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11. Craxì A, Cammà C: Does chemotherapy prevent HCV-related hepatocellular carcinoma? Cons. Dig Liver Dis; 2010 Jul;42 Suppl 3:S287-92
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  • [Title] Does chemotherapy prevent HCV-related hepatocellular carcinoma? Cons.
  • The accuracy and the reliability of well-recognized clinical, virologic, histologic, and molecular risk factors for hepatocellular carcinoma (HCC) are still insufficient.
  • A strategy aiming at preventing chronic liver disease of any etiology (HCV and HBV infection, alcohol, obesity, others) may be required to prevent HCC in low and intermediate incidence areas, and hence, worldwide.
  • In the setting of secondary chemoprevention, literature data pooling suggests a slight preventive effect of interferon (IFN) on HCC development in patients with HCV-related cirrhosis.
  • So, there is no sound evidence to support a recommendation for widespread use of IFN to prevent HCC in HCV-related cirrhosis.
  • [MeSH-major] Antiviral Agents / therapeutic use. Carcinoma, Hepatocellular / prevention & control. Hepatitis C, Chronic / drug therapy. Interferon-alpha / therapeutic use. Liver Neoplasms / prevention & control. Polyethylene Glycols / therapeutic use

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  • [Copyright] Copyright 2010 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd.. All rights reserved.
  • [CommentOn] Dig Liver Dis. 2010 Jul;42 Suppl 3:S281-6 [20547315.001]
  • (PMID = 20547316.001).
  • [ISSN] 1878-3562
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 0 / peginterferon alfa-2a; 30IQX730WE / Polyethylene Glycols; 76543-88-9 / interferon alfa-2a
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12. Riedel F, Goessler UR, Hormann K: Alcohol-related diseases of the mouth and throat. Dig Dis; 2005;23(3-4):195-203
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  • [Title] Alcohol-related diseases of the mouth and throat.
  • In the upper aerodigestive tract, local morphologic, metabolic and functional alterations are present due to alcohol consumption.
  • A clinical link between the chronic consumption of alcohol and head and neck cancer has been observed for decades.
  • While alcohol was described initially as a risk enhancer only in smokers, a number of epidemiological studies have now provided sufficient evidence that chronic alcohol consumption increases the risk of head and neck cancer independent of exposure to tobacco smoke.
  • The systemic effects of alcohol interact with local changes in the morphology and function of the salivary glands.
  • In addition, alcohol leads to accumulation of pathologic microbes within the mucosa, leading to chronic infection.
  • Susceptibility to carcinogens and cell proliferation in the mucosa are increased, resulting in genetic changes with the development of dysplasia, leukoplacia and carcinoma.
  • Chronic alcohol consumption is correlated with an increased risk of cancer and an increased mortality in a dose-effect relationship.
  • A number of biologically plausible mechanisms exist by which alcohol may cause cancer.
  • [MeSH-major] Alcohol Drinking / adverse effects. Alcohol-Related Disorders / diagnosis. Laryngeal Neoplasms / etiology. Mouth Neoplasms / etiology

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  • [Copyright] Copyright 2005 S. Karger AG, Basel.
  • (PMID = 16508283.001).
  • [ISSN] 0257-2753
  • [Journal-full-title] Digestive diseases (Basel, Switzerland)
  • [ISO-abbreviation] Dig Dis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 3K9958V90M / Ethanol
  • [Number-of-references] 101
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13. Polednak AP: Recent trends in incidence rates for selected alcohol-related cancers in the United States. Alcohol Alcohol; 2005 May-Jun;40(3):234-8
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  • [Title] Recent trends in incidence rates for selected alcohol-related cancers in the United States.
  • AIMS: To examine recent trends in incidence rates for cancer types most strongly associated with alcohol use, using data from US cancer registries.
  • The declines in ASIRs were consistent with temporal declines in apparent alcohol consumption by state, although the prevalence of binge and heavy drinking in adults increased in some states.
  • [MeSH-major] Alcohol Drinking / epidemiology. Alcoholism / epidemiology. Neoplasms / epidemiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Carcinoma, Squamous Cell / epidemiology. Esophageal Neoplasms / epidemiology. Female. Humans. Incidence. Laryngeal Neoplasms / epidemiology. Male. Middle Aged. Mouth Neoplasms / epidemiology. Pharyngeal Neoplasms / epidemiology. SEER Program. United States / epidemiology

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  • (PMID = 15797879.001).
  • [ISSN] 0735-0414
  • [Journal-full-title] Alcohol and alcoholism (Oxford, Oxfordshire)
  • [ISO-abbreviation] Alcohol Alcohol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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4. Artifon EL, Lucon AM, Sakai P, Gerhardt R, Srougi M, Takagaki T, Ishioka S, Bhutani MS: EUS-guided alcohol ablation of left adrenal metastasis from non-small-cell lung carcinoma. Gastrointest Endosc; 2007 Dec;66(6):1201-5
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  • [Title] EUS-guided alcohol ablation of left adrenal metastasis from non-small-cell lung carcinoma.
  • OBJECTIVES: We present a case of EUS-guided therapy as alcohol ablation of left adrenal metastases.
  • CT scan revealed an invasive process in the left upper lobe of the lung and a mass in the left adrenal area that was considered highly suspicious for left adrenal metastases from the patient's lung carcinoma.
  • Because the patient's main clinical symptom was disabling abdominal pain, we considered the possibility of injection of alcohol into the left adrenal metastases under EUS guidance to ablate the metastatic lesion and potentially relieve the abdominal pain.
  • EUS-guided alcohol ablation was performed successfully.
  • CONCLUSION: EUS-guided alcohol ablation of left adrenal metastases in patients with non-small-cell lung cancer may provide palliation of cancer-related abdominal pain.
  • [MeSH-major] Adrenal Gland Neoplasms / secondary. Adrenal Gland Neoplasms / surgery. Carcinoma, Non-Small-Cell Lung / pathology. Endosonography / methods. Ethanol / administration & dosage. Lung Neoplasms / pathology

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  • (PMID = 18061721.001).
  • [ISSN] 0016-5107
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 3K9958V90M / Ethanol
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15. Kremsdorf D, Soussan P, Paterlini-Brechot P, Brechot C: Hepatitis B virus-related hepatocellular carcinoma: paradigms for viral-related human carcinogenesis. Oncogene; 2006 Jun 26;25(27):3823-33
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  • [Title] Hepatitis B virus-related hepatocellular carcinoma: paradigms for viral-related human carcinogenesis.
  • As discussed in detail in other chapters of this review, chronic hepatitis B (HBV) infection is a major risk factor for hepatocellular carcinoma (HCC).
  • This review will summarize the current knowledge on the mechanisms involved in HBV-related liver carcinogenesis.
  • It will show in particular how viruses can be viewed as tools to discover and dissect new cellular pathways involved in cancer development and emphasize the potential synergistic effects between HBV and hepatitis C virus, as well as between viral infections and other environmental factors, such as alcohol.
  • [MeSH-major] Carcinoma, Hepatocellular / virology. Hepatitis B virus / pathogenicity. Liver Neoplasms / virology

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  • (PMID = 16799624.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 173
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16. Fan JG, Farrell GC, Asia-Pacific Working Party for Prevention of Hepatocellular Carcinoma: Prevention of hepatocellular carcinoma in nonviral-related liver diseases. J Gastroenterol Hepatol; 2009 May;24(5):712-9
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  • [Title] Prevention of hepatocellular carcinoma in nonviral-related liver diseases.
  • Although chronic infection with hepatitis B virus and/or hepatitis C virus are the most important risk factors for hepatocellular carcinoma (HCC) worldwide, other causes of cirrhosis can also lead to HCC.
  • Given the high prevalence of alcoholism and the worldwide obesity epidemic, the relevant importance of nonviral liver disease-related HCC is expected to increase in the future.
  • Community-based programs to discourage and deal with excessive alcohol intake, to promote tobacco smoking awareness, to avoid exposure to aflatoxin and other food toxins, and measures to reduce the pandemic of obesity and diabetes are vital for effective interruption of the rising tide of HCC from nonviral liver disease.
  • [MeSH-major] Carcinoma, Hepatocellular / prevention & control. Liver Cirrhosis / prevention & control. Liver Neoplasms / prevention & control
  • [MeSH-minor] Alcohol Drinking / adverse effects. Alcohol Drinking / prevention & control. Androgens / adverse effects. Diabetes Mellitus, Type 2 / complications. Diabetes Mellitus, Type 2 / therapy. Diet / adverse effects. Estrogens / adverse effects. Fatty Liver / complications. Fatty Liver / therapy. Food Contamination. Health Knowledge, Attitudes, Practice. Health Promotion. Hemochromatosis / complications. Hemochromatosis / therapy. Humans. Obesity / complications. Obesity / therapy. Risk Assessment. Risk Factors. Smoking / adverse effects. Smoking / prevention & control. Water Pollutants / adverse effects

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  • (PMID = 19646014.001).
  • [ISSN] 1440-1746
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Androgens; 0 / Estrogens; 0 / Water Pollutants
  • [Number-of-references] 86
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17. Bhala N, Bhopal R, Brock A, Griffiths C, Wild S: Alcohol-related and hepatocellular cancer deaths by country of birth in England and Wales: analysis of mortality and census data. J Public Health (Oxf); 2009 Jun;31(2):250-7
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  • [Title] Alcohol-related and hepatocellular cancer deaths by country of birth in England and Wales: analysis of mortality and census data.
  • BACKGROUND: The incidence of and mortality from alcohol-related conditions, liver disease and hepatocellular cancer (HCC) are increasing in the UK.
  • MAIN OUTCOME MEASURES: Standardized mortality ratios (SMRs) for alcohol-related deaths and HCC.
  • RESULTS: Mortality from alcohol-related deaths (23 502 deaths) was particularly high for people born in Ireland (SMR for men [M]: 236, 95% confidence interval [CI]: 219-254; SMR for women [F]: 212, 95% CI: 191-235) and Scotland (SMR-M: 187, CI: 173-213; SMR-F 182, CI: 163-205) and men born in India (SMR-M: 161, CI: 144-181).
  • Low alcohol-related mortality was found in women born in other countries and men born in Bangladesh, Middle East, West Africa, Pakistan, China and Hong Kong, and the West Indies.
  • CONCLUSIONS: These findings show persistent differences in mortality by country of birth for both alcohol-related and HCC deaths and have important clinical and public health implications.
  • [MeSH-major] Alcoholism / complications. Carcinoma, Hepatocellular / chemically induced. Carcinoma, Hepatocellular / mortality. Censuses. Liver Neoplasms / chemically induced. Liver Neoplasms / mortality

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  • (PMID = 19297455.001).
  • [ISSN] 1741-3850
  • [Journal-full-title] Journal of public health (Oxford, England)
  • [ISO-abbreviation] J Public Health (Oxf)
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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18. Fujishima T, Ishikawa T, Shiratori Y, Kanda M, Tateishi R, Akamatsu M, Koike Y, Sato S, Obi S, Hamamura K, Teratani T, Shiina S, Yoshida H, Kawabe T, Omata M: Age-related comparison of the profiles of patients with hepatocellular carcinoma. Hepatogastroenterology; 2006 Nov-Dec;53(72):913-8
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  • [Title] Age-related comparison of the profiles of patients with hepatocellular carcinoma.
  • BACKGROUND/AIMS: It is not known whether the putative etiologic factors and clinical and pathological features of hepatocellular carcinoma differ between young adults and older patients.
  • Younger patients also had a higher ratio of alcohol consumption compared to elderly patients.
  • CONCLUSIONS: There were age-related differences in the clinicopathological characteristics of HCC patients.
  • Of the HCV-related HCC patients, heavy drinking may accelerate the progression from chronic hepatitis to cirrhosis and HCC.
  • [MeSH-major] Carcinoma, Hepatocellular / etiology. Carcinoma, Hepatocellular / pathology. Liver Neoplasms / etiology. Liver Neoplasms / pathology

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  • (PMID = 17153452.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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19. Fukushima W, Tanaka T, Ohfuji S, Habu D, Tamori A, Kawada N, Sakaguchi H, Takeda T, Nishiguchi S, Seki S, Shiomi S, Hirota Y: Does alcohol increase the risk of hepatocellular carcinoma among patients with hepatitis C virus infection? Hepatol Res; 2006 Mar;34(3):141-9
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  • [Title] Does alcohol increase the risk of hepatocellular carcinoma among patients with hepatitis C virus infection?
  • We conducted a hospital-based case-control study to investigate the effects of alcohol drinking on hepatocellular carcinoma (HCC) among patients with hepatitis C virus (HCV) infection, with special reference to the disease course and changes in drinking habits.
  • In conclusion, our results did not demonstrate a strong positive association between alcohol drinking and HCV-related HCC in this population.

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  • (PMID = 16427353.001).
  • [ISSN] 1386-6346
  • [Journal-full-title] Hepatology research : the official journal of the Japan Society of Hepatology
  • [ISO-abbreviation] Hepatol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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20. Werner CW, Seymour RA: Are alcohol containing mouthwashes safe? Br Dent J; 2009 Nov 28;207(10):E19; discussion 488-9
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  • [Title] Are alcohol containing mouthwashes safe?
  • Alcohol (ethanol) is a constituent of many proprietary mouthwashes.
  • In this paper, we reconsider the epidemiological evidence linking alcohol containing mouthwashes with an increased risk of oral cancer.
  • In addition, clinical studies comparing alcohol versus non-alcohol mouthwashes are evaluated.
  • The evidence suggests that the alcohol component of mouthwashes affords little additional benefit to the other active ingredients in terms of plaque and gingivitis control.
  • [MeSH-major] Carcinoma, Squamous Cell / chemically induced. Ethanol / adverse effects. Mouth Neoplasms / chemically induced. Mouthwashes / adverse effects
  • [MeSH-minor] Anti-Infective Agents, Local / therapeutic use. Chlorhexidine / therapeutic use. Dental Plaque / prevention & control. Drug-Related Side Effects and Adverse Reactions. Gingivitis / prevention & control. Humans. Mouth Mucosa / drug effects. Review Literature as Topic. Risk Assessment

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  • [CommentIn] Br Dent J. 2010 Feb 13;208(3):95-6 [20147905.001]
  • (PMID = 19942865.001).
  • [ISSN] 1476-5373
  • [Journal-full-title] British dental journal
  • [ISO-abbreviation] Br Dent J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Infective Agents, Local; 0 / Mouthwashes; 3K9958V90M / Ethanol; R4KO0DY52L / Chlorhexidine
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21. Stroffolini T, Almasio PL, Persico M, Bollani S, Benvegnù L, Di Costanzo G, Pastore G, Aghemo A, Stornaiuolo G, Mangia A, Andreone P, Stanzione M, Mazzella G, Saracco G, Del Poggio P, Bruno S, Italian Association of the Study of the Liver Disease (AISF): Lack of correlation between serum anti-HBcore detectability and hepatocellular carcinoma in patients with HCV-related cirrhosis. Am J Gastroenterol; 2008 Aug;103(8):1966-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of correlation between serum anti-HBcore detectability and hepatocellular carcinoma in patients with HCV-related cirrhosis.
  • BACKGROUND: While the likelihood of developing hepatocellular carcinoma (HCC) in patients coinfected with both HBV and HCV is increased, the role of previous exposure to HBV as a risk factor associated with tumor occurrence in subjects with HCV-related cirrhosis has not been fully investigated.
  • AIM: To assess whether serum anti-HBc positivity, as a marker of previous HBV exposure, is associated with HCC development in HCV-related positive, hepatitis B surface antigen (HBsAg) negative patients with cirrhosis treated with alfa-interferon (IFN) monotherapy.
  • Anti-HBc positive patients were more often men (67.0%vs 58.7%, P= 0.03), had lower transaminase levels (3.3 +/- 2.0 vs 3.8 +/- 2.5 u.l.n., P= 0.004), and had higher rate of alcohol intake (38.3%vs 22.5%, P < 0.001) than anti-HBc negative patients.
  • By Cox multiple regression, there was no association of serum anti-HBc with HCC development (HR 1.03, 95% CI 0.69-1.52) or liver-related deaths incidence (HR 1.21; 95% CI 0.76-1.95).
  • CONCLUSIONS: In comparison with anti-HBc negative subjects, serum anti-HBc positive patients with HCV-related/HBsAg negative cirrhosis treated with IFN monotherapy did not show a greater risk of HCC.
  • [MeSH-major] Antibodies, Viral / blood. Carcinoma, Hepatocellular / blood. Hepatitis B Core Antigens / immunology. Hepatitis B virus / immunology. Hepatitis C / blood. Liver Neoplasms / blood

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  • (PMID = 18637087.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Hepatitis B Core Antigens
  • [Investigator] Boccia S; Di Marco V; Giannini E; Morisco F; Picciotto A; Fagiuoli S; Mazzaro C
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22. Lagiou P, Georgila C, Minaki P, Ahrens W, Pohlabeln H, Benhamou S, Bouchardy C, Slamova A, Schejbalova M, Merletti F, Richiardi L, Kjaerheim K, Agudo A, Castellsague X, Macfarlane TV, Macfarlane GJ, Talamini R, Barzan L, Canova C, Simonato L, Lowry R, Conway DI, McKinney PA, Znaor A, McCartan BE, Healy C, Nelis M, Metspalu A, Marron M, Hashibe M, Brennan PJ: Alcohol-related cancers and genetic susceptibility in Europe: the ARCAGE project: study samples and data collection. Eur J Cancer Prev; 2009 Feb;18(1):76-84
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  • [Title] Alcohol-related cancers and genetic susceptibility in Europe: the ARCAGE project: study samples and data collection.
  • To address these issues, the International Agency for Research on Cancer initiated in 2002 the alcohol-related cancers and genetic susceptibility (ARCAGE) in Europe project, with the participation of 15 centers in 11 European countries.
  • A clear preponderance of smokers and alcohol drinkers among UADT cases compared with controls was observed.
  • [MeSH-major] Alcohol Drinking / adverse effects. Carcinoma, Squamous Cell / etiology. Genetic Predisposition to Disease. Head and Neck Neoplasms / etiology

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  • (PMID = 18830131.001).
  • [ISSN] 1473-5709
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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23. Homann N, König IR, Marks M, Benesova M, Stickel F, Millonig G, Mueller S, Seitz HK: Alcohol and colorectal cancer: the role of alcohol dehydrogenase 1C polymorphism. Alcohol Clin Exp Res; 2009 Mar;33(3):551-6
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  • [Title] Alcohol and colorectal cancer: the role of alcohol dehydrogenase 1C polymorphism.
  • BACKGROUND: Chronic alcohol consumption is a risk factor for colorectal cancer.
  • Animal experiments as well as genetic linkage studies in Japanese individuals with inactive acetaldehyde dehydrogenase leading to elevated acetaldehyde concentrations following ethanol ingestion support the hypothesis that acetaldehyde may be responsible for this carcinogenic effect of alcohol.
  • In Caucasians, a polymorphism of alcohol dehydrogenase 1C (ADH1C) exists resulting in different acetaldehyde concentrations following ethanol oxidation.
  • METHODS: To evaluate whether the association between alcohol consumption and colorectal tumor development is modified by ADH1C polymorphism, we recruited 173 individuals with colorectal tumors diagnosed by colonoscopy and 788 control individuals without colorectal tumors.
  • RESULTS: Genotype ADH1C*1/1 was more frequent in patients with alcohol-associated colorectal neoplasia compared to patients without cancers in the multivariate model controlling for age, gender, and alcohol intake (odds ratio = 1.674, 95% confidence interval = 1.110-2.524, 2-sided p from Wald test = 0.0139).
  • In addition, the joint test of the genetic effect and interaction between ADH1C genotype and alcohol intake (2-sided p = 0.0007) indicated that the difference in ADH1C*1 polymorphisms between controls and colorectal neoplasia is strongly influenced by the alcohol consumption and that only individuals drinking more than 30 g ethanol per day with the genotype ADH1C*1/1 had an increased risk for colorectal tumors.
  • CONCLUSIONS: These data identify ADH1C homozygosity as a genetic risk marker for colorectal tumors in individuals consuming more than 30 g alcohol per day and emphasize the role of acetaldehyde as a carcinogenic agent in alcohol-related colorectal carcinogenesis.
  • [MeSH-major] Adenoma / genetics. Alcohol Dehydrogenase / genetics. Alcohol Drinking / adverse effects. Carcinoma / genetics. Colorectal Neoplasms / genetics

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  • (PMID = 19120062.001).
  • [ISSN] 1530-0277
  • [Journal-full-title] Alcoholism, clinical and experimental research
  • [ISO-abbreviation] Alcohol. Clin. Exp. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.1.1.1 / ADH1C protein, human; EC 1.1.1.1 / Alcohol Dehydrogenase; GO1N1ZPR3B / Acetaldehyde
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24. Polednak AP: Secular trend in U.S. black-white disparities in selected alcohol-related cancer incidence rates. Alcohol Alcohol; 2007 Mar-Apr;42(2):125-30
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  • [Title] Secular trend in U.S. black-white disparities in selected alcohol-related cancer incidence rates.
  • AIMS: To examine secular trends in incidence rates for the cancer types most strongly associated with alcohol in African Americans (blacks) and whites.
  • CONCLUSIONS: Further declines in black-white disparities in cancer rates may occur (allowing for lag times), but the larger disparities for oesophageal cancer support the need to explore etiologic factors interacting with alcohol that continue to differ in prevalence between blacks and whites.
  • [MeSH-major] African Continental Ancestry Group / statistics & numerical data. Alcoholism / epidemiology. Carcinoma, Squamous Cell / epidemiology. European Continental Ancestry Group / statistics & numerical data. Otorhinolaryngologic Neoplasms / epidemiology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Alcohol Drinking / adverse effects. Cause of Death / trends. Cross-Sectional Studies. Female. Fruit. Humans. Incidence. Liver Diseases, Alcoholic / ethnology. Liver Diseases, Alcoholic / mortality. Male. Middle Aged. Registries / statistics & numerical data. Risk Factors. SEER Program. Smoking / adverse effects. Smoking / epidemiology. United States. Vegetables

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  • (PMID = 17255152.001).
  • [ISSN] 0735-0414
  • [Journal-full-title] Alcohol and alcoholism (Oxford, Oxfordshire)
  • [ISO-abbreviation] Alcohol Alcohol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / PC / N01-PC-35133
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
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25. Hu JL, Li ZY, Liu W, Zhang RG, Li GL, Wang T, Ren JH, Wu G: Polymorphism in heme oxygenase-1 (HO-1) promoter and alcohol are related to the risk of esophageal squamous cell carcinoma on Chinese males. Neoplasma; 2010;57(1):86-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polymorphism in heme oxygenase-1 (HO-1) promoter and alcohol are related to the risk of esophageal squamous cell carcinoma on Chinese males.
  • Chronic alcohol drinking is astrong risk factor for esophageal squamous cell carcinoma (ESCC).
  • In this study, the correlation between the HO-1 gene promoter polymorphism and alcohol, along with the risk of ESCC on Chinese males, was analyzed.The case-control study was performed in 143 ESCC patients and 264 cancer-free controls.
  • Reducing alcohol intake might be most protective among L-allele carriers of this polymorphism.
  • KEYWORDS: esophageal squamous cell carcinoma; heme oxygenase-1 promoter polymorphism; alcohol drinking.
  • [MeSH-major] Alcohol Drinking / adverse effects. Carcinoma, Squamous Cell / etiology. Esophageal Neoplasms / etiology. Heme Oxygenase-1 / genetics. Polymorphism, Genetic. Promoter Regions, Genetic

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  • (PMID = 19895178.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] EC 1.14.99.3 / Heme Oxygenase-1
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26. Nguyen VT, Law MG, Dore GJ: Hepatitis B-related hepatocellular carcinoma: epidemiological characteristics and disease burden. J Viral Hepat; 2009 Jul;16(7):453-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hepatitis B-related hepatocellular carcinoma: epidemiological characteristics and disease burden.
  • Worldwide, 350 million people are chronically infected with hepatitis B virus (HBV) who are at greater risk of hepatocellular carcinoma (HCC) compared with uninfected people.
  • Factors associated with increased risk of HCC include demographic characteristics (male sex and older age), lifestyles (heavy alcohol consumption and smoking), viral factors (genotype C, D F, high level of HBV DNA, core/precore mutation) and clinical factors (cirrhosis, elevated alpha-fetoprotein (AFP) and alanine aminotransferase (ALT)).
  • HBV-related HCC has extremely poor prognosis with median survival less than 16 months.
  • Survival rates of HBV-related HCC ranged from 36% to 67% after 1 year and from 15% to 26% after 5 year of diagnosis.
  • Global burden of HBV-related liver disease is still a major challenge for public health in the 21st century.
  • While decreases in incidence of HBV infection have been observed in birth cohorts following the introduction of universal infant HBV vaccination programme, HBV-related HCC incidence in is projected to increase for at least two decades because of the high prevalence of chronic HBV infection and prolonged latency to HCC development.
  • To reduce HBV-related HCC continued expansion of universal infant HBV vaccination is required along with antiviral therapy targeted to those individuals at highest risk of HCC.
  • [MeSH-major] Carcinoma, Hepatocellular / epidemiology. Hepatitis B virus / isolation & purification. Hepatitis B, Chronic / complications

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  • (PMID = 19302335.001).
  • [ISSN] 1365-2893
  • [Journal-full-title] Journal of viral hepatitis
  • [ISO-abbreviation] J. Viral Hepat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 110
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27. Di Costanzo GG, De Luca M, Tritto G, Lampasi F, Addario L, Lanza AG, Tartaglione MT, Picciotto FP, Ascione A: Effect of alcohol, cigarette smoking, and diabetes on occurrence of hepatocellular carcinoma in patients with transfusion-acquired hepatitis C virus infection who develop cirrhosis. Eur J Gastroenterol Hepatol; 2008 Jul;20(7):674-9
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  • [Title] Effect of alcohol, cigarette smoking, and diabetes on occurrence of hepatocellular carcinoma in patients with transfusion-acquired hepatitis C virus infection who develop cirrhosis.
  • AIM: Alcohol drinking, cigarette smoking, and diabetes have been claimed as risk factors for hepatocellular carcinoma in case-control studies.
  • The aim of this study was to define the impact of these risk factors on the development of hepatocellular carcinoma in hepatitis C virus-related liver cirrhosis.
  • METHODS: A historical cohort of 138 patients with posttransfusion hepatitis C virus-related cirrhosis was selected by reviewing all files of patients referred to our liver unit.
  • Sixty-three of them (46%) developed hepatocellular carcinoma.
  • RESULTS: At univariate analysis, risk factors for hepatocellular carcinoma were observed in patients aged above 59 years [P=0.004; relative risk (RR): 2.08, 95% confidence interval (CI): 1.19-3.68], male sex (P<0.001; RR: 2.48, 95% CI: 1.59-3.87), habit of alcohol drinking (P=0.001; RR: 1.89, 95% CI: 1.24-2.88), and duration of alcohol consumption of more than 30 years (P=0.02; RR: 2.08, 95% CI: 0.98-4.40).
  • CONCLUSION: Diabetes, smoking, and alcohol drinking were not independently related to the risk of developing hepatocellular carcinoma in hepatitis C virus-related cirrhosis.
  • [MeSH-major] Alcohol Drinking / adverse effects. Carcinoma, Hepatocellular / etiology. Diabetes Complications. Liver Neoplasms / etiology. Smoking / adverse effects


28. McKillop IH, Schrum LW: Role of alcohol in liver carcinogenesis. Semin Liver Dis; 2009 May;29(2):222-32
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  • [Title] Role of alcohol in liver carcinogenesis.
  • Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in the world and contributes significantly to cancer-related morbidity and mortality.
  • Chronic alcohol consumption has long been associated with progressive liver disease toward the development of hepatic cirrhosis and the subsequent increased risk for developing HCC.
  • In assessing the role of alcohol during hepatic disease, and as a carcinogen, many of the deleterious effects of alcohol can be attributed to alcohol metabolism in hepatocytes.
  • In addition to the direct effects of alcohol/alcohol metabolism on hepatocyte transformation, increasing evidence indicates that other intrahepatic and systemic effects of alcohol are likely to play an equally significant role in the process of hepatic tumorigenesis.
  • [MeSH-major] Alcohol Drinking / adverse effects. Carcinoma, Hepatocellular / etiology. Ethanol / toxicity. Liver / drug effects. Liver Diseases, Alcoholic / etiology. Liver Neoplasms / etiology

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  • (PMID = 19387921.001).
  • [ISSN] 1098-8971
  • [Journal-full-title] Seminars in liver disease
  • [ISO-abbreviation] Semin. Liver Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 3K9958V90M / Ethanol; GO1N1ZPR3B / Acetaldehyde
  • [Number-of-references] 146
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29. Kwon OS, Jung YK, Kim YS, Kim SG, Kim YS, Lee JI, Lee JW, Kim YS, Chun BC, Kim JH: Effect of alcohol on the development of hepatocellular carcinoma in patients with hepatitis B virus-related cirrhosis: a cross-sectional case-control study. Korean J Hepatol; 2010 Sep;16(3):308-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of alcohol on the development of hepatocellular carcinoma in patients with hepatitis B virus-related cirrhosis: a cross-sectional case-control study.
  • BACKGROUND/AIMS: Whether alcohol intake increases the risk of hepatocellular carcinoma (HCC) in patients with chronic hepatitis B virus (HBV) infection remains controversial.
  • The aim of this study was to determine the effect of alcohol intake on the development of HCC.
  • All cases and controls were HBsAg positive, and had a history of lifetime alcohol intake.
  • The basal laboratory data, distribution of Child-Pugh class, HBeAg positivity (31.5% vs. 37.7%), HBV DNA level (5.74±2.35 vs. 5.98±2.29 log10 copies/mL), and proportion with a lifetime alcohol intake of more than 292 kg (30.8% vs. 34.9%) did not differ between cases and controls.
  • The cumulative alcohol intake and the proportion of heavy drinkers did not differ between the two groups in male patients.
  • CONCLUSIONS: Alcohol intake might not increase the risk of HCC in patients with HBV infection.
  • [MeSH-major] Alcohol Drinking / adverse effects. Carcinoma, Hepatocellular / etiology. Hepatitis B, Chronic / complications. Liver Cirrhosis / complications. Liver Neoplasms / etiology

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  • [Cites] Cancer. 1998 Mar 1;82(5):827-35 [9486570.001]
  • [Cites] Am J Epidemiol. 1997 Jun 1;145(11):1039-47 [9169913.001]
  • [Cites] Clin Liver Dis. 2005 Feb;9(1):151-69 [15763234.001]
  • [Cites] JAMA. 2006 Jan 4;295(1):65-73 [16391218.001]
  • [Cites] Gastroenterology. 2006 Mar;130(3):678-86 [16530509.001]
  • [Cites] Gastroenterology. 2007 Jun;132(7):2557-76 [17570226.001]
  • [Cites] Liver Int. 2007 Dec;27(10):1356-63 [17900245.001]
  • [Cites] Gut. 2008 Jan;57(1):91-7 [17502344.001]
  • [Cites] Carcinogenesis. 2008 Jan;29(1):106-12 [17999990.001]
  • [Cites] Hepatology. 2009 May;49(5 Suppl):S56-60 [19399807.001]
  • [Cites] Korean J Hepatol. 2009 Sep;15(3):391-423 [19783891.001]
  • [Cites] Hepatology. 2010 Jan;51(1):307-28 [20034030.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2000 Jun;12(6):687-93 [10912490.001]
  • [Cites] J Gastroenterol Hepatol. 2000 May;15 Suppl:E20-4 [10921377.001]
  • [Cites] Alcohol Clin Exp Res. 2001 May;25(5 Suppl ISBRA):40S-45S [11391047.001]
  • [Cites] Am J Gastroenterol. 2001 Aug;96(8):2462-7 [11513191.001]
  • [Cites] Hepatology. 2001 Oct;34(4 Pt 1):714-8 [11584367.001]
  • [Cites] Br J Cancer. 2001 Nov 30;85(11):1700-5 [11742491.001]
  • [Cites] Am J Epidemiol. 2002 Feb 15;155(4):323-31 [11836196.001]
  • [Cites] Lancet Oncol. 2001 Sep;2(9):533-43 [11905707.001]
  • [Cites] N Engl J Med. 2002 Jul 18;347(3):168-74 [12124405.001]
  • [Cites] Hepatology. 2002 Nov;36(5):1206-13 [12395331.001]
  • [Cites] Cancer Causes Control. 2003 Dec;14(10):995-1000 [14750539.001]
  • [Cites] Gastroenterology. 2004 Nov;127(5 Suppl 1):S35-50 [15508101.001]
  • [Cites] Br J Addict. 1982 Dec;77(4):357-82 [6762224.001]
  • [Cites] J Med Virol. 1984;13(4):385-91 [6330293.001]
  • [Cites] Gut. 1991 Mar;32(3):294-8 [2013423.001]
  • [Cites] Hepatology. 1993 Jul;18(1):47-53 [7686879.001]
  • [Cites] Alcohol Clin Exp Res. 1996 Feb;20(1 Suppl):91A-94A [8659700.001]
  • [Cites] Alcohol Clin Exp Res. 1996 Jun;20(4):758-62 [8800396.001]
  • [Cites] Hepatology. 1998 Apr;27(4):914-9 [9537428.001]
  • (PMID = 20924214.001).
  • [ISSN] 1738-222X
  • [Journal-full-title] The Korean journal of hepatology
  • [ISO-abbreviation] Korean J Hepatol
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Hepatitis B Surface Antigens
  • [Other-IDs] NLM/ PMC3304590
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30. Peters ES, McClean MD, Liu M, Eisen EA, Mueller N, Kelsey KT: The ADH1C polymorphism modifies the risk of squamous cell carcinoma of the head and neck associated with alcohol and tobacco use. Cancer Epidemiol Biomarkers Prev; 2005 Feb;14(2):476-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The ADH1C polymorphism modifies the risk of squamous cell carcinoma of the head and neck associated with alcohol and tobacco use.
  • Alcohol consumption interacts with tobacco use to increase the risk of head and neck squamous cell carcinoma (HNSCC).
  • Alcohol is eliminated through oxidation by alcohol dehydrogenase (ADH).
  • This polymorphism has been reported to alter the risk of HNSCC associated with alcohol use, although the literature differs in the estimates of both the magnitude and direction of this effect modification.
  • There was a significant interaction of alcohol use and genotype (P = 0.05), with an estimated oral cancer risk in heavy drinkers of 7.1 (95% CI, 2.3-22.0) for homozygous variants compared with an OR of 2.3 (95% CI, 1.4-3.8) for ADH1C homozygous wild type or heterozygous individuals (controlling for smoking, age, race, and gender).
  • These findings suggest that the ADH1C*2-2 genotype is associated with susceptibility to smoking and drinking-related HNSCC by modifying the biologically effective dose of alcohol.
  • [MeSH-major] Alcohol Dehydrogenase / genetics. Alcohol Drinking / adverse effects. Carcinoma, Squamous Cell / genetics. Head and Neck Neoplasms / genetics. Smoking / adverse effects

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  • (PMID = 15734975.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA78609; United States / NIEHS NIH HHS / ES / ES 00002
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.1 / ADH1C protein, human; EC 1.1.1.1 / Alcohol Dehydrogenase
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31. Marcellin P, Pequignot F, Delarocque-Astagneau E, Zarski JP, Ganne N, Hillon P, Antona D, Bovet M, Mechain M, Asselah T, Desenclos JC, Jougla E: Mortality related to chronic hepatitis B and chronic hepatitis C in France: evidence for the role of HIV coinfection and alcohol consumption. J Hepatol; 2008 Feb;48(2):200-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mortality related to chronic hepatitis B and chronic hepatitis C in France: evidence for the role of HIV coinfection and alcohol consumption.
  • BACKGROUND/AIMS: Mortality related to HCV and HBV infections was estimated in France.
  • Physicians who reported the deaths were sent a questionnaire to identify how many deaths were related to HBV/HCV infection.
  • In the HCV infection group, 95 percent had cirrhosis; 33 percent had hepatocellular carcinoma (HCC).
  • Deaths related to HBV or HCV infection occurred at an earlier age in patients with a history of excessive alcohol consumption.
  • CONCLUSIONS: In France, 4000-5000 deaths related to HCV and HBV infection occurred in 2001.
  • Alcohol consumption and HIV infection were important co-factors.
  • [MeSH-major] Alcohol Drinking. HIV Infections / mortality. Hepatitis B, Chronic / mortality. Hepatitis C, Chronic / mortality


32. Rota M, Bellocco R, Scotti L, Tramacere I, Jenab M, Corrao G, La Vecchia C, Boffetta P, Bagnardi V: Random-effects meta-regression models for studying nonlinear dose-response relationship, with an application to alcohol and esophageal squamous cell carcinoma. Stat Med; 2010 Nov 20;29(26):2679-87
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  • [Title] Random-effects meta-regression models for studying nonlinear dose-response relationship, with an application to alcohol and esophageal squamous cell carcinoma.
  • This method is illustrated by a meta-analysis aimed to estimate the shape of the dose-response curve between alcohol consumption and esophageal squamous cell carcinoma (SCC).
  • The meta-analysis provided evidence that ethanol intake was related to esophageal SCC risk in a nonlinear fashion.
  • High levels of alcohol consumption resulted in a substantial risk of esophageal SCC as compared to nondrinkers.
  • However, a statistically significant excess risk for moderate and intermediate doses of alcohol was also observed, with no evidence of a threshold effect.
  • [MeSH-major] Alcohol Drinking / adverse effects. Carcinoma, Squamous Cell / epidemiology. Dose-Response Relationship, Drug. Esophageal Neoplasms / epidemiology. Regression Analysis

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  • [Copyright] Copyright © 2010 John Wiley & Sons, Ltd.
  • (PMID = 20809481.001).
  • [ISSN] 1097-0258
  • [Journal-full-title] Statistics in medicine
  • [ISO-abbreviation] Stat Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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33. Morita M, Kumashiro R, Kubo N, Nakashima Y, Yoshida R, Yoshinaga K, Saeki H, Emi Y, Kakeji Y, Sakaguchi Y, Toh Y, Maehara Y: Alcohol drinking, cigarette smoking, and the development of squamous cell carcinoma of the esophagus: epidemiology, clinical findings, and prevention. Int J Clin Oncol; 2010 Apr;15(2):126-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alcohol drinking, cigarette smoking, and the development of squamous cell carcinoma of the esophagus: epidemiology, clinical findings, and prevention.
  • Both cigarette smoking and alcohol drinking are well-established risk factors for esophageal squamous cell carcinoma (ESCC), and the relationship of dose to cancer risk has already been described.
  • Heavy smoking and heavy drinking are closely related to such multicentric carcinogenesis events in the upper aerodigestive tract (UADT), including the esophagus and head andneck region.
  • Patients with inactive ALDH2, in whom facial flushing is usually observed after the drinking of alcohol, are at high risk for ESCC as well as multiple UADT cancers.
  • For the early detection of the disease, effective follow up using endoscopy with Lugol staining or narrow band imaging endoscopy is strongly recommended for high-risk populations, such as smokers, heavy drinkers, people with experience of flushing after the drinking of alcohol, and patients with UADT cancer.
  • [MeSH-major] Alcohol Drinking / adverse effects. Carcinoma, Squamous Cell / etiology. Esophageal Neoplasms / etiology. Smoking / adverse effects

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  • (PMID = 20224884.001).
  • [ISSN] 1437-7772
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 1.2.1.3 / ALDH2 protein, human; EC 1.2.1.3 / Aldehyde Dehydrogenase
  • [Number-of-references] 74
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34. Klussmann JP, Mooren JJ, Lehnen M, Claessen SM, Stenner M, Huebbers CU, Weissenborn SJ, Wedemeyer I, Preuss SF, Straetmans JM, Manni JJ, Hopman AH, Speel EJ: Genetic signatures of HPV-related and unrelated oropharyngeal carcinoma and their prognostic implications. Clin Cancer Res; 2009 Mar 1;15(5):1779-86

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic signatures of HPV-related and unrelated oropharyngeal carcinoma and their prognostic implications.
  • In comparison with HPV-related OSCC, the HPV-negative tumors harbored: (a) a higher number of chromosomal alterations and amplifications (P=0.03 and 0.039, respectively);.
  • Survival analysis revealed a significantly better disease-free survival for HPV-related OSCC (P=0.02), whereas chromosome amplification was an unfavorable prognostic indicator for disease-free and overall survival (P=0.01 and 0.05, respectively).
  • Interestingly, 16q loss, predominantly identified in HPV-related OSCC, was a strong indicator of favorable outcome (overall survival, P=0.008; disease-free survival, P=0.01) and none of these patients had a tumor recurrence.
  • CONCLUSIONS: Genetic signatures of HPV-related and HPV-unrelated OSCC are different and most likely underlie differences in tumor development and progression.
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Gene Expression Profiling. Human papillomavirus 16 / genetics. Oropharyngeal Neoplasms / genetics. Oropharyngeal Neoplasms / metabolism
  • [MeSH-minor] Alcohol Drinking. Chromosome Aberrations. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 3 / genetics. Comparative Genomic Hybridization. Feasibility Studies. Gene Dosage. Humans. Immunoenzyme Techniques. In Situ Hybridization, Fluorescence. Neoplasm Staging. Papillomavirus Infections / genetics. Papillomavirus Infections / metabolism. Papillomavirus Infections / virology. Polymerase Chain Reaction. Prognosis. Risk Factors. Smoking. Survival Rate

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  • (PMID = 19223504.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16
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35. Seitz HK, Stickel F: Risk factors and mechanisms of hepatocarcinogenesis with special emphasis on alcohol and oxidative stress. Biol Chem; 2006 Apr;387(4):349-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk factors and mechanisms of hepatocarcinogenesis with special emphasis on alcohol and oxidative stress.
  • Established risk factors are chronic hepatitis B and C infection, chronic heavy alcohol consumption, obesity and type 2 diabetes, tobacco use, use of oral contraceptives, and aflatoxin-contaminated food.
  • In Western countries, attributable risks are highest for cirrhosis due to chronic alcohol abuse and viral hepatitis B and C infection.
  • An important mechanism implicated in alcohol-related hepatocarcinogenesis is oxidative stress from alcohol metabolism, inflammation, and increased iron storage.
  • Furthermore, alcohol impairs the antioxidant defense system, resulting in mitochondrial damage and apoptosis.
  • Chronic alcohol exposure elicits hepatocyte hyperregeneration due to the activation of survival factors and interference with retinoid metabolism.
  • Finally, chronic alcohol abuse interferes with methyl group transfer and may thereby alter gene expression.
  • [MeSH-major] Alcohol Drinking. Carcinoma, Hepatocellular / etiology. Liver Neoplasms / etiology. Oxidative Stress

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  • (PMID = 16606331.001).
  • [ISSN] 1431-6730
  • [Journal-full-title] Biological chemistry
  • [ISO-abbreviation] Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Retinoids; 3K9958V90M / Ethanol; E1UOL152H7 / Iron; EC 1.14.13.- / Cytochrome P-450 CYP2E1
  • [Number-of-references] 140
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36. Pekow JR, Bhan AK, Zheng H, Chung RT: Hepatic steatosis is associated with increased frequency of hepatocellular carcinoma in patients with hepatitis C-related cirrhosis. Cancer; 2007 Jun 15;109(12):2490-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hepatic steatosis is associated with increased frequency of hepatocellular carcinoma in patients with hepatitis C-related cirrhosis.
  • Previous studies have suggested that hepatic steatosis is a risk factor for hepatocellular carcinoma in patients with hepatitis C virus (HCV) infection.
  • The authors sought to determine whether hepatic steatosis is associated with hepatocellular carcinoma (HCC) in a cohort of patients with hepatitis C-related cirrhosis.
  • Steatosis, age, sex, body mass index, HCV RNA, HCV genotype, Model for End-Stage Liver Disease (MELD) score, chronic alcohol use, and diabetes were examined in univariate and multivariate analyses for association with HCC.
  • CONCLUSIONS: In patients with HCV-related cirrhosis, the presence of hepatic steatosis is independently associated with the development of hepatocellular carcinoma.
  • [MeSH-major] Carcinoma, Hepatocellular / etiology. Fatty Liver / complications. Hepatitis C, Chronic / virology. Liver Cirrhosis / virology. Liver Neoplasms / etiology

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  • [Copyright] Copyright 2007 American Cancer Society.
  • (PMID = 17487861.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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37. Grossi S, Sumberaz A, Gosmar M, Mattioli F, Testino G, Martelli A: DNA damage in peripheral blood lymphocytes of patients with cirrhosis related to alcohol abuse or to hepatitis B and C viruses. Eur J Gastroenterol Hepatol; 2008 Jan;20(1):22-5
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  • [Title] DNA damage in peripheral blood lymphocytes of patients with cirrhosis related to alcohol abuse or to hepatitis B and C viruses.
  • BACKGROUND: Both alcohol abuse and hepatitis B or C virus infections are implicated in the development of hepatocellular carcinoma, but it is still controversial whether the pathogenetic mechanism is epigenetic or genotoxic.
  • AIM: Considering that alcohol promotes the generation of reactive oxygen species and both viruses infect peripheral lymphocytes, in this study we investigated the occurrence of DNA fragmentation in peripheral blood lymphocytes from patients with alcoholic cirrhosis and from patients with cirrhosis related to B and C viruses, and analyzed the correlation between the degree of DNA fragmentation and the Child-Pugh score used to assess the degree of hepatic insufficiency.
  • CONCLUSION: The occurrence of DNA fragmentation in peripheral blood lymphocytes reflects a direct genotoxic effect of either alcohol or HBV and HCV and suggests that the same genotoxic effect may operate in the liver and contribute to hepatocarcinogenesis.
  • [MeSH-minor] Carcinoma, Hepatocellular / genetics. Comet Assay / methods. Female. Humans. Liver Neoplasms / genetics. Male. Middle Aged. Oxidative Stress / immunology

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  • (PMID = 18090985.001).
  • [ISSN] 0954-691X
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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38. Brechot C, Kremsdorf D, Soussan P, Pineau P, Dejean A, Paterlini-Brechot P, Tiollais P: Hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC): molecular mechanisms and novel paradigms. Pathol Biol (Paris); 2010 Aug;58(4):278-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC): molecular mechanisms and novel paradigms.
  • Chronic hepatitis B (HBV) infection is a major risk factor for hepatocellular carcinoma (HCC).
  • This review will summarise the current knowledge on the mechanisms involved in HBV-related liver carcinogenesis.
  • It will show in particular how viruses can be viewed as tools to discover and dissect new cellular pathways involved in cancer development and emphasize the potential synergistic effects between HBV and hepatitis C virus (HCV), as well as between viral infections and other environmental factors, such as alcohol.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / virology. Hepatitis B, Chronic / complications. Liver Neoplasms / genetics. Liver Neoplasms / virology

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  • [Copyright] Copyright 2010. Published by Elsevier SAS.
  • (PMID = 20667665.001).
  • [ISSN] 1768-3114
  • [Journal-full-title] Pathologie-biologie
  • [ISO-abbreviation] Pathol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Hepatitis B Surface Antigens; 0 / Trans-Activators; 0 / hepatitis B virus X protein
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39. Miki D, Aikata H, Uka K, Saneto H, Kawaoka T, Azakami T, Takaki S, Jeong SC, Imamura M, Kawakami Y, Takahashi S, Itamoto T, Asahara T, Arihiro K, Chayama K: Clinicopathological features of elderly patients with hepatitis C virus-related hepatocellular carcinoma. J Gastroenterol; 2008;43(7):550-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinicopathological features of elderly patients with hepatitis C virus-related hepatocellular carcinoma.
  • BACKGROUND: It is well known that the incidence of hepatocellular carcinoma (HCC) in patients with hepatitis C virus (HCV) correlates with progression of liver fibrosis.
  • The aim of this study was to elucidate the clinicopathological features of elderly patients with HCV-related HCC.
  • Next, we selected pure HCV-related HCC patients by excluding the patients with other probable factors for hepatocarcinogenesis (anti-HBc, interferon therapy, and alcohol) and compared the two groups again.
  • RESULTS: Higher platelet count, lower male/female ratio, lower rate of habitual alcohol consumption, and better Child-Pugh class were recognized in the elderly group thant the younger group, statistically.
  • After selection of pure HCV-related HCC patients, in a stepwise multi variate analysis, male sex and platelet count <10 x 10(4)/mm3 were significant variables associated with age <70.
  • In addition to fibrosis, aging could be a factor affecting HCV-related hepatocarcinogenesis.
  • [MeSH-major] Carcinoma, Hepatocellular / virology. Hepatitis C, Chronic / complications. Liver Neoplasms / virology

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  • (PMID = 18648742.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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40. Sun L, König IR, Jacobs A, Seitz HK, Junghanns K, Wagner T, Ludwig D, Jacrobs A, Homann N: Mean corpuscular volume and ADH1C genotype in white patients with alcohol-associated diseases. Alcohol Clin Exp Res; 2005 May;29(5):788-93

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mean corpuscular volume and ADH1C genotype in white patients with alcohol-associated diseases.
  • BACKGROUND: Alcohol abuse is associated with several gastrointestinal diseases, such as esophageal carcinoma, chronic alcoholic pancreatitis, and liver cirrhosis.
  • Increased mean corpuscular volume (MCV) has been recognized as a biomarker for alcohol abuse and heavy drinkers.
  • Recent studies from Japan revealed that macrocytosis is related to ALDH-2/2 genotype, leading to increased acetaldehyde accumulation.
  • Therefore, the aim of the current study was to investigate possible associations of MCV value with polymorphisms of ADH1C in white patients with alcohol-associated esophageal carcinoma, chronic alcoholic pancreatitis, and alcoholic cirrhosis as well as in heavy drinkers without organ damage.
  • METHODS: In this study, a total of 510 alcoholic patients were enrolled with esophageal cancer (n = 98), chronic pancreatitis (n = 98), alcoholic liver cirrhosis (n = 151), and alcohol abuse without gastrointestinal disease (n = 163).
  • RESULTS: In univariate analysis, higher alcohol consumption was associated with increased MCV.
  • In multiple linear regression analysis, after adjustment for age and smoking, higher alcohol consumption and female sex were independently associated with higher MCV values.
  • No other variables, including which alcohol-associated disease the patient had, had an independent effect.
  • The role of ADH1C polymorphism in increasing MCV and the potential use of MCV as a marker for esophageal carcinoma are still pending.
  • [MeSH-major] Alcohol Dehydrogenase / genetics. Alcohol-Induced Disorders / blood. Alcohol-Induced Disorders / genetics. Erythrocyte Indices / genetics

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  • (PMID = 15897724.001).
  • [ISSN] 0145-6008
  • [Journal-full-title] Alcoholism, clinical and experimental research
  • [ISO-abbreviation] Alcohol. Clin. Exp. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-49-2 / DNA; EC 1.1.1.1 / ADH1C protein, human; EC 1.1.1.1 / Alcohol Dehydrogenase
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41. Gitto S, Micco L, Conti F, Andreone P, Bernardi M: Alcohol and viral hepatitis: a mini-review. Dig Liver Dis; 2009 Jan;41(1):67-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alcohol and viral hepatitis: a mini-review.
  • Due to their high prevalence in the general population, alcohol use and abuse can be associated with hepatitis B and C virus infections and it has been demonstrated that alcohol plays a role as a co-morbid factor in the development of liver disease.
  • There is evidence that alcohol abuse accelerates the progression of liver fibrosis and affects the survival of patients with chronic hepatitis C.
  • The mechanism by which alcohol worsens hepatitis C virus-related liver disease has not been fully clarified, but enhanced viral replication, increased oxidative stress, cytotoxicity and impairment of immune response could play a relevant role.
  • Alcohol abuse also seems to reduce both sensitivity to interferon and adherence to treatment.
  • However, more studies are warranted to improve our knowledge about the interaction between alcohol intake and hepatitis B virus infection.
  • In conclusion alcohol abuse is associated with an accelerated progression of liver injury, leading to an earlier development of cirrhosis, higher incidence of hepatocellular carcinoma, and higher mortality.
  • [MeSH-minor] Antiviral Agents / therapeutic use. Carcinoma, Hepatocellular / epidemiology. Comorbidity. Disease Progression. Ethanol / pharmacology. Ethanol / poisoning. Humans. Interferons / therapeutic use. Liver Cirrhosis / chemically induced. Liver Cirrhosis / physiopathology. Liver Cirrhosis / virology. Oxidative Stress / drug effects. Treatment Outcome

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  • (PMID = 18602355.001).
  • [ISSN] 1878-3562
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antiviral Agents; 3K9958V90M / Ethanol; 9008-11-1 / Interferons
  • [Number-of-references] 45
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42. Siegmund SV, Singer MV: [Effects of alcohol on the upper gastrointestinal tract and the pancreas--an up-to-date overview]. Z Gastroenterol; 2005 Aug;43(8):723-36
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  • [Title] [Effects of alcohol on the upper gastrointestinal tract and the pancreas--an up-to-date overview].
  • The oesophagus, stomach and pancreas are primary target organs for ethanol-related diseases.
  • Chronic consumption of alcohol causes a significant increase in the risk for squamous carcinoma of the oesophagus.
  • All of these effects are mainly caused by direct contact of alcohol or its metabolite acetaldehyde with the mucosa.
  • In the exocrine pancreas, alcohol induces secretory alterations that are mainly affected by the manner and duration of alcohol exposure, the additional administration of food, the type of beverage or the basal secretory state of the gland.
  • Chronic alcohol abuse may cause chronic alcoholic pancreatitis after recurrent subclinical inflammatory episodes.
  • Future research needs to define the exact molecular mechanisms and the role of different genetic predispositions for alcohol-induced diseases as well as the effects of the non-alcoholic components of alcoholic beverages.
  • [MeSH-minor] Acute Disease. Carcinoma, Squamous Cell / etiology. Esophageal Neoplasms / etiology. Gastric Acid / secretion. Gastritis / etiology. Gastrointestinal Motility / drug effects. Genetic Predisposition to Disease. Humans. Risk Factors. Time Factors

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  • (PMID = 16088770.001).
  • [ISSN] 0044-2771
  • [Journal-full-title] Zeitschrift für Gastroenterologie
  • [ISO-abbreviation] Z Gastroenterol
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 3K9958V90M / Ethanol
  • [Number-of-references] 192
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43. Saladi RN, Nektalova T, Fox JL: Induction of skin carcinogenicity by alcohol and ultraviolet light. Clin Exp Dermatol; 2010 Jan;35(1):7-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of skin carcinogenicity by alcohol and ultraviolet light.
  • In western societies, casual consumption of alcohol during such outdoor activities as barbecuing and sunbathing is common.
  • The current literature shows that alcohol drinkers have increased episodes of sunburn and a higher prevalence of skin cancer.
  • Moreover, recent evidence suggests that the combination of subcarcinogenic (minimal) ultraviolet (UV) exposure with other behavioural, environmental and xenobiotic factors has resulted in increased incidents of skin-related health problems that also result in skin-cancer formation.
  • We hypothesize that the combination of alcohol consumption with UV radiation can potentiate the skin carcinogenic effects through the intermediate biproducts or metabolites of alcohol, which serve as the photosensitizers, consequently enhancing the cellular damage.
  • We have proposed a mechanism that explains the combined alcohol-UV radiation carcinogenicity and its potential involvement in enhancing skin damage in the multistep skin carcinogenesis process.
  • Previous literature has explored this mutual effect but no studies have definitively ascribed the reasons for increased skin cancer prevalence among alcohol drinkers.
  • [MeSH-major] Alcohol Drinking / adverse effects. Carcinoma, Basal Cell / etiology. Carcinoma, Squamous Cell / etiology. Neoplasms, Radiation-Induced / etiology. Sunburn / complications. Ultraviolet Rays / adverse effects

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  • [CommentIn] Clin Exp Dermatol. 2010 Dec;35(8):923-5 [20500519.001]
  • (PMID = 19778305.001).
  • [ISSN] 1365-2230
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 34
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44. Potash AE, Karnell LH, Christensen AJ, Vander Weg MW, Funk GF: Continued alcohol use in patients with head and neck cancer. Head Neck; 2010 Jul;32(7):905-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Continued alcohol use in patients with head and neck cancer.
  • BACKGROUND: The effect of posttreatment alcohol consumption on health-related quality of life (QOL) and factors predicting overall QOL and continued alcohol consumption were examined in patients with head and neck cancer.
  • METHODS: Self-reported alcohol use and abuse 1 year after diagnosis was analyzed.
  • Oral function was the only predictor of 12-month alcohol use.
  • Alcohol consumption was not associated with QOL, but was associated with better oral function, which in turn predicted better QOL.
  • Alcohol consumption itself does not improve QOL in this population, and these patients should be counseled regarding detrimental effects of continued drinking after treatment.
  • [MeSH-major] Alcohol Drinking / epidemiology. Alcoholism / epidemiology. Carcinoma / psychology. Head and Neck Neoplasms / psychology. Quality of Life

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  • [Copyright] (c) 2009 Wiley Periodicals, Inc.
  • (PMID = 19918984.001).
  • [ISSN] 1097-0347
  • [Journal-full-title] Head & neck
  • [ISO-abbreviation] Head Neck
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106908
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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45. Crous-Bou M, Porta M, López T, Jariod M, Malats N, Morales E, Guarner L, Rifà J, Carrato A, Real FX, PANKRAS II Study Group: Lifetime history of alcohol consumption and K-ras mutations in pancreatic ductal adenocarcinoma. Environ Mol Mutagen; 2009 Jun;50(5):421-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lifetime history of alcohol consumption and K-ras mutations in pancreatic ductal adenocarcinoma.
  • BACKGROUND: In pancreatic ductal adenocarcinoma (PDA), evidence on the etiopathogenic role of alcohol consumption in the occurrence of K-ras mutations is scant, and the role of alcohol in pancreatic carcinogenesis is not well established.
  • We analyzed the relation between lifetime consumption of alcohol and mutations in codon 12 of the K-ras oncogene in patients with PDA.
  • METHODS: Incident cases of PDA were prospectively identified and interviewed face-to-face during hospital admission about lifetime alcohol consumption and other lifestyle factors.
  • Total grams of alcohol and years of consumption were higher in mutated than in wild-type cases: the ORa for lifetime alcohol consumption over 507,499 g was 3.35 (95% CI: 0.81-13.88); and for more than 40 years of alcohol consumption it was 4.47 (95% CI: 1.05-19.02).
  • Age at onset of alcohol consumption and years of abstinence were also associated with the presence of K-ras mutations.
  • There were no significant differences in alcohol dependency.
  • CONCLUSIONS: Alcohol consumption is weakly associated with an increased risk of having a K-ras mutated PDA.
  • To confirm or to refute the hypothesis that ethanol, acetaldehyde or other alcohol-related substances might influence the acquisition or persistence of K-ras mutations in the pancreatic epithelium, large and unselected studies are warranted.
  • [MeSH-major] Alcohol Drinking / adverse effects. Carcinoma, Pancreatic Ductal / genetics. Genes, ras / genetics

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  • (PMID = 19326463.001).
  • [ISSN] 1098-2280
  • [Journal-full-title] Environmental and molecular mutagenesis
  • [ISO-abbreviation] Environ. Mol. Mutagen.
  • [Language] eng
  • [Grant] United States / PHS HHS / / 04-C-N272
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon
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46. El-Serag HB: Epidemiology of hepatocellular carcinoma in USA. Hepatol Res; 2007 Sep;37 Suppl 2:S88-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epidemiology of hepatocellular carcinoma in USA.
  • Hepatocellular carcinoma (HCC) is increasing in frequency the USA.
  • There are striking differences in the incidence of HCC related to age, gender, race, and geographic region.
  • Hepatitis C virus (HCV) infection acquired 2-4 decades ago explains at least half of the observed increase in HCC; HCV-related HCC is likely tocontinue to increase for the next decade.
  • A variable but significant proportion of cases (15-50%) do not have evidence for the risk factors of either viral hepatitis or heavy alcohol consumption.

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  • (PMID = 17877502.001).
  • [ISSN] 1386-6346
  • [Journal-full-title] Hepatology research : the official journal of the Japan Society of Hepatology
  • [ISO-abbreviation] Hepatol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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47. Suzuki T, Matsuo K, Hasegawa Y, Hiraki A, Wakai K, Hirose K, Saito T, Sato S, Ueda R, Tajima K: One-carbon metabolism-related gene polymorphisms and risk of head and neck squamous cell carcinoma: case-control study. Cancer Sci; 2007 Sep;98(9):1439-46
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  • [Title] One-carbon metabolism-related gene polymorphisms and risk of head and neck squamous cell carcinoma: case-control study.
  • Low consumption of vegetables and fruits, which leads to insufficient folate intake, is associated with increased risk of several types of cancer, including head and neck squamous cell carcinoma (HNSCC).
  • The results suggest that there may be interactions between one-carbon metabolism-related polymorphisms and alcohol drinking for HNSCC risk.
  • [MeSH-major] Carbon / metabolism. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Genetic Predisposition to Disease. Head and Neck Neoplasms / genetics. Head and Neck Neoplasms / metabolism. Polymorphism, Genetic
  • [MeSH-minor] 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase / genetics. Aged. Alcohol Drinking / genetics. Alcohol Drinking / metabolism. Case-Control Studies. Diet. Female. Ferredoxin-NADP Reductase / genetics. Folic Acid / administration & dosage. Humans. Male. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Middle Aged. Random Allocation. Risk Factors. Thymidylate Synthase / genetics

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  • (PMID = 17596206.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 7440-44-0 / Carbon; 935E97BOY8 / Folic Acid; EC 1.18.1.- / methionine synthase reductase; EC 1.18.1.2 / Ferredoxin-NADP Reductase; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2); EC 2.1.1.13 / 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; EC 2.1.1.45 / Thymidylate Synthase
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48. Chen JD, Yang HI, Iloeje UH, You SL, Lu SN, Wang LY, Su J, Sun CA, Liaw YF, Chen CJ, Risk Evaluation of Viral Load Elevation and Associated Liver Disease/Cancer in HBV (REVEAL-HBV) Study Group: Carriers of inactive hepatitis B virus are still at risk for hepatocellular carcinoma and liver-related death. Gastroenterology; 2010 May;138(5):1747-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Carriers of inactive hepatitis B virus are still at risk for hepatocellular carcinoma and liver-related death.
  • METHODS: Participants in the Risk Evaluation of Viral Load Elevation and Associated Liver Disease/Cancer-Hepatitis B Virus (REVEAL-HBV) study who were seronegative for hepatitis B e antigen; had serum levels of HBV DNA <10,000 copies/mL; and did not have cirrhosis, hepatocellular carcinoma, or increased serum levels of alanine aminotransferase were classified as carriers of inactive HBV (n = 1932).
  • Liver-related death and new cases of hepatocellular carcinoma were ascertained through computerized data linkage with National Cancer Registry and Death Certification profiles.
  • Annual incidence rates of hepatocellular carcinoma and liver-related death were 0.06% and 0.04%, respectively, for inactive HBV carriers; rates were 0.02%, and 0.02% for controls, respectively.
  • The multivariate-adjusted hazard ratios for carriers of inactive HBV, compared to controls, were 4.6 (95% confidence interval: 2.5-8.3) for hepatocellular carcinoma and 2.1 (95% confidence interval: 1.1-4.1) for liver-related death.
  • Older age and alcohol drinking habits were independent predictors of risk for carriers of inactive HBV to develop hepatocellular carcinoma.
  • CONCLUSIONS: Carriers of inactive HBV have a substantial risk of hepatocellular carcinoma and liver-related death compared with individuals not infected with HBV.
  • [MeSH-major] Carcinoma, Hepatocellular / virology. Carrier State. Hepatitis B / diagnosis. Hepatitis B virus / pathogenicity. Liver Neoplasms / virology. Virus Inactivation
  • [MeSH-minor] Adult. Age Factors. Alcohol Drinking. Case-Control Studies. DNA, Viral / blood. Female. Hepatitis B Surface Antigens / blood. Hepatitis B e Antigens / blood. Hepatitis C Antibodies / blood. Humans. Incidence. Male. Middle Aged. Proportional Hazards Models. Registries. Risk Assessment. Risk Factors. Taiwan / epidemiology. Time Factors. Viral Load

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  • [Copyright] Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20114048.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Hepatitis B Surface Antigens; 0 / Hepatitis B e Antigens; 0 / Hepatitis C Antibodies
  • [Investigator] Hsieh C; Lee HS; Yang PM; Chen CH; Huang SP; Jan CF; Chen TH; Wu MH; Chen SY; Chu KE; Ho SC; Lu TG; Wu WP; Ou TY; Lin CG; Shih KC; Chung WS; Li C; Chen CC; How WC
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49. Ndububa DA, Ojo OS, Adetiloye VA, Aladegbaiye AO, Adebayo RA, Adekanle O: The contribution of alcohol to chronic liver disease in patients from South-west Nigeria. Niger J Clin Pract; 2010 Dec;13(4):360-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The contribution of alcohol to chronic liver disease in patients from South-west Nigeria.
  • OBJECTIVE: This study aimed at determining the level and type of alcohol consumed by patients diagnosed with chronic liver disease (CLD) and, hence, the extent to which alcohol may have contributed to the development of the condition.
  • Alcohol consumption was considered significant if a patient took >50 g/day for > 10 years.
  • Fifty-one (35.2%) patients, all males, drank significant alcohol while consumption was not significant in 43 (29.6%) patients.
  • Alcohol was not consumed at all by 51 (35.2%) patients made up of 18 males (35.3%) and 33 females (64.7%).
  • Beer was the commonest form of alcohol consumed (70.2%) followed by palm wine (50%) and locally-brewed gin (20.2%).
  • The diagnoses made were liver cirrhosis [LC] (60, 41.38%), chronic hepatitis [CH] (54, 37.20%), hepatocellular carcinoma [HCC] (23, 15.86%), alcoholic liver disease [ALD] (6, 4.14%) and non-alcoholic fatty liver disease [NAFLD] (2, 1.38%).
  • The liver disease spectrum did not differ between the patients who drank significant alcohol and those who did not.
  • However, the proportion of LC/HCC cases increased relative to CH with increasing age and consumption of alcohol.
  • CONCLUSIONS: The proportion of CLD directly attributable to alcohol (i.e.
  • However, the burden of LC and HCC is directly related to age and the amount of alcohol consumed and the determinants of alcohol abuse are gender and affluence.
  • [MeSH-major] Alcohol Drinking / adverse effects. Liver Diseases, Alcoholic / diagnosis. Liver Diseases, Alcoholic / epidemiology

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  • (PMID = 21220846.001).
  • [ISSN] 1119-3077
  • [Journal-full-title] Nigerian journal of clinical practice
  • [ISO-abbreviation] Niger J Clin Pract
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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50. Homann N, Stickel F, König IR, Jacobs A, Junghanns K, Benesova M, Schuppan D, Himsel S, Zuber-Jerger I, Hellerbrand C, Ludwig D, Caselmann WH, Seitz HK: Alcohol dehydrogenase 1C*1 allele is a genetic marker for alcohol-associated cancer in heavy drinkers. Int J Cancer; 2006 Apr 15;118(8):1998-2002
MedlinePlus Health Information. consumer health - Alcohol.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alcohol dehydrogenase 1C*1 allele is a genetic marker for alcohol-associated cancer in heavy drinkers.
  • Chronic alcohol consumption is associated with an increased risk for upper aerodigestive tract cancer and hepatocellular carcinoma.
  • Increased acetaldehyde production via alcohol dehydrogenase (ADH) has been implicated in the pathogenesis.
  • So far, the association between the ADH1C*1 allele and alcohol-related cancers among heavy drinkers is controversial.
  • ADH1C genotypes were determined by polymerase chain reaction and restriction fragment length polymorphism in a total of 818 patients with alcohol-associated esophageal (n=123), head and neck (n=84) and hepatocellular cancer (n=86) as well as in patients with alcoholic pancreatitis (n=117), alcoholic liver cirrhosis (n=217), combined liver cirrhosis and pancreatitis (n=17) and in alcoholics without gastrointestinal organ damage (n=174).
  • The ADH1C*1 allele and genotype ADH1C*1/1 were significantly more frequent in patients with alcohol-related cancers than that in individuals with nonmalignant alcohol-related organ damage.
  • Using multivariate analysis, ADH1C*1 allele frequency and rate of homozygosity were significantly associated with an increased risk for alcohol-related cancers (p<0.001 in all instances).
  • The data identify genotype ADH1C*1/1 as an independent risk factor for the development of alcohol-associated tumors among heavy drinkers, indicating a genetic predisposition of individuals carrying this genotype.
  • [MeSH-major] Alcohol Dehydrogenase / genetics. Alcohol Dehydrogenase / metabolism. Alcohol Drinking / adverse effects. Alcohol Drinking / genetics. Genetic Markers. Genetic Predisposition to Disease

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16287084.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; EC 1.1.1.1 / Alcohol Dehydrogenase
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51. Schacherer D, Schoelmerich J, Zuber-Jerger I: [The diagnostic approach to hepatocellular carcinoma]. Z Gastroenterol; 2007 Oct;45(10):1067-74
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  • [Title] [The diagnostic approach to hepatocellular carcinoma].
  • Risk factors and symptoms of hepatocellular carcinoma (HCC): The main risk factors of HCC include infection with hepatitis B or C virus, as well as alcohol consumption.
  • Among the various staging systems used in the context of HCC, the Barcelona-Clinic-Liver-Cancer (BCLC) staging system is currently the only staging system that takes into account tumour stage, liver function, physical status and cancer-related symptoms.
  • [MeSH-major] Carcinoma, Hepatocellular / diagnosis. Liver Neoplasms / diagnosis

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  • (PMID = 17924305.001).
  • [ISSN] 0044-2771
  • [Journal-full-title] Zeitschrift für Gastroenterologie
  • [ISO-abbreviation] Z Gastroenterol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 49
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52. Kim SO, Choi YH: The ethyl alcohol extract of Hizikia fusiforme inhibits matrix metalloproteinase activity and regulates tight junction related protein expression in Hep3B human hepatocarcinoma cells. J Med Food; 2010 Feb;13(1):31-8
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  • [Title] The ethyl alcohol extract of Hizikia fusiforme inhibits matrix metalloproteinase activity and regulates tight junction related protein expression in Hep3B human hepatocarcinoma cells.
  • We tested the correlation between the tightness of tight junctions (TJs) and the anti-invasive activity of the ethyl alcohol extract of Hizikia fusiforme (EHF) in Hep3B human hepatocarcinoma cells.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Carcinoma, Hepatocellular / drug therapy. Liver Neoplasms / drug therapy. Matrix Metalloproteinases / metabolism. Phaeophyta. Plant Extracts / therapeutic use. Tight Junctions / drug effects

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  • (PMID = 20136433.001).
  • [ISSN] 1557-7600
  • [Journal-full-title] Journal of medicinal food
  • [ISO-abbreviation] J Med Food
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Cadherins; 0 / Claudins; 0 / Plant Extracts; 0 / RNA, Messenger; 0 / Thrombospondin 1; EC 2.7.10.1 / Receptor, IGF Type 1; EC 3.4.24.- / Matrix Metalloproteinases
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53. Cui R, Kamatani Y, Takahashi A, Usami M, Hosono N, Kawaguchi T, Tsunoda T, Kamatani N, Kubo M, Nakamura Y, Matsuda K: Functional variants in ADH1B and ALDH2 coupled with alcohol and smoking synergistically enhance esophageal cancer risk. Gastroenterology; 2009 Nov;137(5):1768-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional variants in ADH1B and ALDH2 coupled with alcohol and smoking synergistically enhance esophageal cancer risk.
  • BACKGROUND & AIMS: Esophageal squamous cell carcinoma (ESCC) is prevalent among Asian populations, with marked regional variations in incidence and mortality.
  • Multiple logistic regression analysis revealed SNP rs671, rs1229984, alcohol drinking, and smoking as the independent risk factors for ESCC (odds ratios of 1.66, 1.85, 1.92, and 1.79, respectively).
  • Moreover, individuals who had both genetic and lifestyle-related risk factors had a nearly 190 times higher risk of ESCC than those who had neither of these.
  • CONCLUSIONS: We found 2 known functional variants involved in the metabolism of alcohol and tobacco by-products as the most significant risk factors for the development of ESCC in a Japanese population.
  • [MeSH-major] Alcohol Dehydrogenase / genetics. Alcohol Drinking. Aldehyde Dehydrogenase / genetics. Carcinoma, Squamous Cell / genetics. Esophageal Neoplasms / genetics. Polymorphism, Single Nucleotide / genetics. Smoking

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  • [CommentIn] Gastroenterology. 2009 Nov;137(5):1573-6 [19789091.001]
  • (PMID = 19698717.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.1 / ADH1B protein, human; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / ALDH2 protein, human; EC 1.2.1.3 / Aldehyde Dehydrogenase
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54. Schütte K, Bornschein J, Malfertheiner P: Hepatocellular carcinoma--epidemiological trends and risk factors. Dig Dis; 2009;27(2):80-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hepatocellular carcinoma--epidemiological trends and risk factors.
  • Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related deaths worldwide with about 600,000 patients dying from the disease annually.
  • In regions with a high incidence the majority of cases are related to HBV and HCV hepatitis.
  • In developed countries, in addition to virus-related HCC, high consumption of alcohol as well as non-alcoholic fatty liver disease often in the context of metabolic syndromes are the prevalent causes.
  • Improvement in clinical management of patients with liver cirrhosis and the control of related complications are the key for the rising incidence of HCC.
  • [MeSH-major] Carcinoma, Hepatocellular / epidemiology. Hepatitis / complications. Liver Neoplasms / epidemiology
  • [MeSH-minor] Aflatoxins / adverse effects. Alcohol Drinking / adverse effects. Coffee. Diabetes Complications. Diet / adverse effects. Fatty Liver / complications. Female. Hemochromatosis / complications. Humans. Incidence. Male. Risk Factors. alpha 1-Antitrypsin Deficiency / complications

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19546545.001).
  • [ISSN] 1421-9875
  • [Journal-full-title] Digestive diseases (Basel, Switzerland)
  • [ISO-abbreviation] Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Aflatoxins; 0 / Coffee
  • [Number-of-references] 140
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55. Hu L, Liu J, Chen X, Zhang Y, Liu L, Zhu J, Chen J, Shen H, Qiang F, Hu Z: CTLA-4 gene polymorphism +49 A/G contributes to genetic susceptibility to two infection-related cancers-hepatocellular carcinoma and cervical cancer. Hum Immunol; 2010 Sep;71(9):888-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CTLA-4 gene polymorphism +49 A/G contributes to genetic susceptibility to two infection-related cancers-hepatocellular carcinoma and cervical cancer.
  • In the present study, we expanded our study to two infection-related cancers, namely, hepatocellular carcinoma (HCC) and cervical cancer.
  • [MeSH-major] Antigens, CD / genetics. Carcinoma, Hepatocellular / genetics. Genetic Predisposition to Disease / genetics. Liver Neoplasms / genetics. Polymorphism, Single Nucleotide / genetics. Uterine Cervical Neoplasms / genetics
  • [MeSH-minor] Adult. Age Factors. Aged. Alcohol Drinking / adverse effects. Alcohol Drinking / epidemiology. CTLA-4 Antigen. Carcinoma, Squamous Cell / complications. China. Female. Gene Frequency / genetics. Genotype. Hepatitis B / complications. Hepatitis B / epidemiology. Hepatitis C / complications. Hepatitis C / epidemiology. Humans. Male. Menarche. Middle Aged. Parity. Parturition. Pregnancy. Premenopause. Risk Factors. Smoking / adverse effects. Smoking / epidemiology

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  • [Copyright] Copyright 2010 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20538028.001).
  • [ISSN] 1879-1166
  • [Journal-full-title] Human immunology
  • [ISO-abbreviation] Hum. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human
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56. Polesel J, Talamini R, Montella M, Maso LD, Crovatto M, Parpinel M, Izzo F, Tommasi LG, Serraino D, La Vecchia C, Franceschi S: Nutrients intake and the risk of hepatocellular carcinoma in Italy. Eur J Cancer; 2007 Nov;43(16):2381-7
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  • [Title] Nutrients intake and the risk of hepatocellular carcinoma in Italy.
  • Although hepatitis C and B viruses and alcohol consumption are the major risk factors for hepatocellular carcinoma (HCC), dietary habits may also be relevant.
  • In conclusion, a diet rich in linoleic acid containing foods (e.g. white meats and fish) and beta-carotene was inversely related to HCC risk.
  • [MeSH-major] Alcohol Drinking / adverse effects. Carcinoma, Hepatocellular / etiology. Diet / adverse effects. Liver Neoplasms / etiology

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  • (PMID = 17719221.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 01YAE03M7J / beta Carotene; 9KJL21T0QJ / Linoleic Acid
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57. Kim RH, Chang MS, Kim HJ, Song KS, Kim YS, Choi BY, Kim WH: Medical history and lifestyle factors contributing to Epstein-Barr virus-associated gastric carcinoma and conventional gastric carcinoma in Korea. Anticancer Res; 2010 Jun;30(6):2469-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Medical history and lifestyle factors contributing to Epstein-Barr virus-associated gastric carcinoma and conventional gastric carcinoma in Korea.
  • BACKGROUND: Epstein-Barr virus-associated gastric carcinoma (EBV-GC) has been characterized as a special gastric cancer subset.
  • A history of previous gastric ulcer was associated with EBV-GC, whereas frequent and heavy alcohol drinking was related to non-EBV-GC.
  • Alcohol drinking was more related to non-EBV-GC than EBV-GC.
  • [MeSH-minor] Alcohol Drinking. Female. Food Habits. Helicobacter Infections / complications. Helicobacter pylori. Humans. Male. Medical Records. Middle Aged. Risk Factors. Smoking. Socioeconomic Factors

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  • (PMID = 20651410.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
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58. Hashibe M, Boffetta P, Zaridze D, Shangina O, Szeszenia-Dabrowska N, Mates D, Janout V, Fabiánová E, Bencko V, Moullan N, Chabrier A, Hung R, Hall J, Canzian F, Brennan P: Evidence for an important role of alcohol- and aldehyde-metabolizing genes in cancers of the upper aerodigestive tract. Cancer Epidemiol Biomarkers Prev; 2006 Apr;15(4):696-703
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  • [Title] Evidence for an important role of alcohol- and aldehyde-metabolizing genes in cancers of the upper aerodigestive tract.
  • This increase is likely to be due to patterns of alcohol and tobacco consumption.
  • We analyzed six SNPs in three genes related to ethanol metabolism: alcohol dehydrogenase 1B and 1C (ADH1B, ADH1C) and aldehyde dehydrogenase 2 (ALDH2).
  • When results were analyzed by subsite, strong main effects were observed for squamous cell carcinoma of the esophagus for all six variants.
  • Among carriers who drank alcohol at least thrice to four times a week, the AF(c) for having at least one ALDH2 variant was 49% (21.3-66.8%) for all upper aerodigestive tract cancers, increasing to 68.9% (42.9-83.1%) for esophageal cancer.
  • CONCLUSIONS: Polymorphisms in the ADH1B and ALDH2 genes are associated with upper aerodigestive tract cancer in Central European populations and interact substantially with alcohol consumption.
  • [MeSH-major] Alcohol Dehydrogenase / genetics. Aldehyde Dehydrogenase / genetics. Head and Neck Neoplasms / epidemiology. Head and Neck Neoplasms / etiology

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  • (PMID = 16614111.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA92039
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.1 / ADH1C protein, human; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / ALDH2 protein, human; EC 1.2.1.3 / Aldehyde Dehydrogenase
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59. Woolley E, Magennis P, Shokar P, Lowe D, Edwards D, Rogers SN: The correlation between indices of deprivation and health-related quality of life in patients with oral and oropharyngeal squamous cell carcinoma. Br J Oral Maxillofac Surg; 2006 Jun;44(3):177-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The correlation between indices of deprivation and health-related quality of life in patients with oral and oropharyngeal squamous cell carcinoma.
  • Health-related quality of life (HR-QoL) is an important measure of outcome but there is little on this subject and its correlation with deprivation in patients with oral and oropharyngeal cancer.
  • Validated measures of deprivation scores (Townsend, Carstairs, Jarman and Index of Multiple Deprivation 2000) were calculated, as well as patient-based indicators of social circumstances (marital status, smoking habit, alcohol intake).
  • [MeSH-major] Carcinoma, Squamous Cell / epidemiology. Mouth Neoplasms / epidemiology. Oropharyngeal Neoplasms / epidemiology. Poverty. Quality of Life


60. Dítĕ P, Novotný I, Precechtĕlová M, Růzicka M, Záková A, Hermanová M, Trna J, Nechutová H: Incidence of pancreatic carcinoma in patients with chronic pancreatitis. Hepatogastroenterology; 2010 Jul-Aug;57(101):957-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence of pancreatic carcinoma in patients with chronic pancreatitis.
  • BACKGROUND/AIMS: Pancreatic carcinoma belongs to the area of conditions with late diagnosis and there is no effective screening method.
  • In this 14-year period we performed classical biochemical tests, endoscopic ultrasound, CT scans and ERCP, we asked about the number of cigarettes smoked per year and classified individuals consuming regularly more than 80 g of alcohol per day for 5 years for men and 50 g of alcohol per day for 5 years for women as having the alcoholic form of chronic pancreatitis.
  • RESULTS: Alcohol-related etiology was detected in 73.1% of patients, 21.5% had the chronic obstructive form and only 5.4% were classified as idiopathic pancreatitis.
  • Pancreatic carcinoma was detected in 13 patients with chronic pancreatitis (5.8%), three patients were diagnosed with gastric carcinoma and one with esophageal carcinoma.
  • In the 14 year period 11 subjects died, out of which eight cases were related to pancreatic carcinoma.

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  • (PMID = 21033259.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
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61. Li CI, Chlebowski RT, Freiberg M, Johnson KC, Kuller L, Lane D, Lessin L, O'Sullivan MJ, Wactawski-Wende J, Yasmeen S, Prentice R: Alcohol consumption and risk of postmenopausal breast cancer by subtype: the women's health initiative observational study. J Natl Cancer Inst; 2010 Sep 22;102(18):1422-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alcohol consumption and risk of postmenopausal breast cancer by subtype: the women's health initiative observational study.
  • BACKGROUND: Alcohol consumption is a well-established risk factor for breast cancer.
  • This association is thought to be largely hormonally driven, so alcohol use may be more strongly associated with hormonally sensitive breast cancers.
  • Few studies have evaluated how alcohol-related risk varies by breast cancer subtype.
  • METHODS: We assessed the relationship between self-reported alcohol consumption and postmenopausal breast cancer risk among 87 724 women in the Women's Health Initiative Observational Study prospective cohort from 1993 through 1998.
  • In multivariable adjusted analyses, alcohol consumption was positively related to risk of invasive breast cancer overall, invasive lobular carcinoma, and hormone receptor-positive tumors (all P(trend) ≤ .022).
  • However, alcohol consumption was more strongly related to risk of certain types of invasive breast cancer compared with others.
  • Compared with never drinkers, women who consumed seven or more alcoholic beverages per week had an almost twofold increased risk of hormone receptor-positive invasive lobular carcinoma (HR = 1.82; 95% CI = 1.18 to 2.81) but not a statistically significant increased risk of hormone receptor-positive invasive ductal carcinoma (HR = 1.14; 95% CI = 0.87 to 1.50; difference in HRs per drink per day among current drinkers = 1.15; 95% CI = 1.01 to 1.32, P = .042).
  • CONCLUSIONS: Alcohol use may be more strongly associated with risk of hormone-sensitive breast cancers than hormone-insensitive subtypes, suggesting distinct etiologic pathways for these two breast cancer subtypes.

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  • [Cites] Cancer. 2000 Jun 1;88(11):2570-7 [10861435.001]
  • [Cites] Int J Cancer. 2008 Apr 15;122(8):1832-41 [18067133.001]
  • [Cites] J Natl Cancer Inst. 2001 May 2;93(9):710-5 [11333294.001]
  • [Cites] JAMA. 2001 Nov 7;286(17):2143-51 [11694156.001]
  • [Cites] J Clin Oncol. 2002 Feb 1;20(3):699-706 [11821451.001]
  • [Cites] JAMA. 2002 Feb 13;287(6):734-41 [11851540.001]
  • [Cites] J Natl Cancer Inst. 2002 Apr 17;94(8):606-16 [11959894.001]
  • [Cites] Br J Cancer. 2002 Nov 18;87(11):1234-45 [12439712.001]
  • [Cites] Cancer. 2002 Dec 15;95(12):2455-64 [12467057.001]
  • [Cites] Cancer Causes Control. 2003 Apr;14(3):225-33 [12814201.001]
  • [Cites] JAMA. 2003 Jun 25;289(24):3243-53 [12824205.001]
  • [Cites] JAMA. 2003 Jun 25;289(24):3254-63 [12824206.001]
  • [Cites] Arch Intern Med. 2003 Oct 13;163(18):2149-53 [14557212.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 Oct;12(10):1061-6 [14578143.001]
  • [Cites] Control Clin Trials. 1998 Feb;19(1):61-109 [9492970.001]
  • [Cites] Ann Epidemiol. 1999 Apr;9(3):178-87 [10192650.001]
  • [Cites] Br J Cancer. 2005 Oct 31;93(9):1046-52 [16175185.001]
  • [Cites] Breast Cancer Res. 2006;8(1):R11 [16507159.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 May;15(5):946-54 [16702375.001]
  • [Cites] Cancer Causes Control. 2006 Aug;17(6):759-70 [16783604.001]
  • [Cites] Lancet Oncol. 2006 Nov;7(11):910-8 [17081916.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2482-8 [17164374.001]
  • [Cites] Breast Cancer Res. 2007;9(1):R6 [17239243.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Dec;16(12):2773-80 [18086787.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Jan;17(1):43-50 [18199710.001]
  • [Cites] Am J Clin Pathol. 2001 Jan;115(1):85-98 [11190811.001]
  • (PMID = 20733117.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / WHI NIH HHS / WH / N01WH22110; United States / WHI NIH HHS / WH / N01WH42129-32; United States / WHI NIH HHS / WH / N01WH32100-2; United States / WHI NIH HHS / WH / N01WH32108-9; United States / WHI NIH HHS / WH / N01WH42107-26; United States / WHI NIH HHS / WH / N01WH32122; United States / WHI NIH HHS / WH / N01WH32105-6; United States / WHI NIH HHS / WH / N01WH32111-13; United States / WHI NIH HHS / WH / N01WH32118-32119; United States / WHI NIH HHS / WH / N01WH32115; United States / WHI NIH HHS / WH / N01WH44221; United States / WHI NIH HHS / WH / N01WH24152
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone
  • [Other-IDs] NLM/ PMC2943525
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62. Hill-Baskin AE, Markiewski MM, Buchner DA, Shao H, DeSantis D, Hsiao G, Subramaniam S, Berger NA, Croniger C, Lambris JD, Nadeau JH: Diet-induced hepatocellular carcinoma in genetically predisposed mice. Hum Mol Genet; 2009 Aug 15;18(16):2975-88
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  • [Title] Diet-induced hepatocellular carcinoma in genetically predisposed mice.
  • Hepatocellular carcinoma (HCC) is one of the leading causes of cancer death worldwide, with approximately 70% of cases resulting from hepatitis B and C viral infections, aflatoxin exposure, chronic alcohol use or genetic liver diseases.
  • The remaining approximately 30% of cases are associated with obesity, type 2 diabetes and related metabolic diseases, although a direct link between these pathologies and HCCs has not been established.

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  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):19075-80 [16365291.001]
  • [Cites] N Engl J Med. 2005 Oct 27;353(17):1793-801 [16251535.001]
  • [Cites] J Clin Invest. 2006 Jun;116(6):1582-95 [16710476.001]
  • [Cites] Cancer Lett. 2006 Aug 28;240(2):157-69 [16239065.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 15;103(33):12481-6 [16885212.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2006 Oct;291(4):G575-83 [16710052.001]
  • [Cites] Hepatology. 2006 Oct;44(4):1003-11 [17006931.001]
  • [Cites] Int J Cancer. 2006 Dec 1;119(11):2557-66 [16988945.001]
  • [Cites] Diabetes. 2007 Jan;56(1):161-7 [17192478.001]
  • [Cites] J Biol Chem. 2007 Apr 13;282(15):11197-204 [17227769.001]
  • [Cites] Clin Liver Dis. 2007 Feb;11(1):191-207, x-xi [17544979.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Sep 11;104(37):14771-6 [17785413.001]
  • [Cites] RNA. 2008 Jan;14(1):35-42 [18025253.001]
  • [Cites] Stem Cells. 2008 Jan;26(1):17-29 [17916804.001]
  • [Cites] J Clin Invest. 2008 Feb;118(2):683-94 [18188449.001]
  • [Cites] Asian Pac J Cancer Prev. 2007;8 Suppl:35-80 [18260705.001]
  • [Cites] Oncology. 2007;72(5-6):397-402 [18196926.001]
  • [Cites] Cancer Res. 2008 Apr 1;68(7):2391-9 [18381447.001]
  • [Cites] Am Fam Physician. 2008 Jun 1;77(11):1573-8 [18581838.001]
  • [Cites] Adv Exp Med Biol. 2008;630:72-93 [18637486.001]
  • [Cites] Semin Liver Dis. 2008 Nov;28(4):370-9 [18956293.001]
  • [Cites] RNA. 2008 Nov;14(11):2290-6 [18812437.001]
  • [Cites] Mamm Genome. 2009 Feb;20(2):71-82 [19137372.001]
  • [Cites] Int J Cancer. 2006 Jun 15;118(12):3030-44 [16404738.001]
  • [Cites] Nat Genet. 2000 May;25(1):25-9 [10802651.001]
  • [Cites] J Biol Chem. 2001 Jan 5;276(1):629-38 [11024029.001]
  • [Cites] Cancer Res. 2001 Jul 1;61(13):5016-23 [11431335.001]
  • [Cites] Hepatology. 2001 Nov;34(5):935-42 [11679964.001]
  • [Cites] Nat Genet. 2002 Aug;31(4):339-46 [12149612.001]
  • [Cites] Semin Liver Dis. 2004 Feb;24(1):99-106 [15085490.001]
  • [Cites] Science. 2004 Apr 16;304(5669):445-8 [15031436.001]
  • [Cites] Curr Opin Genet Dev. 2004 Feb;14(1):37-42 [15108803.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 22;101(25):9309-14 [15184677.001]
  • [Cites] Gastroenterology. 2004 Nov;127(5 Suppl 1):S218-24 [15508087.001]
  • [Cites] Metabolism. 1995 May;44(5):645-51 [7752914.001]
  • [Cites] PLoS Biol. 2004 Nov;2(11):e363 [15502875.001]
  • [Cites] Bioinformatics. 2004 Nov 22;20(17):3108-27 [15217816.001]
  • [Cites] Nat Genet. 2004 Dec;36(12):1306-11 [15565109.001]
  • [Cites] Alcohol. 2004 Aug;34(1):67-79 [15670668.001]
  • [Cites] Intervirology. 2005;48(1):6-9 [15785083.001]
  • [Cites] Diabetes. 2005 May;54(5):1314-23 [15855315.001]
  • [Cites] Hepatobiliary Pancreat Dis Int. 2005 May;4(2):173-7 [15908310.001]
  • [Cites] Acta Pharmacol Sin. 2005 Jun;26(6):659-65 [15916730.001]
  • [Cites] Carcinogenesis. 2005 Jun;26(6):1013-20 [15677630.001]
  • [Cites] Nucleic Acids Res. 2005 Jul 1;33(Web Server issue):W627-32 [15980550.001]
  • [Cites] Hepatology. 2005 Oct;42(4):880-5 [16175608.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] Nucleic Acids Res. 2006 Jan 1;34(Database issue):D140-4 [16381832.001]
  • (PMID = 19454484.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] ENG
  • [Grant] None / None / / P40 RR012305-07; United States / NIDDK NIH HHS / DK / DK075040-04; United States / NCRR NIH HHS / RR / P40 RR012305-07; United States / NIAID NIH HHS / AI / AI068730; United States / NCRR NIH HHS / RR / P40 RR012305-09; United States / NCRR NIH HHS / RR / P40 RR012305; None / None / / P40 RR012305-09; United States / NCRR NIH HHS / RR / RR12305; United States / NIDDK NIH HHS / DK / R01 DK075040-04; None / None / / P40 RR012305-08; United States / NIDDK NIH HHS / DK / R01 DK075040; United States / NCRR NIH HHS / RR / P40 RR012305-08; United States / NCI NIH HHS / CA / U54CA116867; United States / NIDDK NIH HHS / DK / DK075040
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dietary Fats
  • [Other-IDs] NLM/ PMC2714725
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63. Takahashi H, Mizuta T, Kawazoe S, Eguchi Y, Kawaguchi Y, Otuka T, Oeda S, Ario K, Iwane S, Akiyama T, Ozaki I, Fujimoto K: Efficacy and safety of radiofrequency ablation for elderly hepatocellular carcinoma patients. Hepatol Res; 2010 Oct;40(10):997-1005

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  • [Title] Efficacy and safety of radiofrequency ablation for elderly hepatocellular carcinoma patients.
  • AIM:   This study was conducted to evaluate the efficacy and safety of radiofrequency ablation (RFA) therapy in elderly patients with hepatocellular carcinoma (HCC).
  • RESULTS:   In the elderly group, the proportion of men, alcohol consumption, serum alanine aminotransferase and γ-glutamyl transpeptidase levels were significantly lower compared with those in the non-elderly group.
  • In multivariate analysis, Child-Pugh grade and tumor-related factors were significant factors associated with survival, but age was not.

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  • [Copyright] © 2010 The Japan Society of Hepatology.
  • (PMID = 20887335.001).
  • [ISSN] 1872-034X
  • [Journal-full-title] Hepatology research : the official journal of the Japan Society of Hepatology
  • [ISO-abbreviation] Hepatol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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64. Lee CH, Wu DC, Lee JM, Wu IC, Goan YG, Kao EL, Huang HL, Chan TF, Chou SH, Chou YP, Ho CK, Wu MT: Anatomical subsite discrepancy in relation to the impact of the consumption of alcohol, tobacco and betel quid on esophageal cancer. Int J Cancer; 2007 Apr 15;120(8):1755-62
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Anatomical subsite discrepancy in relation to the impact of the consumption of alcohol, tobacco and betel quid on esophageal cancer.
  • We carried out a multicenter case-control study in Taiwan to assess anatomical subsite risk discrepancy for this neoplasm in regard to the consumption of alcohol, tobacco and betel quid.
  • All consumption of the three substances was related to the development of each subsite of EC, with a heterogeneously higher risk for current smokers (adjusted odds ratio (AOR) = 6.2) found in M/3-EC and for current chewers, in U/3-EC (AOR = 4.9).
  • In conclusion, tumor subsite discrepancy risk is related to prolonged exposure to tobacco and betel quid with inflorescence.
  • Alcohol interacts with tobacco in a stronger supra-multiplicative way in the middle portion of the esophagus, probably explaining why esophageal SCC occurs more commonly at this anatomical location.
  • [MeSH-major] Alcohol Drinking / adverse effects. Areca / adverse effects. Carcinoma, Squamous Cell / etiology. Esophageal Neoplasms / etiology. Smoking / adverse effects

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17230518.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drug Combinations
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65. Yoshikawa M, Kato H, Miyazaki T, Nakajima M, Kamiyama Y, Fukai Y, Tajima K, Masuda N, Ojima H, Tsukada K, Kuwano H: Expression of p53 in esophageal carcinoma with multiple areas unstained by iodine. Hepatogastroenterology; 2005 Sep-Oct;52(65):1444-7
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  • [Title] Expression of p53 in esophageal carcinoma with multiple areas unstained by iodine.
  • BACKGROUND/AIMS: Esophageal squamous cell carcinoma is occasionally associated with multiple areas in the surrounding mucosa unstained with iodine.
  • METHODOLOGY: We examined 21 male patients with superficial esophageal carcinoma.
  • Group 1 consisted of 4 cases of superficial esophageal carcinoma associated with multiple lesions that did not stain with iodine.
  • We assessed the correlation between clinicopathological factors, a history of tobacco and alcohol consumption, and p53 expression in the two groups.
  • RESULTS: We found four cases (group 1) of superficial esophageal squamous cell carcinoma where there were a total of 10 satellite tumors in addition to the main tumor.
  • These patients tended to have a higher daily consumption of tobacco and alcohol than those in group 2.
  • CONCLUSIONS: We have found that higher tobacco and alcohol consumption are closely related to multiple lesions unstained by iodine and abnormal expression of the p53 gene.
  • [MeSH-major] Carcinoma, Squamous Cell / metabolism. Esophageal Neoplasms / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adult. Alcohol Drinking / epidemiology. Coloring Agents. Esophagus / pathology. Humans. Immunohistochemistry. Iodides. Male. Middle Aged. Mucous Membrane / pathology. Risk Factors. Smoking / epidemiology

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  • (PMID = 16201092.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / Iodides; 0 / Tumor Suppressor Protein p53; T66M6Y3KSA / Lugol's solution
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66. Sakamoto T, Higaki Y, Hara M, Ichiba M, Horita M, Mizuta T, Eguchi Y, Yasutake T, Ozaki I, Yamamoto K, Onohara S, Kawazoe S, Shigematsu H, Koizumi S, Tanaka K: hOGG1 Ser326Cys polymorphism and risk of hepatocellular carcinoma among Japanese. J Epidemiol; 2006 Nov;16(6):233-9
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  • [Title] hOGG1 Ser326Cys polymorphism and risk of hepatocellular carcinoma among Japanese.
  • BACKGROUND: The Ser326Cys polymorphism in human oxoguanine glycosylase 1 (hOGG1), which is involved in the repair of 8-hydroxy-2-deoxyguanine in oxidatively damaged DNA, has been associated with susceptibility to certain cancers, but has not been examined in causation of hepatocellular carcinoma (HCC).
  • METHODS: We conducted a case-control study to investigate whether this polymorphism was related to HCC risk with any interaction with alcohol consumption and cigarette smoking.
  • We could not detect any significant gene-alcohol interaction (p = 0.95 or 0.16) or gene-smoking interaction (p = 0.70 or 0.69).

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  • (PMID = 17085873.001).
  • [ISSN] 0917-5040
  • [Journal-full-title] Journal of epidemiology
  • [ISO-abbreviation] J Epidemiol
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 452VLY9402 / Serine; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / oxoguanine glycosylase 1, human
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67. Murakami A, Fukushima C, Yositomi K, Sueoka K, Nawata S, Fujimoto M, Nakamura K, Sugino N: Tumor-related protein, the squamous cell carcinoma antigen binds to the intracellular protein carbonyl reductase. Int J Oncol; 2010 Jun;36(6):1395-400
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  • [Title] Tumor-related protein, the squamous cell carcinoma antigen binds to the intracellular protein carbonyl reductase.
  • Squamous cell carcinoma antigen (SCCA) is a useful tumor marker for diagnosis and management of squamous cell carcinoma.
  • Third, Western blotting was performed to analyze the expression levels of this protein in keratinocytes and six kinds of uterine squamous cell carcinoma cell lines.
  • The CR expression levels in six kinds of squamous cell carcinoma cell lines were lower compared to those in keratinocytes.
  • [MeSH-major] Alcohol Oxidoreductases / metabolism. Antigens, Neoplasm / metabolism. Epithelial Cells / immunology. Keratinocytes / metabolism. Serpins / metabolism
  • [MeSH-minor] Blotting, Western. Carcinoma, Squamous Cell / metabolism. Cell Line, Tumor. Cytoplasm / metabolism. Humans. Immunohistochemistry. Immunoprecipitation

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  • (PMID = 20428762.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Serpins; 0 / squamous cell carcinoma-related antigen; EC 1.1.- / Alcohol Oxidoreductases
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68. Kane RC, Farrell AT, Madabushi R, Booth B, Chattopadhyay S, Sridhara R, Justice R, Pazdur R: Sorafenib for the treatment of unresectable hepatocellular carcinoma. Oncologist; 2009 Jan;14(1):95-100
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  • [Title] Sorafenib for the treatment of unresectable hepatocellular carcinoma.
  • Food and Drug Administration (FDA) review and approval of sorafenib (Nexavar; Bayer Pharmaceuticals Corp., Montville, NJ, and Onyx Pharmaceuticals Corp., Emeryville, CA), an oral kinase inhibitor, for the treatment of patients with unresectable hepatocellular carcinoma (HCC).
  • Underlying liver diseases included hepatitis B (18%), hepatitis C (28%), and alcohol-related (26%).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzenesulfonates / therapeutic use. Carcinoma, Hepatocellular / drug therapy. Liver Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyridines / therapeutic use

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  • [CommentIn] Oncologist. 2009 Jan;14(1):92-4 [19144679.001]
  • (PMID = 19144678.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib
  • [Number-of-references] 2
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69. McGlynn KA, London WT: Epidemiology and natural history of hepatocellular carcinoma. Best Pract Res Clin Gastroenterol; 2005 Feb;19(1):3-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epidemiology and natural history of hepatocellular carcinoma.
  • Hepatocellular carcinoma (HCC) is a major contributor to cancer incidence and mortality.
  • In contrast, hepatitis C virus and alcohol consumption are more important risk factors in low-risk countries.
  • Reasons for both trends are not completely understood, but are likely related to public health efforts in Asia and the increase in hepatitis C virus infection in low-risk countries.
  • [MeSH-major] Carcinoma, Hepatocellular / epidemiology. Global Health. Liver Neoplasms / epidemiology
  • [MeSH-minor] Aflatoxins / adverse effects. Alcohol Drinking. Chemoprevention. Food Contamination. Genetic Predisposition to Disease. Hepatitis B / complications. Hepatitis C / complications. Humans. Incidence. Liver Cirrhosis / complications. Risk Factors

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  • (PMID = 15757802.001).
  • [ISSN] 1521-6918
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aflatoxins
  • [Number-of-references] 130
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70. Kirchner G, Kirovski G, Hebestreit A, Schölmerich J, Schlitt HJ, Stoeltzing O, Hellerbrand C: Epidemiology and survival of patients with hepatocellular carcinoma in Southern Germany. Int J Clin Exp Med; 2010;3(2):169-79
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  • [Title] Epidemiology and survival of patients with hepatocellular carcinoma in Southern Germany.
  • Hepatocellular carcinoma (HCC) belongs to the most frequent tumors worldwide with an incidence still rising.
  • The results indicate that chronic alcohol abuse was the most common risk factor (57.2%), followed by infection with hepatitis B and C viruses (HBV: 10.9% and HCV: 20.5%).
  • We conclude that chronic alcohol abuse is frequently associated with HCC in low hepatitis virus endemic areas, such as Germany.
  • Our study suggests the CLIP score as a valuable prognostic marker for patients' survival, particularly of patients with alcohol related HCC.

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  • [Cites] Eur J Gastroenterol Hepatol. 1999 Nov;11(11):1215-20 [10563529.001]
  • [Cites] Hepatology. 1998 Sep;28(3):751-5 [9731568.001]
  • [Cites] Dig Dis. 2001;19(4):345-51 [11935095.001]
  • [Cites] Minerva Gastroenterol Dietol. 2005 Mar;51(1):1-5 [15756142.001]
  • [Cites] Jpn J Clin Oncol. 2008 Oct;38(10):683-8 [18753360.001]
  • [Cites] J Gastroenterol Hepatol. 2009 Mar;24(3):346-53 [19220670.001]
  • [Cites] J Hepatol. 1998 Dec;29(6):944-52 [9875641.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2000 Jan;12(1):61-6 [10656212.001]
  • [Cites] Hepatology. 2000 Apr;31(4):840-5 [10733537.001]
  • [Cites] Scand J Infect Dis. 2000;32(2):147-52 [10826899.001]
  • [Cites] Liver. 2000 Jul;20(4):312-8 [10959810.001]
  • [Cites] J Med Virol. 2001 Feb;63(2):96-102 [11170044.001]
  • [Cites] Gesundheitswesen. 2001 Dec;63(12):775-82 [11735072.001]
  • [Cites] World J Gastroenterol. 2001 Apr;7(2):208-15 [11819762.001]
  • [Cites] Cancer. 2002 Mar 15;94(6):1760-9 [11920539.001]
  • [Cites] J Surg Oncol. 2002 Dec;81(4):195-202 [12451624.001]
  • [Cites] Hepatology. 2003 Mar;37(3):520-7 [12601348.001]
  • [Cites] Cancer. 1954 May;7(3):462-503 [13160935.001]
  • [Cites] Gut. 2005 Mar;54(3):411-8 [15710992.001]
  • [Cites] J Hepatol. 2006 Jan;44(1):158-66 [16290309.001]
  • [Cites] Liver Int. 2006 Aug;26(6):680-7 [16842324.001]
  • [Cites] Ann Oncol. 2007 Mar;18(3):581-92 [17287242.001]
  • [Cites] J Gastroenterol Hepatol. 2008 Mar;23(3):459-66 [17854425.001]
  • [Cites] J Gastroenterol Hepatol. 2007 Nov;22(11):1936-41 [17914973.001]
  • [Cites] Gesundheitswesen. 2008 Jan;70(1):28-37 [18273761.001]
  • [Cites] J Clin Gastroenterol. 2008 May-Jun;42(5):527-32 [18277889.001]
  • [Cites] Cancer. 1985 Aug 15;56(4):918-28 [2990661.001]
  • [Cites] Hepatology. 1995 Oct;22(4 Pt 1):1027-33 [7557847.001]
  • [Cites] Cancer. 1996 Jun 1;77(11):2217-22 [8635087.001]
  • [Cites] Gut. 2001 Jan;48(1):103-9 [11115830.001]
  • (PMID = 20607043.001).
  • [ISSN] 1940-5901
  • [Journal-full-title] International journal of clinical and experimental medicine
  • [ISO-abbreviation] Int J Clin Exp Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2894652
  • [Keywords] NOTNLM ; CLIP score / HCC / epidemiology / hepatocellular carcinoma / survival
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71. Galeone C, Pelucchi C, Levi F, Negri E, Talamini R, Franceschi S, La Vecchia C: Folate intake and squamous-cell carcinoma of the oesophagus in Italian and Swiss men. Ann Oncol; 2006 Mar;17(3):521-5
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  • [Title] Folate intake and squamous-cell carcinoma of the oesophagus in Italian and Swiss men.
  • BACKGROUND: Dietary folate has been inversely related to the risk of several cancers.
  • PATIENTS AND METHODS: Using data from a multicentric case-control study conducted in Italy and Switzerland between 1992 and 1999, we investigated the association between dietary folate intake and oesophageal squamous-cell carcinoma (OSCC) among 351 men with incident, histologically confirmed OSCC and 875 hospital controls admitted for acute, non-neoplastic conditions, unrelated to alcohol and smoking consumption.
  • The inverse relation was somewhat stronger in strata of high methionine, vitamin B6 and alcohol intake, and did not vary substantially according to age and smoking habits.
  • CONCLUSION: Dietary folate was inversely related to OSCC risk in this population with high alcohol consumption and infrequent use of supplements and multivitamins.

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  • (PMID = 16344275.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 8059-24-3 / Vitamin B 6; 935E97BOY8 / Folic Acid; AE28F7PNPL / Methionine
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72. Ascha MS, Hanouneh IA, Lopez R, Tamimi TA, Feldstein AF, Zein NN: The incidence and risk factors of hepatocellular carcinoma in patients with nonalcoholic steatohepatitis. Hepatology; 2010 Jun;51(6):1972-8
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  • [Title] The incidence and risk factors of hepatocellular carcinoma in patients with nonalcoholic steatohepatitis.
  • Nonalcoholic steatohepatitis (NASH) is a well-recognized cause of cirrhosis and has been increasingly associated with the development of hepatocellular carcinoma (HCC).
  • The aims of this study were to (1) estimate the incidence of HCC in patients with NASH-related cirrhosis, (2) compare incidence in NASH-related cirrhosis with hepatitis C virus (HCV)-related cirrhosis, and (3) identify risk factors of HCC in patients with NASH-related cirrhosis compared with HCV-related cirrhosis.
  • Multivariate regression analysis revealed that older age (P = 0.006) and alcohol consumption (P = 0.002) were independent variables associated with development of HCC in patients with NASH-cirrhosis.
  • Compared with nondrinkers, patients who reported any regular alcohol consumption were at greater risk for HCC development (hazard ratio: 3.6; P25, P75: 1.5, 8.3).
  • Alcohol consumption, a modifiable risk factor, appears to be the most significant factor associated with risk of HCC development in our study population.
  • [MeSH-major] Carcinoma, Hepatocellular / epidemiology. Fatty Liver / complications. Hepatitis C / complications. Liver Cirrhosis / complications. Liver Neoplasms / epidemiology
  • [MeSH-minor] Alcohol Drinking / adverse effects. Female. Humans. Incidence. Male. Middle Aged. Retrospective Studies. Risk Factors. United States / epidemiology

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  • [CommentIn] Hepatology. 2010 Sep;52(3):1172 [20683933.001]
  • (PMID = 20209604.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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73. Ikeda K, Marusawa H, Osaki Y, Nakamura T, Kitajima N, Yamashita Y, Kudo M, Sato T, Chiba T: Antibody to hepatitis B core antigen and risk for hepatitis C-related hepatocellular carcinoma: a prospective study. Ann Intern Med; 2007 May 1;146(9):649-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antibody to hepatitis B core antigen and risk for hepatitis C-related hepatocellular carcinoma: a prospective study.
  • BACKGROUND: Previous exposure to hepatitis B virus (HBV) and occult HBV infection may have an important role in the development of hepatocellular carcinoma (HCC) in patients with chronic liver disease related to hepatitis C virus (HCV).
  • OBJECTIVE: To prospectively study the association between antibody to hepatitis B core antigen (anti-HBc) and clinical outcomes in patients with HCV-related chronic liver disease.
  • Hepatocellular carcinoma occurred in 237 of 846 patients (28.0%) during follow-up.
  • Among patients with cirrhosis, HCC was diagnosed in 85 of 141 patients (60.3%) with anti-HBc and 58 of 129 patients (45.0%) without HBV-related serologic markers.
  • LIMITATIONS: The study included only 1 assessment of smoking and alcohol consumption at study entry and did not precisely determine the duration of smoking or alcohol use.
  • CONCLUSIONS: Anti-HBc-positive results on serologic testing are a marker of high risk for HCC among patients with HCV-related cirrhosis.
  • [MeSH-major] Carcinoma, Hepatocellular / virology. Hepatitis B Antibodies / blood. Hepatitis B Core Antigens / immunology. Hepatitis C, Chronic / immunology. Liver Neoplasms / virology

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  • [CommentIn] Ann Intern Med. 2008 Jan 15;148(2):166-7; author reply 167 [18195343.001]
  • [SummaryForPatientsIn] Ann Intern Med. 2007 May 1;146(9):I59 [17470828.001]
  • (PMID = 17470833.001).
  • [ISSN] 1539-3704
  • [Journal-full-title] Annals of internal medicine
  • [ISO-abbreviation] Ann. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Hepatitis B Antibodies; 0 / Hepatitis B Core Antigens; 0 / Interferon-alpha; 77238-31-4 / Interferon-beta
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74. Merion RM: Current status and future of liver transplantation. Semin Liver Dis; 2010 Nov;30(4):411-21
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  • Indications for liver transplant have evolved to include previously contraindicated conditions such as hepatocellular carcinoma and alcohol-related liver disease.
  • [MeSH-minor] Body Dysmorphic Disorders. Carcinoma, Hepatocellular / surgery. End Stage Liver Disease / surgery. Hepatitis C, Chronic / surgery. Humans. Liver Neoplasms / surgery. Living Donors. Patient Selection. Severity of Illness Index. Tissue and Organ Procurement. Treatment Outcome. Waiting Lists

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  • [Copyright] © Thieme Medical Publishers.
  • (PMID = 20960380.001).
  • [ISSN] 1098-8971
  • [Journal-full-title] Seminars in liver disease
  • [ISO-abbreviation] Semin. Liver Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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75. Ladero JM, Martínez C, García-Martín E, Ropero P, Briceño O, Villegas A, Díaz-Rubio M, Agúndez JA: Glutathione S-transferase M1 and T1 genetic polymorphisms are not related to the risk of hepatocellular carcinoma: a study in the Spanish population. Eur J Cancer; 2006 Jan;42(1):73-7
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  • [Title] Glutathione S-transferase M1 and T1 genetic polymorphisms are not related to the risk of hepatocellular carcinoma: a study in the Spanish population.
  • Glutathione S-transferases constitute a superfamily of enzymes that catalyse the inactivating conjugation of endogenous and environmental substrates involved in the pathogenesis of hepatocellular carcinoma (HCC) and glutathione.
  • Gender, age at diagnosis, tobacco use, chronic infection with hepatitis B or C virus and alcohol abuse did not influence these results.
  • In conclusion, polymorphisms in GSTM1 and GSTT1 genes are not related to the incidence of HCC in a high-risk Spanish population.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Glutathione Transferase / genetics. Liver Neoplasms / genetics. Polymorphism, Genetic / genetics

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  • (PMID = 16314088.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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76. Castro MA, Dedivitis RA, Ribeiro KC: Comorbidity measurement in patients with laryngeal squamous cell carcinoma. ORL J Otorhinolaryngol Relat Spec; 2007;69(3):146-52
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  • [Title] Comorbidity measurement in patients with laryngeal squamous cell carcinoma.
  • OBJECTIVE: It was the aim of this study to measure comorbidities in patients with laryngeal squamous cell carcinoma.
  • PATIENTS AND METHODS: Ninety adult patients treated for newly diagnosed laryngeal squamous cell carcinoma were studied.
  • We measured comorbid illness applying the following validated scales: the Cumulative Illness Rating Scale (CIRS), the Kaplan-Feinstein Classification (KFC), the Charlson index, the Index of Coexistent Disease (ICED), the Adult Comorbidity Evaluation-27 (ACE-27), the Alcohol-Tobacco-Related Comorbidities Index (ATC), and the Washington University Head and Neck Comorbidity Index (WUHNCI).
  • [MeSH-major] Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / pathology. Laryngeal Neoplasms / epidemiology

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  • [Copyright] Copyright (c) 2007 S. Karger AG, Basel.
  • (PMID = 17264530.001).
  • [ISSN] 0301-1569
  • [Journal-full-title] ORL; journal for oto-rhino-laryngology and its related specialties
  • [ISO-abbreviation] ORL J. Otorhinolaryngol. Relat. Spec.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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77. Chan YY, Chang CS, Chien LH, Wu TF: Apoptotic effects of a high performance liquid chromatography (HPLC) fraction of Antrodia camphorata mycelia are mediated by down-regulation of the expressions of four tumor-related genes in human non-small cell lung carcinoma A549 cell. J Ethnopharmacol; 2010 Feb 17;127(3):652-61
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  • [Title] Apoptotic effects of a high performance liquid chromatography (HPLC) fraction of Antrodia camphorata mycelia are mediated by down-regulation of the expressions of four tumor-related genes in human non-small cell lung carcinoma A549 cell.
  • In this study we determined the inhibitory effects of alcohol extract and individual fractions of alcohol extract on the proliferation of human non-small cell lung carcinoma A549 cell and clarified the mechanism underlying the anti-cancer activities.
  • MATERIALS AND METHODS: Alcohol extracts of Antrodia camphorata mycelia were prepared by the serial extraction with the solvents with increasing polarity and fractionated using HPLC.
  • The impacts of HPLC fractions on the expression levels of apoptosis- and cancer-related proteins were evaluated by western blotting.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antrodia. Apoptosis / drug effects. Biological Products / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Cell Proliferation / drug effects

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  • [Copyright] Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 19995598.001).
  • [ISSN] 1872-7573
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / ARHGDIA protein, human; 0 / Antineoplastic Agents; 0 / Biological Products; 0 / Galectin 1; 0 / Guanine Nucleotide Dissociation Inhibitors; 0 / Peptide Initiation Factors; 0 / RNA-Binding Proteins; 0 / eukaryotic translation initiation factor 5A; 0 / rho Guanine Nucleotide Dissociation Inhibitor alpha; 0 / rho-Specific Guanine Nucleotide Dissociation Inhibitors; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.22.- / Calpain
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78. Nemes J, Boda R, Redl P, Márton I: [Oral squamous cell carcinoma in north-eastern Hungary. II. Etiological factors]. Fogorv Sz; 2006 Oct;99(5):179-85
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  • [Title] [Oral squamous cell carcinoma in north-eastern Hungary. II. Etiological factors].
  • The purpose of this study is to determine the possible etiological factors of oral squamous cell carcinoma (OSCC) in North-Eastern Hungary.
  • The following risk factors were investigated: tobacco and alcohol consumption, dental status, rural vs. urban residence, and high risk HPV infection.
  • Smoking significantly correlated with younger age, male gender, advanced clinical stages and alcohol consumption.
  • The majority of the patients (75.5%) consumed alcohol, 41.1% regularly over the acceptable range.
  • HPV DNA presence was not related to gender, clinical stage, histological grade or other risk factors.
  • In the study population the most important risk factor for developing oral cancer is tobacco smoking followed by alcohol consumption.
  • Avoidance of tobacco smoking and a reduced amount of alcohol, together with healthy nutrition and regular dental care should be emphasized.
  • [MeSH-major] Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / etiology. Mouth Neoplasms / epidemiology. Mouth Neoplasms / etiology
  • [MeSH-minor] Age Factors. Aged. Alcohol Drinking / adverse effects. Female. HIV Infections / complications. Humans. Hungary / epidemiology. Male. Middle Aged. Risk Factors. Rural Population / statistics & numerical data. Smoking / adverse effects. Survival Rate. Tooth Diseases / complications. Urban Population / statistics & numerical data


79. Lundell LR: Etiology and risk factors for esophageal carcinoma. Dig Dis; 2010;28(4-5):641-4
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  • [Title] Etiology and risk factors for esophageal carcinoma.
  • Trends toward increasing incidence rates were observed for esophageal and gastric cardia adenocarcinoma in Western countries and were associated with trends toward stabilizing or declining incidence rates for esophageal squamous cell carcinoma, suggesting that these tumors might be associated with distinct risk factors.
  • Overweight and obesity have been consistently related to esophageal adenocarcinoma, but not to squamous cell carcinoma.
  • Body mass index seems to be inversely related to the risk of esophageal squamous cell carcinoma.
  • The influence of obesity on esophageal adenocarcinoma and gastric cardia adenocarcinoma may be related to higher incidence of gastroesophageal reflux in obese persons since the risk of gastroesophageal reflux is strongly related to the risk for Barrett's esophagus.
  • Tobacco smoking is a strong risk factor for esophageal squamous cell carcinoma, but is only a weak risk factor for esophageal adenocarcinoma.
  • Alcohol consumption is a strong risk factor for esophageal squamous cell carcinoma, but is not consistently related to esophageal adenocarcinoma.
  • It has been suggested that infection with H. pylori is protective to adenocarcinoma, but might be a risk factor for squamous cell carcinoma, although the role of H. pylori in the etiology of these cancers remains somewhat unclear.

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  • [Copyright] Copyright © 2010 S. Karger AG, Basel.
  • (PMID = 21088416.001).
  • [ISSN] 1421-9875
  • [Journal-full-title] Digestive diseases (Basel, Switzerland)
  • [ISO-abbreviation] Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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80. Gomaa AI, Khan SA, Toledano MB, Waked I, Taylor-Robinson SD: Hepatocellular carcinoma: epidemiology, risk factors and pathogenesis. World J Gastroenterol; 2008 Jul 21;14(27):4300-8
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  • [Title] Hepatocellular carcinoma: epidemiology, risk factors and pathogenesis.
  • Hepatocellular carcinoma (HCC) is the commonest primary malignant cancer of the liver in the world.
  • Given that the burden of chronic liver disease is expected to rise owing to increasing rates of alcoholism, hepatitis B and C prevalence and obesity-related fatty liver disease, it is expected that the incidence of HCC will also increase in the foreseeable future.
  • This article summarizes the international epidemiology, the risk factors and the pathogenesis of HCC, including the roles of viral hepatitis, toxins, such as alcohol and aflatoxin, and insulin resistance.

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  • [Cites] Lancet. 2003 Dec 20;362(9401):2083-8 [14697812.001]
  • [Cites] Kurume Med J. 2004;51(2):141-9 [15373231.001]
  • [Cites] Carcinogenesis. 2004 Oct;25(10):2023-32 [15180947.001]
  • [Cites] Gastroenterology. 2004 Nov;127(5 Suppl 1):S5-S16 [15508102.001]
  • [Cites] Nature. 1991 Apr 4;350(6317):429-31 [1672732.001]
  • [Cites] Dig Dis Sci. 1991 Aug;36(8):1134-6 [1650690.001]
  • [Cites] Virology. 1992 May;188(1):331-41 [1314459.001]
  • [Cites] Lancet. 1992 Aug 15;340(8816):427 [1353577.001]
  • [Cites] Cancer Res. 1992 Nov 15;52(22):6358-64 [1330291.001]
  • [Cites] N Engl J Med. 1992 Dec 31;327(27):1906-11 [1454085.001]
  • [Cites] Cancer Res. 1993 Feb 15;53(4):790-4 [8381328.001]
  • [Cites] J Egypt Public Health Assoc. 1992;67(3-4):223-36 [1296960.001]
  • [Cites] J Infect Dis. 1993 Sep;168(3):789-90 [8394867.001]
  • [Cites] Jpn J Cancer Res. 1993 Jul;84(7):708-14 [8396564.001]
  • [Cites] Am J Trop Med Hyg. 1993 Oct;49(4):440-7 [7692754.001]
  • [Cites] Virology. 1994 Feb;198(2):489-503 [8291231.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Mar 15;91(6):2230-4 [8134379.001]
  • [Cites] J Hepatol. 1994 Aug;21(2):159-66 [7527435.001]
  • [Cites] Br J Haematol. 1994 Jul;87(3):555-61 [7993796.001]
  • [Cites] Hepatology. 1995 Jan;21(1):77-82 [7806171.001]
  • [Cites] J Hepatol. 1994 Oct;21(4):656-66 [7814813.001]
  • [Cites] J Virol. 1995 Mar;69(3):1851-9 [7853526.001]
  • [Cites] Lancet. 1995 Feb 18;345(8947):413-5 [7772123.001]
  • [Cites] N Engl J Med. 1995 Jun 1;332(22):1463-6 [7739682.001]
  • [Cites] Acta Trop. 1995 May;59(2):155-61 [7545863.001]
  • [Cites] Vaccine. 1995;13 Suppl 1:S47-9 [7571830.001]
  • [Cites] Hepatology. 1996 Apr;23(4):695-9 [8666319.001]
  • [Cites] J Hepatol. 1996 Mar;24(3):277-85 [8778193.001]
  • [Cites] Gastroenterology. 1996 Sep;111(3):691-700 [8780574.001]
  • [Cites] J Hepatol. 1996 Jan;24(1):27-32 [8834021.001]
  • [Cites] J Natl Cancer Inst. 1996 Oct 16;88(20):1472-7 [8841022.001]
  • [Cites] Prog Clin Biol Res. 1996;395:211-22 [8895991.001]
  • [Cites] Hepatology. 1997 Feb;25(2):449-58 [9021963.001]
  • [Cites] Nat Med. 1998 Sep;4(9):1065-7 [9734402.001]
  • [Cites] Carcinogenesis. 1998 Aug;19(8):1369-75 [9744531.001]
  • [Cites] N Engl J Med. 1999 Mar 11;340(10):745-50 [10072408.001]
  • [Cites] Hepatology. 1999 Mar;29(3):664-9 [10051466.001]
  • [Cites] Bull World Health Organ. 1998;76 Suppl 2:152-3 [10063701.001]
  • [Cites] Int J Cancer. 1999 Mar 15;80(6):827-41 [10074914.001]
  • [Cites] Cancer. 1999 May 15;85(10):2132-7 [10326690.001]
  • [Cites] Int J Hyg Environ Health. 2005;208(5):329-39 [16217918.001]
  • [Cites] Liver Int. 2005 Dec;25(6):1097-107 [16343058.001]
  • [Cites] Methods Enzymol. 2005;401:307-41 [16399395.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Feb 17;340(3):916-28 [16403455.001]
  • [Cites] Gastroenterology. 2006 Mar;130(3):678-86 [16530509.001]
  • [Cites] Gastroenterology. 2006 Apr;130(4):1153-68 [16618410.001]
  • [Cites] Clin Chem Lab Med. 2006;44(5):653-6 [16681440.001]
  • [Cites] Hepatology. 2006 May;43(5):915-22 [16628669.001]
  • [Cites] Oncogene. 2006 Jun 26;25(27):3771-7 [16799618.001]
  • [Cites] J Infect Dis. 2006 Sep 1;194(5):594-9 [16897657.001]
  • [Cites] Am J Gastroenterol. 2006 Aug;101(8):1797-803 [16817842.001]
  • [Cites] N Engl J Med. 1976 Apr 1;294(14):746-9 [943694.001]
  • [Cites] Lancet. 1981 Nov 21;2(8256):1129-33 [6118576.001]
  • [Cites] Gastroenterology. 1986 Feb;90(2):263-7 [2416625.001]
  • [Cites] Int J Cancer. 1988 Dec 15;42(6):872-6 [2847988.001]
  • [Cites] Cancer Res. 1989 Feb 15;49(4):1049-51 [2912550.001]
  • [Cites] Hum Pathol. 1989 Jun;20(6):594-8 [2656500.001]
  • [Cites] Lancet. 1989 Oct 28;2(8670):1004-6 [2572739.001]
  • [Cites] Lancet. 1989 Oct 28;2(8670):1006-8 [2572740.001]
  • [Cites] Hepatology. 1990 Jan;11(1):74-80 [2295475.001]
  • [Cites] Hepatology. 1990 Oct;12(4 Pt 1):671-5 [2170265.001]
  • [Cites] Cancer. 1991 Jan 15;67(2):429-33 [1845946.001]
  • [Cites] Hepatology. 1999 Aug;30(2):517-25 [10421662.001]
  • [Cites] BMJ. 1999 Sep 4;319(7210):640 [10473489.001]
  • [Cites] Gastroenterology. 2004 Dec;127(6):1733-8 [15578511.001]
  • [Cites] Dis Mon. 2004 Oct;50(10):556-73 [15616490.001]
  • [Cites] Gastroenterology. 2005 Jan;128(1):24-32 [15633120.001]
  • [Cites] Food Chem Toxicol. 2005 Mar;43(3):433-41 [15680679.001]
  • [Cites] J Natl Cancer Inst. 2005 Feb 16;97(4):265-72 [15713961.001]
  • [Cites] Gut. 2005 Apr;54(4):533-9 [15753540.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] J Hepatol. 2005 Apr;42(4):444-6 [15763323.001]
  • [Cites] Int J Cancer. 2005 Jun 10;115(2):290-5 [15688396.001]
  • [Cites] Semin Liver Dis. 2005;25(2):143-54 [15918143.001]
  • [Cites] Liver Int. 2005 Aug;25(4):696-703 [15998418.001]
  • [Cites] Lancet Infect Dis. 2005 Sep;5(9):558-67 [16122679.001]
  • [Cites] World J Gastroenterol. 2005 Sep 7;11(33):5193-8 [16127751.001]
  • [Cites] Int J Cancer. 2006 Dec 15;119(12):2916-21 [16998792.001]
  • [Cites] J Med Virol. 2007 Jan;79(1):92-6 [17133558.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2521-5 [17164379.001]
  • [Cites] Cancer Sci. 2007 Feb;98(2):214-8 [17233838.001]
  • [Cites] Int J Cancer. 2007 Apr 1;120(7):1555-9 [17205531.001]
  • [Cites] J Viral Hepat. 2007 Mar;14(3):153-60 [17305880.001]
  • [Cites] Am J Med. 2007 Mar;120(3):194-202 [17349437.001]
  • [Cites] J Chin Med Assoc. 2007 Apr;70(4):141-5 [17475593.001]
  • [Cites] Hepatology. 2007 Aug;46(2):430-5 [17580359.001]
  • [Cites] Clin Liver Dis. 2007 Nov;11(4):797-816, viii [17981229.001]
  • [Cites] J Infect Dis. 2000 May;181(5):1528-36 [10823750.001]
  • [Cites] Teratog Carcinog Mutagen. 2000;20(4):229-40 [10910473.001]
  • [Cites] Eur J Epidemiol. 2000 May;16(5):419-23 [10997828.001]
  • [Cites] Immunol Lett. 2000 Oct 3;74(2):117-20 [10996386.001]
  • [Cites] Cell Immunol. 2000 Aug 1;203(2):111-23 [11006009.001]
  • [Cites] Infection. 2000 Nov-Dec;28(6):341-5 [11139151.001]
  • [Cites] Am J Gastroenterol. 2001 Jan;96(1):179-83 [11197250.001]
  • [Cites] Gastroenterology. 2001 Jul;121(1):91-100 [11438497.001]
  • [Cites] J Clin Gastroenterol. 2001 Aug;33(2):123-6 [11468438.001]
  • [Cites] J Clin Epidemiol. 2001 Aug;54(8):823-9 [11470392.001]
  • [Cites] J Hepatol. 2001 Sep;35(3):421-30 [11592607.001]
  • [Cites] J Gastroenterol. 2001 Oct;36(10):651-60 [11686474.001]
  • [Cites] Ann Intern Med. 2001 Nov 6;135(9):796-800 [11694104.001]
  • [Cites] Lancet. 1997 Mar 22;349(9055):825-32 [9121257.001]
  • [Cites] N Engl J Med. 1997 Jun 26;336(26):1855-9 [9197213.001]
  • [Cites] Eur J Cancer. 1997 Apr;33(4):629-34 [9274446.001]
  • [Cites] Hepatology. 1997 Sep;26(3 Suppl 1):2S-10S [9305656.001]
  • [Cites] J Natl Cancer Inst. 1997 Sep 17;89(18):1360-5 [9308706.001]
  • [Cites] J Virol. 1997 Oct;71(10):7387-92 [9311817.001]
  • [Cites] Zhonghua Yi Xue Za Zhi (Taipei). 1997 Jul;60(1):40-7 [9316327.001]
  • [Cites] Liver. 1997 Oct;17(5):215-23 [9387912.001]
  • [Cites] Int J Cancer. 1998 Jan 30;75(3):347-54 [9455792.001]
  • [Cites] Hepatology. 1998 Jun;27(6):1730-5 [9620350.001]
  • [Cites] J Gastroenterol Hepatol. 1998 Apr;13(4):419-26 [9641308.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 21;95(15):8847-51 [9671767.001]
  • [Cites] Hepatology. 1998 Sep;28(3):805-9 [9731576.001]
  • [Cites] Hepatology. 1999 Dec;30(6):1356-62 [10573511.001]
  • [Cites] Hepatology. 2000 Feb;31(2):513-20 [10655279.001]
  • [Cites] Int J Cancer. 2000 Feb 15;85(4):498-502 [10699921.001]
  • [Cites] J Hepatol. 2000;32(1 Suppl):225-37 [10728807.001]
  • [Cites] Lancet. 2000 Mar 11;355(9207):887-91 [10752705.001]
  • [Cites] J Gastroenterol Hepatol. 2000 Apr;15(4):357-68 [10824878.001]
  • [Cites] Ann N Y Acad Sci. 2002 Jun;963:13-20 [12095924.001]
  • [Cites] Gastroenterology. 2002 Jul;123(1):134-40 [12105842.001]
  • [Cites] J Vasc Interv Radiol. 2002 Sep;13(9 Pt 2):S169-71 [12354833.001]
  • [Cites] Am J Gastroenterol. 2002 Nov;97(11):2886-95 [12425564.001]
  • [Cites] J Hepatol. 2002 Dec;37(6):806-13 [12445422.001]
  • [Cites] Jpn J Cancer Res. 2002 Dec;93(12):1287-92 [12495467.001]
  • [Cites] Gastroenterology. 2003 Feb;124(2):327-34 [12557138.001]
  • (PMID = 18666317.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] ENG
  • [Grant] United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aflatoxins
  • [Number-of-references] 134
  • [Other-IDs] NLM/ PMC2731180
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81. Gao C, Yao SK: Diabetes mellitus: a "true" independent risk factor for hepatocellular carcinoma? Hepatobiliary Pancreat Dis Int; 2009 Oct;8(5):465-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diabetes mellitus: a "true" independent risk factor for hepatocellular carcinoma?
  • BACKGROUND: Diabetes mellitus (DM) is thought to be associated with an increased risk of hepatocellular carcinoma (HCC) in some published studies.
  • DATA SOURCES: MEDLINE and PubMed searches were conducted for published studies (between January 1966 and June 2009) to identify relevant articles using the keywords "diabetes", "insulin resistance" and "hepatocellular carcinoma", including "primary liver cancer".
  • (1) the significant synergy between DM, hepatitis virus infection, and heavy alcohol consumption in HCC;.
  • Related issues should be clarified by more research.
  • [MeSH-major] Carcinoma, Hepatocellular / epidemiology. Diabetes Complications / complications. Liver Neoplasms / epidemiology
  • [MeSH-minor] Alcohol Drinking / adverse effects. Hepatitis C, Chronic / complications. Humans. Risk Factors

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  • (PMID = 19822488.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Number-of-references] 41
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82. Saunders D, Seidel D, Allison M, Lyratzopoulos G: Systematic review: the association between obesity and hepatocellular carcinoma - epidemiological evidence. Aliment Pharmacol Ther; 2010 May;31(10):1051-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systematic review: the association between obesity and hepatocellular carcinoma - epidemiological evidence.
  • We examined such evidence for hepatocellular carcinoma.
  • AIM: To review the effect of increased levels of body mass index on hepatocellular carcinoma risk.
  • METHODS: We reviewed systematically the literature examining the association between increased body mass index and hepatocellular carcinoma risk.
  • Of the cohort studies, 75% of person-years related to North Americans, 15% to East Asians, and 10% to Europeans.
  • Three cohort studies adjusted for alcohol consumption, only one cohort study adjusted for hepatitis infection status.
  • Seven cohort studies found a positive association between obesity (body mass index > or =30 kg/m(2)) and hepatocellular carcinoma risk (relative risks ranging from 1.4 to 4.1); two reported no association; and one reported a significant inverse association for a population subgroup (relative risk = 0.7, 95% confidence interval: 0.5-0.9).
  • CONCLUSION: Although most studies did not adjust for confounders and most data relate to a single world region, the overall evidence is suggestive of an increased hepatocellular carcinoma risk in obese and overweight individuals.
  • [MeSH-major] Carcinoma, Hepatocellular / complications. Liver Neoplasms / complications. Obesity / complications

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  • [CommentIn] Aliment Pharmacol Ther. 2010 Jul;32(2):304-5 [20636625.001]
  • (PMID = 20175765.001).
  • [ISSN] 1365-2036
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 56
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83. Cao W, Cai L, Rao JY, Pantuck A, Lu ML, Dalbagni G, Reuter V, Scher H, Cordon-Cardo C, Figlin RA, Belldegrun A, Zhang ZF: Tobacco smoking, GSTP1 polymorphism, and bladder carcinoma. Cancer; 2005 Dec 1;104(11):2400-8
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  • [Title] Tobacco smoking, GSTP1 polymorphism, and bladder carcinoma.
  • BACKGROUND: Although cigarette smoking is considered a major risk factor for bladder carcinoma, little is known about the interaction between metabolic genes such as glutathione-S-transferase P1 and tobacco smoking in this process.
  • GSTP1 may play a role in detoxification of tobacco-related carcinogens.
  • METHODS: In this case-control study of 145 cases with bladder carcinoma (male:female = 7.5:1) and 170 noncancer controls (male:female = 3.7:1), the relation between genetic polymorphisms of GSTP1 and susceptibility to bladder carcinoma was investigated and the gene-environment interaction between tobacco smoking and GSTP1 polymorphism was evaluated.
  • RESULTS: Cigarette smoking was confirmed as a risk factor of bladder carcinoma with an OR of 3.1 (95% CI: 1.7-5.9) after controlling for potential confounding factors.
  • CONCLUSIONS: The results indicate that the Ile 105 allele is associated with an increased risk of bladder carcinoma and suggest that individuals who smoke and possess the Ile allele might be at increased risk for bladder carcinoma.
  • [MeSH-minor] Alcohol Drinking / genetics. Case-Control Studies. DNA, Neoplasm / blood. DNA, Neoplasm / isolation & purification. Female. Humans. Isoleucine / genetics. Male. Middle Aged. Odds Ratio. Patient Selection

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  • (PMID = 16240451.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA09142; United States / NIEHS NIH HHS / ES / ES06718; United States / NCI NIH HHS / CA / U01 CA96116
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 04Y7590D77 / Isoleucine; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi
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84. Sturgis EM, Pytynia KB: After the smoke clears: environmental and occupational risks for carcinoma of the upper aerodigestive tract. Cancer J; 2005 Mar-Apr;11(2):96-103
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  • [Title] After the smoke clears: environmental and occupational risks for carcinoma of the upper aerodigestive tract.
  • Both environmental and occupational exposures are associated with the development of carcinomas of the upper aerodigestive tract, although most squamous cell carcinomas of the upper aerodigestive tract are related to smoking and drinking.
  • This review discusses environmental and occupational risk factors, other than tobacco and alcohol, for carcinoma of the upper aerodigestive tract and the difficulties encountered when attempts are made to study these environmental and occupational exposures.
  • [MeSH-major] Carcinoma, Squamous Cell / etiology. Head and Neck Neoplasms / etiology. Occupational Exposure / adverse effects. Tobacco Smoke Pollution / adverse effects

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  • (PMID = 15969982.001).
  • [ISSN] 1528-9117
  • [Journal-full-title] Cancer journal (Sudbury, Mass.)
  • [ISO-abbreviation] Cancer J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tobacco Smoke Pollution
  • [Number-of-references] 72
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85. Otani K, Korenaga M, Beard MR, Li K, Qian T, Showalter LA, Singh AK, Wang T, Weinman SA: Hepatitis C virus core protein, cytochrome P450 2E1, and alcohol produce combined mitochondrial injury and cytotoxicity in hepatoma cells. Gastroenterology; 2005 Jan;128(1):96-107
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  • [Title] Hepatitis C virus core protein, cytochrome P450 2E1, and alcohol produce combined mitochondrial injury and cytotoxicity in hepatoma cells.
  • BACKGROUND & AIMS: Alcohol consumption exacerbates liver injury in chronic hepatitis C, and enhanced mitochondrial oxidative stress is one possible mechanism.
  • The aim of this study was to determine whether hepatitis C virus core protein and alcohol-inducible cytochrome P450 2E1 contribute to reactive oxygen species production and cytotoxicity in human hepatoma cells.
  • Alcohol further depletes mitochondrial reduced glutathione, which exacerbates depolarization and cell death.
  • Sensitization of mitochondria to oxidative insults is thus a potential mechanism for alcohol-related exacerbation of liver injury in chronic hepatitis C.
  • [MeSH-minor] Carcinoma, Hepatocellular. Cell Death / physiology. Cell Line, Tumor. Chronic Disease. Glutathione. Humans. Liver Neoplasms. Models, Biological. Oxidative Stress / physiology. Reactive Oxygen Species / metabolism. Tumor Necrosis Factor-alpha

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  • [CommentIn] Gastroenterology. 2005 Jan;128(1):232-4 [15633141.001]
  • (PMID = 15633127.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NIAAA NIH HHS / AA / AA 12863
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alcohols; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; 0 / Viral Core Proteins; 0 / nucleocapsid protein, Hepatitis C virus; 3K9958V90M / Ethanol; EC 1.14.13.- / Cytochrome P-450 CYP2E1; GAN16C9B8O / Glutathione
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86. Yokoi Y, Suzuki S, Baba S, Inaba K, Konno H, Nakamura S: Clinicopathological features of hepatocellular carcinomas (HCCs) arising in patients without chronic viral infection or alcohol abuse: a retrospective study of patients undergoing hepatic resection. J Gastroenterol; 2005 Mar;40(3):274-82
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  • [Title] Clinicopathological features of hepatocellular carcinomas (HCCs) arising in patients without chronic viral infection or alcohol abuse: a retrospective study of patients undergoing hepatic resection.
  • BACKGROUND: This study was carried out to clarify the etiology and clinicopathological features of hepatocellular carcinomas (HCCs) arising in patients without chronic viral infection or alcohol abuse.
  • METHODS: HCC patients who underwent resection were divided into three groups: a non-B non-C (NBNC) group (n = 13), who were seronegative for hepatitis B surface antigen (HBs Ag) and anti-hepatitis C antibody (HCV Ab), excluding a history of alcohol abuse; a B group (n = 25), who were seropositive for HBs Ag only; and a C group (n = 116), who were seropositive for HCV Ab only.
  • We analyzed the features of tumor- and host-related factors and the outcome of the NBNC group.
  • There were no significant differences in tumor-related factors, except for higher serum levels of alpha-fetoprotein in the NBNC group.
  • [MeSH-major] Carcinoma, Hepatocellular / etiology. Hepatectomy. Liver / pathology. Liver Neoplasms / etiology

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  • (PMID = 15830287.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Hepatitis B Antigens; 0 / Hepatitis C Antibodies; 0 / alpha-Fetoproteins
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87. Capocaccia R, Sant M, Berrino F, Simonetti A, Santi V, Trevisani F, EUROCARE Working Group: Hepatocellular carcinoma: trends of incidence and survival in Europe and the United States at the end of the 20th century. Am J Gastroenterol; 2007 Aug;102(8):1661-70; quiz 1660, 1671
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hepatocellular carcinoma: trends of incidence and survival in Europe and the United States at the end of the 20th century.
  • OBJECTIVES: There is large geographic variation in incidence levels and time trends of hepatocellular carcinoma.
  • METHODS: Since comparisons based on cancer registry data are problematic because of variations in liver cancer definition and coding, we considered a subset of cases likely to be mainly hepatocellular carcinoma, suitable for international comparison.
  • CONCLUSIONS: Increasing incidence in southern Europe is probably related to hepatitis B and C infection and increasing alcohol intake, while improving survival may be due to greater surveillance for cirrhosis.
  • [MeSH-major] Carcinoma, Hepatocellular / epidemiology. Liver Neoplasms / epidemiology

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  • (PMID = 17555459.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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88. Lansford CD, Guerriero CH, Kocan MJ, Turley R, Groves MW, Bahl V, Abrahamse P, Bradford CR, Chepeha DB, Moyer J, Prince ME, Wolf GT, Aebersold ML, Teknos TN: Improved outcomes in patients with head and neck cancer using a standardized care protocol for postoperative alcohol withdrawal. Arch Otolaryngol Head Neck Surg; 2008 Aug;134(8):865-72
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  • [Title] Improved outcomes in patients with head and neck cancer using a standardized care protocol for postoperative alcohol withdrawal.
  • OBJECTIVE: To show clinical benefit in the main outcome measures by the use of a standardized protocol for identification, characterization, and treatment of alcohol withdrawal syndrome (AWS) in postoperative patients with head and neck cancer.
  • RESULTS: Protocol patients demonstrated significantly fewer AWS-related ICU transfers and less delirium and violence than preprotocol patients.
  • CONCLUSION: Use of the standardized AWS symptom-triggered protocol decreased delirium, violence, and AWS-related ICU transfers without significantly increasing hospital charges.
  • [MeSH-major] Alcoholism / rehabilitation. Carcinoma, Squamous Cell / surgery. Ethanol / toxicity. Otorhinolaryngologic Neoplasms / surgery. Postoperative Complications / rehabilitation. Substance Withdrawal Syndrome / rehabilitation
  • [MeSH-minor] Adult. Aged. Alcohol Withdrawal Delirium / diagnosis. Alcohol Withdrawal Delirium / rehabilitation. Cohort Studies. Female. Humans. Intensive Care Units. Male. Mass Screening. Middle Aged. Outcome and Process Assessment (Health Care). Patient Admission. Prospective Studies. Retrospective Studies. Treatment Outcome

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  • (PMID = 18711062.001).
  • [ISSN] 1538-361X
  • [Journal-full-title] Archives of otolaryngology--head & neck surgery
  • [ISO-abbreviation] Arch. Otolaryngol. Head Neck Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 3K9958V90M / Ethanol
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89. ElSaadany S, Giulivi A: Epidemiology of hepatocellular carcinoma in Canada, 1995: analysis of death certificates. Chronic Dis Can; 2006;27(3):125-9
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  • [Title] Epidemiology of hepatocellular carcinoma in Canada, 1995: analysis of death certificates.
  • A descriptive analysis of hepatocellular carcinoma (HCC) deaths in Canada for 1995 was undertaken.
  • Of these, the largest proportion (45 percent) was of unknown type while 23 patients (22 percent) had alcohol-related cirrhosis.
  • [MeSH-major] Carcinoma, Hepatocellular / epidemiology. Death Certificates. Liver Neoplasms / epidemiology

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  • (PMID = 17306064.001).
  • [ISSN] 0228-8699
  • [Journal-full-title] Chronic diseases in Canada
  • [ISO-abbreviation] Chronic Dis Can
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
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90. Czerninski R, Kaplan I, Almoznino G, Maly A, Regev E: Oral squamous cell carcinoma around dental implants. Quintessence Int; 2006 Oct;37(9):707-11
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  • [Title] Oral squamous cell carcinoma around dental implants.
  • It is well documented that oral squamous cell carcinoma (OSCC) is related to risk factors such as smoking and alcohol consumption as well as premalignant lesions and conditions such as leukoplakia, oral lichen planus (OLP), and previous malignancy of the upper respiratory system and gastrointestinal tract.
  • [MeSH-major] Carcinoma, Squamous Cell / diagnosis. Dental Implants / adverse effects. Gingival Neoplasms / diagnosis. Mandibular Neoplasms / diagnosis

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  • (PMID = 17017632.001).
  • [ISSN] 0033-6572
  • [Journal-full-title] Quintessence international (Berlin, Germany : 1985)
  • [ISO-abbreviation] Quintessence Int
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Dental Implants
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91. Rossi L, Zoratto F, Papa A, Iodice F, Minozzi M, Frati L, Tomao S: Current approach in the treatment of hepatocellular carcinoma. World J Gastrointest Oncol; 2010 Sep 15;2(9):348-59

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current approach in the treatment of hepatocellular carcinoma.
  • Hepatocellular carcinoma (HCC) is the most common malignant hepatobiliary disease; it is responsible for about 1 million deaths per year.
  • Risk factors include hepatitis B and C, hepatic cirrhosis, including alcohol related hepatitis, metabolic and nutritional hepatic damage.

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  • (PMID = 21160806.001).
  • [ISSN] 1948-5204
  • [Journal-full-title] World journal of gastrointestinal oncology
  • [ISO-abbreviation] World J Gastrointest Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2999141
  • [Keywords] NOTNLM ; Hepatocarcinogenesis / Hepatocarcinoma / Local treatments / Sorafenib / Systemic treatments / Targeted therapy
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92. Yeh CB, Tsai HT, Chen YC, Kuo WH, Chen TY, Hsieh YH, Chou MC, Yang SF: Genetic polymorphism of CCR2-64I increased the susceptibility of hepatocellular carcinoma. J Surg Oncol; 2010 Sep 1;102(3):264-70
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  • [Title] Genetic polymorphism of CCR2-64I increased the susceptibility of hepatocellular carcinoma.
  • BACKGROUND AND OBJECTIVES: The purpose of this study was to investigate genetic impact of monocyte chemoattractant protein-1 (MCP-1) and its receptor chemokine receptor-2 (CCR2) gene polymorphisms on the susceptibility and clinicopathological characteristics of hepatocellular carcinoma (HCC).
  • There was no synergistic effect between gene polymorphism and environmental risk factors, including tobacco and alcohol consumptions, as well as clinicopathological parameters of HCC for MCP-1 -2518G/A and CCR2 V64I genes, respectively.
  • CONCLUSIONS: CCR2-64I gene polymorphism is an important factor for the susceptibility of HCC but it might not influence the clinical pathological progression of HCC, and the contribution of CCR2-64I gene polymorphism on the susceptibility of HCC could be not through the affection of liver injury-related clinical pathological characteristics.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Genetic Predisposition to Disease. Liver Neoplasms / genetics. Polymorphism, Genetic. Receptors, CCR2 / genetics

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  • [Copyright] 2010 Wiley-Liss, Inc.
  • (PMID = 20740585.001).
  • [ISSN] 1096-9098
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCL2 protein, human; 0 / CCR2 protein, human; 0 / Chemokine CCL2; 0 / Receptors, CCR2
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93. Barazani Y, Hiatt JR, Tong MJ, Busuttil RW: Chronic viral hepatitis and hepatocellular carcinoma. World J Surg; 2007 Jun;31(6):1243-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic viral hepatitis and hepatocellular carcinoma.
  • BACKGROUND: Hepatocellular carcinoma (HCC) is the third leading cause of death from malignancy worldwide, and its increasing incidence parallels rising global rates of hepatitis B (HBV) and hepatitis C (HCV).
  • Hepatitis B patients exhibited stronger family histories of liver disease (54%) and HCC (33%), whereas HCV risk factors included blood transfusion (56%), intravenous drug abuse (31%), and alcohol consumption (44%; p < 0.0001 for all comparisons).
  • CONCLUSIONS: Patients with HBV- and HCV-related HCC have different epidemiologic, clinical, and survival characteristics.
  • [MeSH-major] Carcinoma, Hepatocellular / diagnosis. Hepatitis B, Chronic / complications. Hepatitis C, Chronic / complications. Liver Neoplasms / diagnosis

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  • (PMID = 17440771.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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94. Teramoto R, Minagawa H, Honda M, Miyazaki K, Tabuse Y, Kamijo K, Ueda T, Kaneko S: Protein expression profile characteristic to hepatocellular carcinoma revealed by 2D-DIGE with supervised learning. Biochim Biophys Acta; 2008 May;1784(5):764-72
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  • [Title] Protein expression profile characteristic to hepatocellular carcinoma revealed by 2D-DIGE with supervised learning.
  • Hepatocellular carcinoma (HCC) is one of the most common and aggressive human malignancies.
  • Although several major risks related to HCC, e.g., hepatitis B and/or hepatitis C virus infection, aflatoxin B1 exposure, alcohol drinking and genetic defects have been revealed, the molecular mechanisms leading to the initiation and progression of HCC have not been clarified.
  • We confirmed that SGB is able to identify the known HCC-related proteins, e.g., heat shock proteins, carbonic anhydrase 2.
  • Moreover, we identified the differentially expressed proteins associated with histological grade of HCC and AFP level and found that aldo-keto reductase 1B10 (AKR1B10) is related to well differentiated HCC, keratin 8 (KRT8) is related to both histological grade and AFP level and protein disulfide isomerase-associated 3 (PDIA3) is associated with both HCC and AFP level.
  • [MeSH-major] Carcinoma, Hepatocellular / chemistry. Liver Neoplasms / chemistry. Proteomics

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  • (PMID = 18359300.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / alpha-Fetoproteins
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95. Asia-Pacific Working Party on Prevention of Hepatocellular Carcinoma: Prevention of hepatocellular carcinoma in the Asia-Pacific region: consensus statements. J Gastroenterol Hepatol; 2010 Apr;25(4):657-63
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  • [Title] Prevention of hepatocellular carcinoma in the Asia-Pacific region: consensus statements.
  • Among approximately 650,000 people who die from hepatocellular carcinoma (HCC) each year, at least two-thirds live in Asia.
  • Separate reviews have summarized epidemiology of HCC, preventive approaches related to hepatitis B virus (HBV), hepatitis C virus (HCV) and non-viral liver diseases, and the role of surveillance to detect HCC at a curative stage.
  • There is currently insufficient evidence to give firm recommendations on alcohol, obesity/metabolic risk factors and other liver diseases.
  • [MeSH-major] Carcinoma, Hepatocellular / prevention & control. Hepatitis B, Chronic / prevention & control. Hepatitis C, Chronic / prevention & control. Liver Neoplasms / prevention & control. Mass Screening. Primary Prevention

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  • (PMID = 20492323.001).
  • [ISSN] 1440-1746
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Practice Guideline; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Hepatitis B Vaccines
  • [Investigator] Farrell GC; Chan HL; Yuen MF; Amarapurkar DN; Chutaputti A; Fan JG; Hou JL; Han KH; Kao JH; Lim SG; Mohamed R; Sollano J; Ueno Y
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96. Huang TT, Hsu LP, Hsu YH, Chen PR: Surgical outcome in patients with oral verrucous carcinoma: long-term follow-up in an endemic betel quid chewing area. ORL J Otorhinolaryngol Relat Spec; 2009;71(6):323-8
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  • [Title] Surgical outcome in patients with oral verrucous carcinoma: long-term follow-up in an endemic betel quid chewing area.
  • BACKGROUND/AIMS: To evaluate the clinical features and prognosis of patients with oral verrucous carcinoma (OVC) in an endemic betel quid chewing area.
  • All patients had been exposed to betel quid, cigarette smoking, and/or alcohol.
  • [MeSH-major] Alcohol Drinking / adverse effects. Areca / adverse effects. Carcinoma, Verrucous. Mouth Neoplasms. Smoking / adverse effects

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 20029242.001).
  • [ISSN] 1423-0275
  • [Journal-full-title] ORL; journal for oto-rhino-laryngology and its related specialties
  • [ISO-abbreviation] ORL J. Otorhinolaryngol. Relat. Spec.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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97. Psyrri A, Gouveris P, Vermorken JB: Human papillomavirus-related head and neck tumors: clinical and research implication. Curr Opin Oncol; 2009 May;21(3):201-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human papillomavirus-related head and neck tumors: clinical and research implication.
  • HPV-associated HNSCCs represent a different disease entity from those associated with the traditional risk factors of tobacco and alcohol use.
  • RECENT FINDINGS: In recent years, there has been an increase in the annual incidence of HPV-related HNSCC in the United States and Europe.
  • HPV-associated HNSCCs have a better prognosis compared with stage-matched non-HPV-related HNSCC in the majority of studies.
  • SUMMARY: The increasing incidence of HPV-related HNSCC has led to the development of novel research strategies in HNSCC.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Squamous Cell / complications. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / therapy. Carcinoma, Squamous Cell / virology. Humans. Prognosis

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  • (PMID = 19370803.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 37
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98. Luo RH, Zhao ZX, Zhou XY, Gao ZL, Yao JL: Risk factors for primary liver carcinoma in Chinese population. World J Gastroenterol; 2005 Jul 28;11(28):4431-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk factors for primary liver carcinoma in Chinese population.
  • AIM: To evaluate the risk factors for primary liver carcinoma (PLC) in Chinese population.
  • All the related literatures were screened, and the risk factors for PLC in Chinese population were studied.
  • Ten factors related to PLC were demonstrated by sensitive analysis and funnel plot analysis.
  • CONCLUSION: The main risk factors for PLC in China are liver diseases, family history of liver carcinoma, poor psychic status, aflatoxin, and some unhealthy behaviors.
  • [MeSH-minor] Alcohol Drinking / epidemiology. China / epidemiology. Family Health. Food Contamination. Health Behavior. Humans. Risk Factors

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  • (PMID = 16038048.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Number-of-references] 5
  • [Other-IDs] NLM/ PMC4434676
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99. Chatzimichalis M, Xenellis J, Tzagaroulakis A, Sarof P, Banis K, Gazouli M, Bibas A: GSTT1, GSTM1, GSTM3 and NAT2 polymorphisms in laryngeal squamous cell carcinoma in a Greek population. J Laryngol Otol; 2010 Mar;124(3):318-23
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  • [Title] GSTT1, GSTM1, GSTM3 and NAT2 polymorphisms in laryngeal squamous cell carcinoma in a Greek population.
  • OBJECTIVE: It is well known that laryngeal squamous cell carcinoma is strongly related to tobacco and alcohol consumption.
  • Accumulating evidence suggests that alterations of detoxification enzymes, such as glutathione S-transferases and N-acetyltransferases, influence the risk of cancers associated with tobacco smoke and alcohol.
  • The study group consisted of 88 Greek patients with laryngeal squamous cell carcinoma; there were also 102 control subjects.
  • CONCLUSION: This study demonstrated a significant relationship between rapid acetylator genotypes and laryngeal squamous cell carcinoma in a Greek population.
  • [MeSH-major] Arylamine N-Acetyltransferase / genetics. Carcinoma, Squamous Cell / genetics. Glutathione Transferase / genetics. Laryngeal Neoplasms / genetics
  • [MeSH-minor] Acetylation. Aged. Alcohol Drinking / adverse effects. Case-Control Studies. Female. Gene Frequency. Genetic Predisposition to Disease. Greece / epidemiology. Humans. Isoenzymes / genetics. Male. Middle Aged. Phenotype. Polymerase Chain Reaction / methods. Polymorphism, Genetic / genetics. Retrospective Studies. Smoking / adverse effects

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  • (PMID = 19922706.001).
  • [ISSN] 1748-5460
  • [Journal-full-title] The Journal of laryngology and otology
  • [ISO-abbreviation] J Laryngol Otol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Isoenzymes; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / NAT2 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1; EC 2.5.1.18 / glutathione transferase M3-3
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100. Haddad R, Crum C, Chen Z, Krane J, Posner M, Li Y, Burk R: HPV16 transmission between a couple with HPV-related head and neck cancer. Oral Oncol; 2008 Aug;44(8):812-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HPV16 transmission between a couple with HPV-related head and neck cancer.
  • Although squamous cell carcinoma of the head and neck (SCCHN) is closely linked to tobacco and alcohol use, there is an increasing incidence HPV16-related SCCHN arising in the oropharynx.
  • Here, we report a couple-husband and wife diagnosed synchronously with squamous cell carcinoma of the head and neck wherein the tumors were positive for HPV16 by PCR diagnosis.
  • Both viral genomes were genetically identical and closely related to the revised European prototype, HPV16R.
  • [MeSH-major] Carcinoma, Squamous Cell / virology. Head and Neck Neoplasms / virology. Human papillomavirus 16 / isolation & purification. Papillomavirus Infections / transmission. Spouses

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  • (PMID = 18061523.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Viral
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