regression models were utilized to calculate odds ratio (OR) and 95% confidence interval (CI) to determine HCC associations with risk factors. RESULTS The study confirmed that HCV infection and obesity were important risk factors for HCC, ORs 110 (95% CI 59.2-204) and 2.13 (95% CI 1.52-3.00), respectively. High BMI and HCV infection had synergy in association with elevated HCC risk. Patients both obese and infected with HCV had HCC detected on average nearly 10 years earlier than those with neither factor. Diabetes, cigarette smoking and heavy alcohol intake were all associated with increased risk of HCC, whereas aspirin and other NSAID use were associated with reduced risk. HCC cases tended to attain less education, with lower household incomes, unmarried, and to have had more sexual partners than the controls. CONCLUSIONS Individuals at risk of HCC in the US comprise a unique population with low socioeconomic status and unhealthy lifestyle choices. Given the multifactorial nature, a comprehensive approach is needed in HCC prevention.
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Affiliation(s)
- Yi Shen
- Epidemiology Program, University of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA
| | - Harvey Risch
- Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT, USA
| | - Lingeng Lu
- Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT, USA
| | - Xiaomei Ma
- Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT, USA
| | - Melinda L Irwin
- Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT, USA
| | - Joseph K Lim
- Department of Internal Medicine, Yale School of Medicine, New Haven, CT, USA
| | - Tamar Taddei
- Department of Internal Medicine, Yale School of Medicine, New Haven, CT, USA
| | - Karen Pawlish
- New Jersey State Cancer Registry, New Jersey Department of Health, Trenton, NJ, USA
| | - Antoinette Stroup
- Rutgers Cancer Institute, Rutgers School of Public Health, New Brunswick, NJ, USA
| | - Robert Brown
- Department of Medicine, Weill Cornell Medical College, College of Physicians & Surgeons, Columbia University, New York, NY, USA
| | - Zhanwei Wang
- Epidemiology Program, University of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA
| | - Wei Jia
- Epidemiology Program, University of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA
| | - Linda Wong
- Epidemiology Program, University of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA
| | - Susan T Mayne
- Center for Food Safety and Applied Nutrition, US Food and Drug Administration, College Park, MD, USA
| | - Herbert Yu
- Epidemiology Program, University of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA.
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Kolly P, Knöpfli M, Dufour JF. Effect of smoking on survival of patients with hepatocellular carcinoma. Liver Int 2017; 37:1682-1687. [PMID: 28467657 DOI: 10.1111/liv.13466] [Citation(s) in RCA: 24] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/10/2016] [Accepted: 04/22/2017] [Indexed: 02/13/2023]
Abstract
BACKGROUND & AIMS Lifestyle factors such as smoking, obesity and physical activity have gained interest in the field of hepatocellular carcinoma. These factors play a significant role in the development of hepatocellular carcinoma. Several studies revealed the impact of tobacco consumption on the development of hepatocellular carcinoma and its synergistic effects with viral etiologies (hepatitis B and C). The effects of smoking on survival in patients with a diagnosed hepatocellular carcinoma have not yet been investigated in a Western cohort where hepatitis C infection is a major risk factor. METHODS Using data from a prospective cohort of patients with hepatocellular carcinoma who were followed at the University Hospital of Bern, Switzerland, survival was compared by Kaplan-Meier analysis in smokers and nonsmokers, and multivariate Cox regression was applied to control for confounding variables. RESULTS Of 238 eligible hepatocellular carcinoma patients, 64 were smokers at the time of inclusion and 174 were nonsmokers. Smokers had a significant worse overall survival than nonsmokers (hazard ratio 1.77, 95% confidence interval: 1.22-2.58, P=.003). Analysis of patients according to their underlying liver disease, revealed that smoking, and not nonsmoking, affected survival of hepatitis B virus and C virus-infected patients only. In this subgroup, smoking was an independent predictor for survival (hazard ratio 2.99, 95% confidence interval: 1.7-5.23, P<.001) and remained independently predictive when adjusted for confounding variables. CONCLUSIONS This study shows that smoking is an independent predictor of survival in hepatitis B virus/hepatitis C virus-infected patients with hepatocellular carcinoma.
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Affiliation(s)
- Philippe Kolly
- Hepatology, Department of Clinical Research, University of Bern, Bern, Switzerland.,University Clinic for Visceral Surgery and Medicine, Inselspital, Bern, Switzerland
| | - Marina Knöpfli
- University Clinic for Visceral Surgery and Medicine, Inselspital, Bern, Switzerland
| | - Jean-François Dufour
- Hepatology, Department of Clinical Research, University of Bern, Bern, Switzerland.,University Clinic for Visceral Surgery and Medicine, Inselspital, Bern, Switzerland
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Abdel-Rahman O, Helbling D, Schöb O, Eltobgy M, Mohamed H, Schmidt J, Giryes A, Mehrabi A, Iype S, John H, Tekbas A, Zidan A, Oweira H. Cigarette smoking as a risk factor for the development of and mortality from hepatocellular carcinoma: An updated systematic review of 81 epidemiological studies. J Evid Based Med 2017; 10:245-254. [PMID: 28891275 DOI: 10.1111/jebm.12270] [Citation(s) in RCA: 81] [Impact Index Per Article: 10.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/05/2017] [Accepted: 08/13/2017] [Indexed: 01/11/2023]
Abstract
BACKGROUND AND AIMS Hepatocellular carcinoma (HCC) is the sixth most common cancer worldwide and its incidence has increased during the past decade. While hepatitis B and C virus infections and alcohol were established risk factors, the impact of smoking on the incidence and mortality of HCC was needed to be confirmed. METHODS We reviewed cohort and case-control studies evaluating the association between cigarette smoking and incidence and mortality of HCC from MEDLINE and Google Scholar. We also checked reference lists of original studies and review articles manually for cross-references up to February 2016. We extracted the relevant information on participant characteristics and study outcomes, as well as information on the methodology of the studies. We also assessed the quality of the included trials using critical appraisal skills program checklists. Meta-analysis was performed by using RevMan 5.3 software. RESULTS A total of 81 studies were included in the systematic review. Pooled OR for HCC development with current smokers was 1.55 (95% CI: 1.46 to 1.65; P < 0.00001). Pooled OR for HCC development with former smokers was 1.39 (95% CI: 1.26 to 1.52; P < 0.00001) and pooled OR for HCC development with heavy smokers was 1.90 (95% CI: 1.68 to 2.14; P < 0.00001). Pooled OR for the mortality of current smokers with HCC was 1.29 (95% CI: 1.23 to 1.34; P < 0.00001); and for former smokers with HCC, it was 1.20 (95% CI: 1.00 to 1.42; P = 0.04). CONCLUSIONS Cigarette smoking increases the incidence and mortality of HCC. Further studies are needed to evaluate possible impact of quitting smoking on decreasing this risk.
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Affiliation(s)
- Omar Abdel-Rahman
- Clinical Oncology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt
- Department of Medical Oncology, Gastrointestinal Tumor Center Zurich, Zurich, Switzerland
| | - Daniel Helbling
- Department of Medical Oncology, Gastrointestinal Tumor Center Zurich, Zurich, Switzerland
| | - Othmar Schöb
- Surgical Center Zurich, Hirslanden Hospital Zurich, Zurich, Switzerland
| | - Mostafa Eltobgy
- Clinical Oncology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt
| | - Hadeer Mohamed
- Clinical Oncology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt
| | - Jan Schmidt
- Surgical Center Zurich, Hirslanden Hospital Zurich, Zurich, Switzerland
| | - Anwar Giryes
- Department of Medical Oncology, Gastrointestinal Tumor Center Zurich, Zurich, Switzerland
| | - Arianeb Mehrabi
- Department of General, Visceral and Transplant Surgery, University of Heidelberg, Heidelberg, Germany
| | - Satheesh Iype
- Department of Surgery, Cambridge University Hospital, Cambridge, United Kingdom
| | - Hannah John
- Department of Surgery, Cambridge University Hospital, Cambridge, United Kingdom
| | - Aysun Tekbas
- Department of General, Visceral and Transplant Surgery, University of Heidelberg, Heidelberg, Germany
| | - Ahmad Zidan
- Department of HPB and Liver Transplantation, Rajhy Liver Hospital, Assiut University, Assiut, Egypt
| | - Hani Oweira
- Surgical Center Zurich, Hirslanden Hospital Zurich, Zurich, Switzerland
- Department of General, Visceral and Transplant Surgery, University of Heidelberg, Heidelberg, Germany
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6
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Liang Z, Wu R, Xie W, Xie C, Wu J, Geng S, Li X, Zhu M, Zhu W, Zhu J, Huang C, Ma X, Xu W, Zhong C, Han H. Effects of Curcumin on Tobacco Smoke-induced Hepatic MAPK Pathway Activation and Epithelial-Mesenchymal Transition In Vivo. Phytother Res 2017; 31:1230-1239. [PMID: 28585748 DOI: 10.1002/ptr.5844] [Citation(s) in RCA: 25] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/29/2016] [Revised: 05/09/2017] [Accepted: 05/10/2017] [Indexed: 12/11/2022]
Abstract
Tobacco smoke is a major risk factor for hepatic cancer. Epithelial-mesenchymal transition (EMT) induced by tobacco smoke is crucially involved in the initiation and development of cancer. Mitogen-activated protein kinase (MAPK) pathways play important roles in tobacco smoke-associated carcinogenesis including EMT process. The chemopreventive effect of curcumin supplementation against cancers has been reported. In this study, we investigated the effects of tobacco smoke on MAPK pathway activation and EMT alterations, and then the preventive effect of curcumin was examined in the liver of BALB/c mice. Our results indicated that exposure of mice to tobacco smoke for 12 weeks led to activation of ERK1/2, JNK, p38 and ERK5 pathways as well as activator protein-1 (AP-1) proteins in liver tissue. Exposure of mice to tobacco smoke reduced the hepatic mRNA and protein expression of the epithelial markers, while the hepatic mRNA and protein levels of the mesenchymal markers were increased. Treatment of curcumin effectively attenuated tobacco smoke-induced activation of ERK1/2 and JNK MAPK pathways, AP-1 proteins and EMT alterations in the mice liver. Our data suggested the protective effect of curcumin in tobacco smoke-triggered MAPK pathway activation and EMT in the liver of BALB/c mice, thus providing new insights into the chemoprevention of tobacco smoke-associated hepatic cancer. Copyright © 2017 John Wiley & Sons, Ltd.
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Affiliation(s)
- Zhaofeng Liang
- Jiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, 212013, China
- Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, 211166, China
| | - Rui Wu
- Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, 211166, China
- Chongchuanqu Market Supervision Administration, Nantong, 226006, China
| | - Wei Xie
- Institute of Food Safety and Assessment, Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, 211166, China
| | - Chunfeng Xie
- Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, 211166, China
| | - Jieshu Wu
- Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, 211166, China
| | - Shanshan Geng
- Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, 211166, China
| | - Xiaoting Li
- Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, 211166, China
| | - Mingming Zhu
- Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, 211166, China
| | - Weiwei Zhu
- Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, 211166, China
| | - Jianyun Zhu
- Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, 211166, China
| | - Cong Huang
- Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, 211166, China
| | - Xiao Ma
- Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, 211166, China
| | - Wenrong Xu
- Jiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, 212013, China
| | - Caiyun Zhong
- Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, 211166, China
- The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, 211166, China
| | - Hongyu Han
- Department of Clinical Nutrition, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangzhou, 510060, China
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Liu F, Luo L, Wei Y, Wang W, Wen T, Yang J, Xu M, Li B. Association of VEGFA polymorphisms with susceptibility and clinical outcome of hepatocellular carcinoma in a Chinese Han population. Oncotarget 2017; 8:16488-16497. [PMID: 28147320 PMCID: PMC5369979 DOI: 10.18632/oncotarget.14870] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/06/2016] [Accepted: 01/16/2017] [Indexed: 02/05/2023] Open
Abstract
Vascular endothelial growth factor A (VEGFA) is an important angiogenesis regulator, which plays an important role in angiogenesis and progression of tumor, including hepatocellular carcinoma (HCC). We aimed at determining whether single nucleotide polymorphisms of VEGFA gene influence the development and clinical outcomes of HCC. We analyzed four potential functional polymorphisms (936C/T, 634G/C, 1612G/A, 2578C/A) of VEGFA gene in 476 HCC patients and 526 controls using matrix-assisted laser desorption ionization time-of-flight mass spectrometry method. Serum VEGF levels were measured by enzyme-linked immunosorbent assay. The Kaplan-Meier methods with log-rank test and Cox regression models were used to compare survival of resected HCC patients according to the genotype. We found that only the VEGFA 2578C/A polymorphism was significantly associated with decreased risk of HCC (AA/AC vs. CC; adjusted OR = 0.69, 95% CI = 0.51-0.93). Furthermore, the 2578C/A polymorphism was associated with significantly decreased postoperative recurrence (AA/AC vs. CC, adjusted OR = 0.51; 95% CI, 0.29-0.88) and improved overall survival (AA/AC vs. CC, adjusted HR = 0.27, 95% CI = 0.13-0.52) of resected HCC patients. In addition, the VEGF serum levels in HCC patients were significantly higher than those in healthy controls, although no significant association between VEGFA genotype and serum levels of VEGF was observed. These results suggest that the VEGFA 2578 C/A polymorphism may play a potential role in the development and clinical outcome of HCC among Chinese Han population.
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Affiliation(s)
- Fei Liu
- Department of Liver Surgery and Liver Transplantation Center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan Province, China
| | - Limei Luo
- Department of Clinical Immunological Laboratory, West China Hospital, Sichuan University, 610041, China
| | - Yonggang Wei
- Department of Liver Surgery and Liver Transplantation Center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan Province, China
| | - Wentao Wang
- Department of Liver Surgery and Liver Transplantation Center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan Province, China
| | - Tianfu Wen
- Department of Liver Surgery and Liver Transplantation Center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan Province, China
| | - Jiayin Yang
- Department of Liver Surgery and Liver Transplantation Center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan Province, China
| | - Mingqing Xu
- Department of Liver Surgery and Liver Transplantation Center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan Province, China
| | - Bo Li
- Department of Liver Surgery and Liver Transplantation Center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan Province, China
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8
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Deng B, Liu F, Luo L, Wei Y, Li B, Yang H. CASP 3 genetic polymorphisms and risk of Hepatocellular carcinoma: a case-control study in a Chinese population. Tumour Biol 2016; 37:8985-91. [DOI: 10.1007/s13277-015-4779-y] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/25/2015] [Accepted: 12/29/2015] [Indexed: 12/20/2022] Open
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9
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Braillon A. Prediction of hepatocellular carcinoma: using a complex risk model or assisting for smoking cessation? Cancer 2015; 121:1149-50. [PMID: 25470258 DOI: 10.1002/cncr.29182] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/11/2022]
Affiliation(s)
- Alain Braillon
- Hepatology and Public Health, University Hospital, Amiens, France
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10
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Abstract
Hepatocellular carcinoma (HCC) is the most common histologic type of primary liver cancer, accounting for between 85% and 90% of these malignancies. The overall prognosis of patients with liver cancer is poor, and an understanding of this disease and its risk factors is crucial for screening at-risk individuals, early recognition, and timely diagnosis. Most HCCs arise in the background of chronic liver disease caused by hepatitis B virus, hepatitis C virus, and chronic excessive alcohol intake. These underlying causes are characterized by marked variations in geography, gender, and other well-documented risk factors, some of which are potentially preventable.
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Affiliation(s)
- Kelly J Lafaro
- Department of Surgery, Johns Hopkins Hospital, The Johns Hopkins University School of Medicine, 600 North Wolfe Street, Blalock 688, Baltimore, MD 21287, USA
| | - Aram N Demirjian
- Department of Surgery, University of California-Irvine, 333 City Boulevard West, Suite 1205, Orange, CA 92868, USA
| | - Timothy M Pawlik
- Division of Surgical Oncology, Department of Surgery, Johns Hopkins Hospital, 600 North Wolfe Street, Blalock 688, Baltimore, MD 21287, USA.
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11
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Yamada S, Kawaguchi A, Kawaguchi T, Fukushima N, Kuromatsu R, Sumie S, Takata A, Nakano M, Satani M, Tonan T, Fujimoto K, Shima H, Kakuma T, Torimura T, Charlton MR, Sata M. Serum albumin level is a notable profiling factor for non-B, non-C hepatitis virus-related hepatocellular carcinoma: A data-mining analysis. Hepatol Res 2014; 44:837-45. [PMID: 23819517 DOI: 10.1111/hepr.12192] [Citation(s) in RCA: 27] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/24/2013] [Revised: 06/24/2013] [Accepted: 06/25/2013] [Indexed: 12/12/2022]
Abstract
AIM Various factors are underlying for the onset of non-B, non-C hepatitis virus-related hepatocellular carcinoma (NBNC-HCC). We aimed to investigate the independent risk factors and profiles associated with NBNC-HCC using a data-mining technique. METHODS We conducted a case-control study and enrolled 223 NBNC-HCC patients and 669 controls from a health checkup database (n = 176 886). Multivariate analysis, random forest analysis and a decision-tree algorithm were employed to examine the independent risk factors, factors distinguishing between the case and control groups, and to identify profiles for the incidence of NBNC-HCC, respectively. RESULTS In multivariate analysis, besides γ-glutamyltransferase (GGT) levels and the Brinkman index, albumin level was an independent negative risk factor for the incidence of NBNC-HCC (odds ratio = 0.67; 95% confidence interval = 0.60-0.70; P < 0.0001). In random forest analysis, serum albumin level was the highest-ranked variable for distinguishing between the case and control groups (98 variable importance). A decision-tree algorithm was created for albumin and GGT levels, the aspartate aminotransferase-to-platelet ratio index (APRI) and the Brinkman index. The serum albumin level was selected as the initial split variable, and 82.5% of the subjects with albumin levels of less than 4.01 g/dL were found to have NBNC-HCC. CONCLUSION Data-mining analysis revealed that serum albumin level is an independent risk factor and the most distinguishable factor associated with the incidence of NBNC-HCC. Furthermore, we created an NBNC-HCC profile consisting of albumin and GGT levels, the APRI and the Brinkman index. This profile could be used in the screening strategy for NBNC-HCC.
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Affiliation(s)
- Shingo Yamada
- Division of Gastroenterology, Department of Medicine, Kurume University School of Medicine, Japan
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12
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Yu Y, Rajan SS, Essien EJ, Yang M, Abughosh S. The relationship between obesity and prescription of smoking cessation medications. Popul Health Manag 2014; 17:172-9. [PMID: 24784163 DOI: 10.1089/pop.2013.0059] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/09/2023] Open
Abstract
The objective of this study was to examine the differences in prescription of smoking cessation medications among smokers with different body mass index (BMI) classifications. A retrospective cross-sectional study was conducted using National Ambulatory Medical Care Survey data (2006-2010). Self-reported current smokers aged 18 years and older were included in the study. The outcome of interest was receiving a prescription for a Food and Drug Administration-approved smoking cessation medication. Multivariate logistic regression was performed to assess the association between the outcome variable and the main independent variable (BMI classification), controlling for other covariates. The results showed that overweight, obese, and severely obese smokers were less likely to be prescribed a smoking cessation medication as compared to normal weight smokers. Although 5.11% of normal weight smokers were prescribed a smoking cessation medication, only 3.70% of overweight smokers, 3.41% of obese smokers, and 2.50% of severely obese smokers were prescribed a smoking cessation medication. In addition, older smokers, whites, smokers visiting primary care providers, smokers receiving tobacco counseling, and nondiabetic smokers were more likely to be prescribed a smoking cessation medication. Lower prescription of smoking cessation medications among overweight, obese, and severely obese smokers might be driven by patients' health concerns and behavioral factors or providers' treatment preferences or biases. The disparity in smoking cessation medication prescription among smokers with different BMI classifications raises quality of care and health care concerns for overweight, obese, and severely obese smokers.
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Affiliation(s)
- Yuping Yu
- 1 Department of Pharmaceutical Health Outcomes and Policy, College of Pharmacy, University of Houston , Houston, Texas
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Hamed MA, Ali SA. Non-viral factors contributing to hepatocellular carcinoma. World J Hepatol 2013; 5:311-322. [PMID: 23805355 PMCID: PMC3692972 DOI: 10.4254/wjh.v5.i6.311] [Citation(s) in RCA: 46] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/21/2013] [Revised: 05/10/2013] [Accepted: 05/18/2013] [Indexed: 02/06/2023] Open
Abstract
Hepatocellular carcinoma (HCC) is a major cause of cancer death worldwide, accounting for over half a million deaths per year. The geographic pattern of HCC incidence is parallel to exposure to viral etiologic factors. Its incidence is increasing, ranging between 3% and 9% annually depending on the geographical location, and variability in the incidence rates correspond closely to the prevalence and pattern of the primary etiologic factors. Chronic infections with hepatitis B viruses or hepatitis C viruses have both been recognized as human liver carcinogens with a combined attributable fraction of at least 75% of all HCC cases. Multiple non-viral factors have been implicated in the development of HCC. Increased body mass index and diabetes with subsequent development of non-alcoholic steatohepatitis represent significant risk factors for HCC. Other non-viral causes of HCC include iron overload syndromes, alcohol use, tobacco, oral contraceptive, aflatoxin, pesticides exposure and betel quid chewing, a prevalent habit in the developing world. Wilson disease, α-1 antitrypsin deficiency, Porphyrias, autoimmune hepatitis, Schistosoma japonicum associated with positive hepatitis B surface antigen, and thorotrast-ray are also contributing hepatocellualar carcinoma. In addition, primary biliary cirrhosis, congestive liver disease and family history of liver cancer increase the risk of HCC incident. In conclusion, clarification of relevant non-viral causes of HCC will help to focus clinicians on those risk factors that are modifiable. The multilevel preventative approach will hopefully lead to a reduction in incidence of non-viral HCC, and a decrease in the patient morbidity and mortality as well as the societal economic burden associated with HCC.
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Affiliation(s)
- Manal A Hamed
- Manal A Hamed, Sanaa A Ali, Therapeutic Chemistry Department, Pharmaceutical and Drug Industries Division, National Research Centre, Dokki, Giza 12622, Egypt
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14
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Abstract
Hepatocellular carcinoma (HCC) is a major cause of cancer death worldwide, accounting for over half a million deaths per year. The geographic pattern of HCC incidence is parallel to exposure to viral etiologic factors. Its incidence is increasing, ranging between 3% and 9% annually depending on the geographical location, and variability in the incidence rates correspond closely to the prevalence and pattern of the primary etiologic factors. Chronic infections with hepatitis B viruses or hepatitis C viruses have both been recognized as human liver carcinogens with a combined attributable fraction of at least 75% of all HCC cases. Multiple non-viral factors have been implicated in the development of HCC. Increased body mass index and diabetes with subsequent development of non-alcoholic steatohepatitis represent significant risk factors for HCC. Other non-viral causes of HCC include iron overload syndromes, alcohol use, tobacco, oral contraceptive, aflatoxin, pesticides exposure and betel quid chewing, a prevalent habit in the developing world. Wilson disease, α-1 antitrypsin deficiency, Porphyrias, autoimmune hepatitis, Schistosoma japonicum associated with positive hepatitis B surface antigen, and thorotrast-ray are also contributing hepatocellualar carcinoma. In addition, primary biliary cirrhosis, congestive liver disease and family history of liver cancer increase the risk of HCC incident. In conclusion, clarification of relevant non-viral causes of HCC will help to focus clinicians on those risk factors that are modifiable. The multilevel preventative approach will hopefully lead to a reduction in incidence of non-viral HCC, and a decrease in the patient morbidity and mortality as well as the societal economic burden associated with HCC.
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Affiliation(s)
- Manal A Hamed
- Manal A Hamed, Sanaa A Ali, Therapeutic Chemistry Department, Pharmaceutical and Drug Industries Division, National Research Centre, Dokki, Giza 12622, Egypt
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15
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De P, Dryer D, Otterstatter MC, Semenciw R. Canadian trends in liver cancer: a brief clinical and epidemiologic overview. ACTA ACUST UNITED AC 2013; 20:e40-3. [PMID: 23443230 DOI: 10.3747/co.20.1190] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/21/2022]
Abstract
Although primary liver cancer is rare, its incidence rate has been rising quickly in Canada, more than tripling since the early 1980s. This cancer is more common in men than women, and the age-specific incidence rates in men have been increasing significantly in all age groups from 40 years of age onward. The death rate has followed a similar upward trajectory, in part because of the low 5-year survival rate of 18% in both sexes. Infection with the hepatitis B or C virus continues to be the most common risk factor, but other factors may also play a role. Risk reduction strategies, such as viral hepatitis screening, have been recommended in other countries and warrant consideration in Canada as part of a coordinated strategy of disease prevention and control.
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Affiliation(s)
- P De
- Cancer Control Policy, Canadian Cancer Society, Toronto, ON
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16
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Wang S, Sugamori KS, Brenneman D, Hsu I, Calce A, Grant DM. Influence of arylamine N-acetyltransferase, sex, and age on 4-aminobiphenyl-induced in vivo mutant frequencies and spectra in mouse liver. ENVIRONMENTAL AND MOLECULAR MUTAGENESIS 2012; 53:350-357. [PMID: 22508569 DOI: 10.1002/em.21695] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Received: 12/29/2011] [Revised: 03/07/2012] [Accepted: 03/09/2012] [Indexed: 05/31/2023]
Abstract
One model for cancer initiation by 4-aminobiphenyl (ABP) involves N-oxidation by cytochrome P450 CYP1A2 followed by O-conjugation by N-acetyltransferase(s) NAT1 and/or NAT2 and decomposition to a DNA-binding nitrenium ion. We recently observed that neonatal ABP exposure produced liver tumors in male but not in female mice, and that NAT deficiency reduced liver tumor incidence. However, ABP-induced liver tumor incidence did not correlate with liver levels of N-(deoxyguanosin-8-yl)-ABP adducts 24 hr after exposure. In this study, we compared in vivo ABP-induced DNA mutant frequencies and spectra between male and female wild-type and NAT-deficient Muta™Mouse using both the tumor-inducing neonatal exposure protocol and a 28-day repetitive dosing adult exposure protocol. ABP produced an increase in liver DNA mutant frequencies in both neonates and adults. However, we observed no sex or strain differences in mutant frequencies in neonatally exposed mice, and higher frequencies in adult females than males. Neonatal ABP exposure of wild-type mice increased the proportion of G-T transversions in both males and females, while exposure of Nat1/2(-/-) mice produced increased G-T transversions in males and a decrease in females, even though females had higher levels of N-(deoxyguanosin-8-yl)-4-ABP adducts. There was no correlation of mutant frequencies or spectra between mice dosed as neonates or as adults. These results suggest that observed sex- and NAT-dependent differences in ABP-induced liver tumor incidence in mice are not due to differences in either mutation rates or mutational spectra, and that mechanisms independent of carcinogen bioactivation, covalent DNA binding and mutation may be responsible for these differences.
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Affiliation(s)
- Shuang Wang
- Department of Pharmacology & Toxicology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada M5S 1A8
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17
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Ha NB, Ha NB, Ahmed A, Ayoub W, Daugherty TJ, Chang ET, Lutchman GA, Garcia G, Cooper AD, Keeffe EB, Nguyen MH. Risk factors for hepatocellular carcinoma in patients with chronic liver disease: a case–control study. Cancer Causes Control 2012; 23:455-62. [DOI: 10.1007/s10552-012-9895-z] [Citation(s) in RCA: 26] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/03/2011] [Accepted: 01/06/2012] [Indexed: 01/17/2023]
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Abstract
Hepatocellular carcinoma (HCC) is the most common primary liver malignancy and represents an international public health concern as one of the most deadly cancers worldwide. The main etiology of HCC is chronic infection with hepatitis B and hepatitis C viruses. However, there are other important factors that contribute to the international burden of HCC. Among these are obesity, diabetes, non-alcoholic steatohepatitis and dietary exposures. Emerging evidence suggests that the etiology of many cases of HCC is in fact multifactorial, encompassing infectious etiologies, comorbid conditions and environmental exposures. Clarification of relevant non-viral causes of HCC will aid in preventative efforts to curb the rising incidence of this disease.
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Dubois G, Braillon A. Hepatocellular carcinoma: again, tobacco is the first enemy. Int J Epidemiol 2009; 39:1399. [PMID: 19939811 DOI: 10.1093/ije/dyp352] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/13/2022] Open
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20
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Jeng JE, Tsai HR, Chuang LY, Tsai JF, Lin ZY, Hsieh MY, Chen SC, Chuang WL, Wang LY, Yu ML, Dai CY, Chang JG. Independent and additive interactive effects among tumor necrosis factor-alpha polymorphisms, substance use habits, and chronic hepatitis B and hepatitis C virus infection on risk for hepatocellular carcinoma. Medicine (Baltimore) 2009; 88:349-357. [PMID: 19910749 DOI: 10.1097/md.0b013e3181c10477] [Citation(s) in RCA: 33] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022] Open
Abstract
We conducted a case-control study to assess the roles of tumor necrosis factor (TNF)-alpha polymorphisms, substance use habits, and chronic hepatitis B virus (HBV)/hepatitis C virus (HCV) infection on the risk for hepatocellular carcinoma (HCC). We enrolled 200 pairs of sex- and age-matched patients with HCC and unrelated healthy controls. TNF-alpha polymorphisms were detected with polymerase chain reaction and direct sequencing. Serum hepatitis B surface antigen (HBsAg) and antibodies to HCV (anti-HCV) were detected. We used a structured questionnaire to obtain information about substance use habits.Multivariate analysis indicated that TNF308.2 allele (odds ratio [OR], 3.23; p = 0.011), habitual betel quid chewing (OR, 3.70; p = 0.011), HBsAg (OR, 23.62; p = 0.0001), and anti-HCV (OR, 38.73; p = 0.0001) were independent risk factors for HCC. Having at least 2 substance use habits was associated with risk for HCC. The more substance use habits, the higher the OR for HCC (p(for trend) = 0.0001). There were additive interactions among TNF308.2 allele, substance use habits, and chronic HBV/HCV infection. Multivariate analysis indicated that TNF308.2 allele (p = 0.001), cigarette smoking (p = 0.0001), and alcohol drinking (p = 0.0001) were independent risk factors for habitual betel quid chewing. Moreover, patients harboring the TNF308.2 allele and/or those with habits of substance use had low serum albumin concentration and platelet count (each p = 0.0001). In conclusion, there are independent and additive interactive effects among the TNF308.2 allele, substance use habits, and chronic HBV/HCV infection on the risk for HCC. Substance use habits or carrying the TNF308.2 allele correlates with disease severity and hepatic fibrosis, which may contribute to higher risks for HCC.
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Affiliation(s)
- Jen-Eing Jeng
- From Department of Laboratory Medicine (JEJ, JGC), and Internal Medicine (JFT, ZYL, MYH, SCC, WLC, LYW, MLY, CYD), Kaohsiung Medical University Hospital; and Department of Laboratory Medicine (JEJ, JGC), Internal Medicine (JFT, ZYL, MYH, SCC, WLC, LYW, MLY, CYD), and Biochemistry (LYC), Faculty of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; and Department of Internal Medicine (HRT), Sin-Lau Christmas Hospital, Tainan, Taiwan
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21
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Lee YCA, Cohet C, Yang YC, Stayner L, Hashibe M, Straif K. Meta-analysis of epidemiologic studies on cigarette smoking and liver cancer. Int J Epidemiol 2009; 38:1497-511. [PMID: 19720726 DOI: 10.1093/ije/dyp280] [Citation(s) in RCA: 194] [Impact Index Per Article: 12.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022] Open
Abstract
BACKGROUND Whereas the International Agency for Research on Cancer (IARC) Monograph concluded that the evidence for the relationship between cigarette smoking and liver cancer is sufficient, the US Surgeon General's report summarized the data as suggestive but not sufficient. METHODS A meta-analysis of previous epidemiologic studies may help to clarify the potential association. We identified 38 cohort studies and 58 case-control studies in a systematic literature search for studies on liver cancer and cigarette smoking. The meta-relative risk (mRR) of liver cancer and dose-response trends were calculated. Tests for heterogeneity, publication bias assessment and influence analyses were performed. RESULTS Compared with never smokers, the adjusted mRR was 1.51 [95% confidence interval (CI) 1.37-1.67] for current smokers and 1.12 (95% CI 0.78-1.60) for former smokers. The increased liver cancer risk among current smokers appeared to be consistent in strata of different regions, study designs, study sample sizes and publication periods. CONCLUSION The results of our meta-analysis show that tobacco smoking is associated with liver cancer development, which supports the conclusion by the IARC Monograph. This conclusion has an important public health message for areas with high smoking prevalence and high liver cancer incidence such as China.
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Bailey SM, Mantena SK, Millender-Swain T, Cakir Y, Jhala NC, Chhieng D, Pinkerton KE, Ballinger SW. Ethanol and tobacco smoke increase hepatic steatosis and hypoxia in the hypercholesterolemic apoE(-/-) mouse: implications for a "multihit" hypothesis of fatty liver disease. Free Radic Biol Med 2009; 46:928-38. [PMID: 19280709 PMCID: PMC2775483 DOI: 10.1016/j.freeradbiomed.2009.01.003] [Citation(s) in RCA: 46] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/20/2022]
Abstract
Although epidemiologic studies indicate that combined exposure to cigarette smoke and alcohol increase the risk and severity of liver diseases, the molecular mechanisms responsible for hepatotoxicity are unknown. Similarly, emerging evidence indicates a linkage among hepatic steatosis and cardiovascular disease. Herein, we hypothesize that combined exposure to alcohol and environmental tobacco smoke (ETS) on a hypercholesterolemic background increases liver injury through oxidative/nitrative stress, hypoxia, and mitochondrial damage. To test this, male apoE(-/-) mice were exposed to an ethanol-containing diet, ETS alone, or a combination of the two, and histology and functional endpoints were compared to filtered-air-exposed, ethanol-naïve controls.Whereas ethanol consumption induced a mild steatosis, combined exposure to ethanol + ETS resulted in increased hepatic steatosis, inflammation, alpha-smooth muscle actin, and collagen. Exposure to ethanol + ETS induced the largest increase in CYP2E1 and iNOS protein, as well as increased 3-nitrotyrosine, mtDNA damage, and decreased cytochrome c oxidase protein, compared to all other groups. Similarly, the largest increase in HIF1alpha expression was observed in the ethanol + ETS group, indicating enhanced hypoxia. These studies demonstrate that ETS increases alcohol-dependent steatosis and hypoxic stress. Therefore, ETS may be a key environmental "hit" that accelerates and exacerbates alcoholic liver disease in hypercholesterolemic apoE(-/-) mice.
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Affiliation(s)
- Shannon M Bailey
- Department of Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
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Underner M, Hadjadj S, Beauchant M, Bridoux F, Debiais F, Meurice JC. Effets du tabagisme sur la thyroïde, le tube digestif, le rein et l’os. Rev Mal Respir 2008; 25:1261-78. [DOI: 10.1016/s0761-8425(08)75091-5] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/12/2023]
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Hassan MM, Spitz MR, Thomas MB, El-Deeb AS, Glover KY, Nguyen NT, Chan W, Kaseb A, Curley SA, Vauthey JN, Ellis LM, Abdalla E, Lozano RD, Patt YZ, Brown TD, Abbruzzese JL, Li D. Effect of different types of smoking and synergism with hepatitis C virus on risk of hepatocellular carcinoma in American men and women: case-control study. Int J Cancer 2008; 123:1883-91. [PMID: 18688864 PMCID: PMC2673571 DOI: 10.1002/ijc.23730] [Citation(s) in RCA: 61] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022]
Abstract
The International Agency for Research on Cancer has declared smoking to be a risk factor for hepatocellular carcinoma (HCC). However, passive exposure to cigarette smoke and use of noncigarette tobacco products on the risk of HCC has not been examined. Therefore, we evaluated the independent effects of different types of smoking exposure along with multiple risk factors for HCC and determined whether the magnitude of smoking was modified by other risk factors in men and women. We conducted a case-control study at The University of Texas M. D. Anderson Cancer Center where 319 HCC patients and 1,061 healthy control subjects were personally interviewed for several HCC risk factors. Multivariate logistic regression analysis was performed to estimate the adjusted odds ratio (AOR) and 95% confidence interval (CI) for each potential risk factor. Use of smokeless tobacco (chewing tobacco and snuff), cigars, pipes and passive smoking exposure were not related to HCC among noncigarette smokers. However, regular cigarette smoking was associated with HCC in men: AOR, 1.9 (95% CI, 1.1-3.1). Heavy alcohol consumption was associated with HCC in women: AOR, 7.7 (95% CI, 2.3-25.1). Cigarette smoking interacted synergistically with chronic infection of hepatitis C virus in men: AOR, 136.3 (95% CI, 43.2-429.6) and with heavy alcohol consumption in women: AOR, 13.7 (95% CI, 3.2-57.9). We conclude that sex differences were observed in HCC relationship with cigarette smoking and alcohol consumption. Controlling for smoking exposure might be a prudent approach to the prevention of HCC, especially in patients with chronic viral hepatitis infections.
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Affiliation(s)
- Manal M Hassan
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
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25
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Jim MA, Perdue DG, Richardson LC, Espey DK, Redd JT, Martin HJ, Kwong SL, Kelly JJ, Henderson JA, Ahmed F. Primary liver cancer incidence among American Indians and Alaska Natives, US, 1999-2004. Cancer 2008; 113:1244-55. [PMID: 18720380 DOI: 10.1002/cncr.23728] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
BACKGROUND American Indians and Alaska Natives (AI/AN) experience higher morbidity and mortality from primary liver cancer than other United States (US) populations, but racial misclassification in medical records results in underestimates of disease burden. METHODS To reduce misclassification, National Program of Cancer Registries and Surveillance, Epidemiology, and End Results data were linked with Indian Health Service (IHS) enrollment records to compare primary liver cancer incidence and stage at diagnosis between AI/AN and non-Hispanic whites (NHW) living within the regionalized IHS Contract Health Service Delivery Area counties. Incidence rates are expressed per 100,000 persons and age-adjusted by 19 age groups to the 2000 US standard population. RESULTS Overall, AI/AN have a higher proportion of hepatocellular carcinoma compared with NHW, 77.8% versus 66.7%. Liver cancer incidence rates among AI/AN males and females were higher than those among NHW males and females for all regions except for the East. Among males, rates ranged from 7.3 (95% confidence interval [CI], 3.8-12.6) in the East to 17.2 (95% CI, 10.4-26.3) in Alaska. Among females, rates ranged from 3.8 (95% CI, 1.4-8.2) in the East to 6.9 (95% CI, 3.6-11.6) in Alaska. The AI/AN rates for all regions were consistently higher than the NHW rates at every age. An increasing trend among AI/AN was suggested but did not achieve statistical significance. CONCLUSIONS Reducing racial misclassification revealed higher disparities in primary liver cancer incidence between NHW and AI/AN populations than previously reported. Further description of the reasons for regional differences in this disparity is needed, as are programs to reduce risk factors and to diagnose primary liver cancer at earlier, more treatable stages.
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Affiliation(s)
- Melissa A Jim
- Division of Cancer Prevention and Control, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
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Chen Y, Yi Q, Mao Y. Cluster of liver cancer and immigration: a geographic analysis of incidence data for Ontario 1998-2002. Int J Health Geogr 2008; 7:28. [PMID: 18518988 PMCID: PMC2426679 DOI: 10.1186/1476-072x-7-28] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/26/2008] [Accepted: 06/02/2008] [Indexed: 12/17/2022] Open
Abstract
Background Liver cancer is not common in Canada in general; however, clustering of the disease causes a concern. We conducted a spatial analysis to determine the geographic variation of liver cancer and its association with the proportion of immigration in Ontario. Liver cancer incidence data between 1998 and 2002 were obtained from the Ontario Cancer Registry. The Canadian Community Health Survey (CCHS) in 2001 provided information on potential risk factors. Results Age standardized incidence ratios (SIR) for liver cancer and prevalence of potential risk factors were calculated for each of 35 health regions. The SIRs for liver cancer varied across the 35 health regions (p < 0.01). Toronto and York health regions had a significantly higher SIR than other regions, indicated by the Scan method (p < 0.001). Poisson models with and without random effects were fitted to determine independent ecological contributors. After adjustment for sex, age and spatial location, the proportion of immigrants remained a significant determinant. Smoking, alcohol drinking, physical activity, education, income, obesity and diabetes did not substantially explain the geographic variation of liver cancer in Ontario. Conclusion Immigration is an important reason for the clustering of liver cancer in Ontario. More attention should be paid to areas with a high proportion of immigrants.
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Affiliation(s)
- Yue Chen
- Department of Epidemiology and Community Medicine, Faculty of Medicine, University of Ottawa, 451 Smyth Road, Ottawa, Ontario, Canada.
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Mantena SK, King AL, Andringa KK, Landar A, Darley-Usmar V, Bailey SM. Novel interactions of mitochondria and reactive oxygen/nitrogen species in alcohol mediated liver disease. World J Gastroenterol 2007; 13:4967-73. [PMID: 17854139 PMCID: PMC4434620 DOI: 10.3748/wjg.v13.i37.4967] [Citation(s) in RCA: 49] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
Mitochondrial dysfunction is known to be a contributing factor to a number of diseases including chronic alcohol induced liver injury. While there is a detailed understanding of the metabolic pathways and proteins of the liver mitochondrion, little is known regarding how changes in the mitochondrial proteome may contribute to the development of hepatic pathologies. Emerging evidence indicates that reactive oxygen and nitrogen species disrupt mitochondrial function through post-translational modifications to the mitochondrial proteome. Indeed, various new affinity labeling reagents are available to test the hypothesis that post-translational modification of proteins by reactive species contributes to mitochondrial dysfunction and alcoholic fatty liver disease. Specialized proteomic techniques are also now available, which allow for identification of defects in the assembly of multi-protein complexes in mitochondria and the resolution of the highly hydrophobic proteins of the inner membrane. In this review knowledge gained from the study of changes to the mitochondrial proteome in alcoholic hepatotoxicity will be described and placed into a mechanistic framework to increase understanding of the role of mitochondrial dysfunction in liver disease.
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Affiliation(s)
- Sudheer K Mantena
- Department of Environmental Health Sciences, Center for Free Radical Biology, University of Alabama at Birmingham, Ryals Building, Room 623, 1530 3rd Avenue South, Birmingham, AL 35294, USA
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