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1. 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
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anatomical subsite discrepancy in relation to the impact of the consumption of alcohol, tobacco and betel quid on esophageal cancer.
  • The carcinogenetic impact of risk factors on esophageal cancer (EC) may differ according to the portion of the esophagus where the tumor occurs.
  • It is unclear why more esophageal squamous cell carcinomas (SCC) developed in the middle location.
  • 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).
  • Concomitant exposure to these two agents brought the risks of EC at all three subsites up to 10- to 23.9-fold and additional tobacco-free betel quid to a 30.3- to 75.0-fold.
  • 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
  • [MeSH-minor] Adult. Aged. Case-Control Studies. Cocarcinogenesis. Drug Combinations. Drug Synergism. Female. Humans. Incidence. Male. Middle Aged. Risk Factors. Taiwan / epidemiology


2. 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).
  • Overall, 14 case-control studies and one cohort study, including 3000 cases of esophageal SCC, were included.
  • 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


3. Yokoyama A, Omori T: [Alcohol and oropharyngolaryngeal and digestive tract cancer]. Nihon Arukoru Yakubutsu Igakkai Zasshi; 2001 Dec;36(6):551-66
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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 oropharyngolaryngeal and digestive tract cancer].
  • Epidemiology has demonstrated that alcoholic beverages are causally related to oropharyngolaryngeal, esophageal, liver, colorectal, and female breast cancer.
  • Among Japanese male alcoholics screened by endoscopy combined with esophageal iodine staining and immunofecal occult blood tests, 4.2% had esophageal squamous cell carcinoma (SCC); 1.2%, oropharyngolaryngeal SCC; 1.4%, stomach adenocarcinoma; 1.9%, colorectal adenocarcinoma.
  • Inactive ALDH2 was also associated with synchronous and metachronous multiple esophageal cancers.
  • These results suggest a general role of acetaldehyde, an established animal carcinogen, in carcinogenesis of the human alimentary tract.
  • The normal alcohol dehydrogenase-2 (ADH2), encoded by ADH2*1/2*1, is another risk factor for oropharyngolaryngeal and esophageal cancer in Japanese alcoholics.
  • For patients with both normal ADH2 and inactive ALDH2, the risks for oropharyngolaryngeal and esophageal cancer are enhanced in a multiplicative fashion.
  • Use of this questionnaire to obtain information on ALDH2-associated cancer susceptibility could contribute to the prevention of alcohol-related cancer in Asians.
  • [MeSH-minor] Acetaldehyde / metabolism. Alcohol Dehydrogenase / genetics. Alcoholism / complications. Aldehyde Dehydrogenase / deficiency. Aldehyde Dehydrogenase / genetics. Animals. Genotype. Humans. Japan / epidemiology. Polymorphism, Genetic

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  • (PMID = 11828713.001).
  • [ISSN] 1341-8963
  • [Journal-full-title] Nihon Arukōru Yakubutsu Igakkai zasshi = Japanese journal of alcohol studies & drug dependence
  • [ISO-abbreviation] Nihon Arukoru Yakubutsu Igakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [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; GO1N1ZPR3B / Acetaldehyde
  • [Number-of-references] 65
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4. Szalay F: [Alcohol-induced gastrointestinal diseases]. Orv Hetil; 2003 Aug 24;144(34):1659-66
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  • [Title] [Alcohol-induced gastrointestinal diseases].
  • Alcohol induced gastrointestinal diseases are common and significant, and may lead to early death.
  • Although the alcohol itself is not carcinogenic, some maligancies are more common among alcoholics.
  • AIM AND METHODS: In this review the hepatic and extrahepatic metabolism of alcohol, the epidemiology, pathomechanism, clinical signs of the alcohol induced organ damages and the treatment options are summarized.
  • RESULTS: Type IV alcoholdehydrogenase in the stomach has a role in the first pass metabolism.
  • If the amount of alcohol exceeds the metabolising capacity, the toxic substances cause lipidperoxidation, membrane and organ injury.
  • Alcohol metabolism is different in the pancreas, the activity of fatty acid ethanol ester synthase activity is more pronounced.
  • In alcoholics the leukoplakia, oropharingeal carcinoma, oesophagitis, Mallory-Weiss syndrome, liver cirrhosis related oesophageal variceal bleeding, chronic gastritis, liver diseases, pancreatitis, bowel motility disorders, malabsorption and colorectal carcinoma are more frequent.
  • Following steatohepatitis, fibrosis, cirrhosis and liver carcinoma may develop.
  • The possibilities for medical treatment are limited, since some patients do not cooperate properly, and on the other hand, the drugs and measurements can control only a part of the whole process (antioxidants, anti-inflammatory drugs, monoclonal anti-cytokine antibodies), and are appropriate only for the treatment of complications as ascites, portal hypertension, oesophageal varices, portosystemic encephalopathy, malabsortion, infections, vitamin deficiency.
  • The task of the general practitioner and the role of the cooperation among the patient, the physician, the family and the community are very important.
  • [MeSH-major] Alcohol Drinking / adverse effects. Alcoholism / complications. Digestive System Diseases / etiology. Ethanol / metabolism. Liver Diseases, Alcoholic / metabolism
  • [MeSH-minor] Esophageal Diseases / etiology. Humans. Intestinal Diseases / etiology. Pancreatic Diseases / etiology. Stomach Diseases / etiology

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  • (PMID = 14528839.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 3K9958V90M / Ethanol
  • [Number-of-references] 40
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5. Harth V, Brüning T, Bolt HM: Renal carcinogenicity of trichloroethylene: update, mode of action, and fundamentals for occupational standard setting. Rev Environ Health; 2005 Apr-Jun;20(2):103-18
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  • Earlier exposures were related to a slight increase in risk of non-Hodgkin's lymphoma, renal carcinoma, and esophageal carcinoma.
  • Such confounders as coexposure to other industrial solvents (non-Hodgkin's lymphoma) and alcohol drinking (esophageal cancer) must be discussed.
  • In Germany, a new consecutive case-control study on kidney cancer confirmed that the risk of renal cell cancer is significantly elevated in persons reporting long-term (several years) exposure to trichloroethylene.
  • Clear-cell renal carcinoma, preferentially induced by trichloroethylene, is linked with the homozygous inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene.
  • In highly exposed subjects, the local genotoxic effect of trichloroethylene results from bioactivation pathways leading to renal VHL gene damage and renal cell carcinomas.
  • The view that renal cell cancer development after long-term (several years) and high (with prenarcotic episodes) occupational exposure to trichloroethylene is due to chronic damage of the proximal tubule of the kidney as a key step argues for the existence of a practical threshold.
  • Prolonged and unusually high-dose exposure to trichloroethylene is deemed a strong risk factor for the development of renal cell cancer.
  • [MeSH-major] Carcinoma, Renal Cell / chemically induced. Kidney / drug effects. Kidney Neoplasms / chemically induced. Occupational Exposure / adverse effects. Occupational Exposure / standards. Solvents / adverse effects. Trichloroethylene / adverse effects
  • [MeSH-minor] Denmark / epidemiology. Dose-Response Relationship, Drug. Humans

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  • (PMID = 16121833.001).
  • [ISSN] 0048-7554
  • [Journal-full-title] Reviews on environmental health
  • [ISO-abbreviation] Rev Environ Health
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Israel
  • [Chemical-registry-number] 0 / Solvents; 290YE8AR51 / Trichloroethylene
  • [Number-of-references] 69
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6. Ke L, Yu P, Zhang ZX: Novel epidemiologic evidence for the association between fermented fish sauce and esophageal cancer in South China. Int J Cancer; 2002 May 20;99(3):424-6
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  • [Title] Novel epidemiologic evidence for the association between fermented fish sauce and esophageal cancer in South China.
  • Previous studies have suggested that fermented fish sauce is related to an increased risk for nasopharyngeal, thyroid and gastric cancers and has suspicious carcinogenic and promoting effects in the laboratory, but these reports have not investigated the association between this agent and esophageal cancer in population.
  • Therefore, we investigated the relationship between esophageal cancer and consumption of fermented fish sauce, alcohol and tobacco after adjusting other risk factors using data from a large hospital-based case-control study in Chaoshan area of China.
  • The subjects for analysis included 1,248 cases (median age 58.5 [range 29-82] years, 936 males, 312 females, some 50% with the habit of fermented fish sauce eating) with squamous cell carcinoma of the esophagus and the same amount of controls matched by sex and age.
  • A significant increase in risk (OR 3.21; 95% CI 2.45-4.19) for eating fermented fish sauce compared to not eating and a significant dose-response relationship was found with the consumption of fermented fish sauce (p for trend < 0.001).
  • The joint effect of fermented fish sauce (F) and smoking (S) was more than additive (F * S > F + S: 15.5 > 1 + (5.6 - 1) + (6.6 - 1)), but the effect for fermented fish sauce and alcohol was not found.
  • It is concluded that risks of esophageal cancer in the population were substantially associated with fermented fish sauce.
  • Further epidemiologic and experimental study are required to find a biologic causal relationship between them.
  • [MeSH-major] Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / etiology. Esophageal Neoplasms / epidemiology. Esophageal Neoplasms / etiology. Fish Products / adverse effects
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Alcohol Drinking. China. Female. Humans. Male. Middle Aged. Odds Ratio. Smoking

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 11992412.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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7. Paget V, Lechevrel M, Sichel F: Acetaldehyde-induced mutational pattern in the tumour suppressor gene TP53 analysed by use of a functional assay, the FASAY (functional analysis of separated alleles in yeast). Mutat Res; 2008 Mar 29;652(1):12-9
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  • Chronic alcohol consumption is a major risk factor for upper aero-digestive tract cancers, including cancer of the esophagus.
  • Whereas alcohol as such is not thought to be directly carcinogenic, acetaldehyde, its first metabolite, has been proven genotoxic and mutagenic in the HPRT gene.
  • As mutations in the tumour suppressor gene TP53 are the most common genetic alterations involved in human cancers, especially esophageal tumours, the aim of this work was to establish the mutational pattern induced by acetaldehyde in vitro on the TP53 gene, and to compare this pattern with that found in human alcohol-related tumours.
  • Finally, we compared this pattern with that found for esophageal cancers in humans.
  • These results support the notion that acetaldehyde plays a role in TP53 mutations in esophageal cancers.
  • [MeSH-major] Acetaldehyde / toxicity. DNA Mutational Analysis / methods. Genes, p53 / drug effects. Genes, p53 / physiology. Yeasts / genetics
  • [MeSH-minor] Alcohol Drinking / adverse effects. Alleles. Carcinoma, Squamous Cell / chemically induced. Carcinoma, Squamous Cell / genetics. Cells, Cultured. Dose-Response Relationship, Drug. Esophageal Neoplasms / chemically induced. Esophageal Neoplasms / genetics. Humans. Mutagenicity Tests / methods. Mutant Proteins / analysis. Recombination, Genetic / drug effects. Sequence Homology. Transfection

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  • (PMID = 18242117.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Mutant Proteins; GO1N1ZPR3B / Acetaldehyde
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8. Galli J, Frenguelli A, Calò L, Agostino S, Cianci R, Cammarota G: [Role of gastroesophageal reflux in precancerous conditions and in squamous cell carcinoma of the larynx: our experience]. Acta Otorhinolaryngol Ital; 2001 Dec;21(6):350-5
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  • [Title] [Role of gastroesophageal reflux in precancerous conditions and in squamous cell carcinoma of the larynx: our experience].
  • [Transliterated title] Ruolo del reflusso gastroesofageo nelle precancerosi e nel carcinoma squamocellulare della laringe: nostra esperienza.
  • The major risk factors for the onset of precancerous lesions and squamous cell carcinoma of the larynx are, above all, tobacco smoke, alcohol abuse and exposure to viral and toxic agents.
  • In recent years, however, gastro-esophageal reflux (GER) has also aroused significant interest not only as carcinogen but also as co-carcinogen in association with smoking and alcohol consumption.
  • The purpose of the present work is to provide an objective evaluation of the presence of distal and proximal esophageal reflux using multi-electrode pH monitoring in patients with precancerous lesions of the larynx and laryngeal and pharyngolaryngeal neoplasms.
  • A total of 24 patients consecutively hospitalized during 2000 were evaluated: 20 with squamous cell carcinoma of the larynx and/or pharynx-larynx and 4 with precancerous vocal cord lesions.
  • Data analysis showed that in 83.3% of the cases (20/24) pH monitoring was indicative of pathological GER and 63.7% of these patients had no complaints related to reflux.
  • Moreover, 7/24 patients have had a previous gastrectomy (Billroth II) strictly related to the presence of bile reflux.
  • The Authors conclude that, according with recent literature, pH monitoring data further indicate that patients with precancerous or neoplastic pharyngeal-laryngeal lesions present often a positive history of GER, even though no direct cause-effect relationship can yet be established because of the co-existence of other important risk factors such as smoking and alcohol consumption.
  • [MeSH-major] Carcinoma, Squamous Cell / etiology. Gastroesophageal Reflux / complications. Laryngeal Neoplasms / etiology. Precancerous Conditions / etiology

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  • (PMID = 11938707.001).
  • [ISSN] 0392-100X
  • [Journal-full-title] Acta otorhinolaryngologica Italica : organo ufficiale della Società italiana di otorinolaringologia e chirurgia cervico-facciale
  • [ISO-abbreviation] Acta Otorhinolaryngol Ital
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
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9. 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-major] Alcoholism / complications. Esophagus / drug effects. Ethanol / adverse effects. Pancreas / drug effects. Pancreatitis, Alcoholic / etiology. Stomach / drug effects
  • [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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