327 research outputs found
Alcohol and cancer
No full textA causal association has been established between alcohol consumption and cancers of the oral cavity, pharynx, larynx, oesophagus, liver, colon, rectum, and, in women, breast; an association is suspected for cancers of the pancreas and lung. Evidence suggests that the effect of alcohol is modulated by polymorphisms in genes encoding enzymes for ethanol metabolism (eg, alcohol dehydrogenases, aldehyde dehydrogenases, and cytochrome P450 2E1), folate metabolism, and DNA repair. The mechanisms by which alcohol consumption exerts its carcinogenic effect have not been defined fully, although plausible events include: a genotoxic effect of acetaldehyde, the main metabolite of ethanol; increased oestrogen concentration, which is important for breast carcinogenesis; a role as solvent for tobacco carcinogens; production of reactive oxygen species and nitrogen species; and changes in folate metabolism. Alcohol consumption is increasing in many countries and is an important cause of cancer worldwide
Head and neck cancer prevention: From primary prevention to impact of clinicians on reducing burden
No full textSurvival from head and neck cancers (HNCs) of the lip, oral cavity, pharynx, and larynx has increased by 10% over the past few decades. Little over half of patients who develop HNCs will survive beyond 5 years. Survival is lower for individuals in many countries where traditional risk factors such as tobacco smoking, alcohol drinking, and betel quid chewing are highly prevalent but tertiary health care center access is limited or unavailable. Early diagnosis of HNC is the most important prognostic factor for each tumor site. Molecular-based research on HNC tumors holds promise for early stage detection, screening, vaccination, disease follow-up, and progression. Future investments for HNC control must consider both effectiveness and sustainability for both high-and low-resource countries alike, with priority toward risk factor prevention and earlier diagnosis
The epidemiology of neuroblastoma: a review
No full textNeuroblastoma is the most common tumour in children less than 1 year of age. The goal of this review was to summarise the existing epidemiological research on risk factors for neuroblastoma. A comprehensive search of the literature was undertaken using PubMed for epidemiological studies on neuroblastoma risk factors. We ascertained 47 articles which examined the risk factors. Ten studies employed population-based case-control designs; six were hospital-based case-control studies; two were cohort studies; and five employed ecological designs. Studies ranged in size from 42 to 538 cases. Three studies showed evidence of an increased risk of disease with use of alcohol during pregnancy (OR range 1.1, 12.0). Protective effects were seen with maternal vitamin intake during pregnancy (OR range 0.5, 0.7) in two studies, while risk of disease increased with maternal intake of diuretics (OR range 1.2, 5.8) in three studies. Three studies reported a decrease in risk for children with a history of allergic disease prior to neuroblastoma diagnosis (OR range 0.2, 0.4). The rarity of neuroblastoma makes this disease particularly challenging to study epidemiologically. We review the methodological limitations of prior research and make suggestions for further areas of study. © 2008 Blackwell Publishing Ltd
The burden of cancer attributable to alcohol drinking
No full textWe estimated the number of cancer cases and deaths attributable to alcohol drinking in 2002 by sex and WHO subregion, based on relative risks of cancers of the oral cavity, pharynx, esophagus, liver, colon, rectum, larynx and female breast obtained from recent meta- and pooled analyses and data on prevalence of drinkers obtained from the WHO Global Burden of Disease project. A total of 389,100 cases of cancer are attributable to alcohol drinking worldwide, representing 3.6% of all cancers (5.2% in men, 1.7% in women). The corresponding figure for mortality is 232,900 deaths (3.5% of all cancer deaths). This proportion is particularly high among men in Central and Eastern Europe. Among women, breast cancer comprises 60% of alcohol-attributable cancers. Although our estimates are based on simplified assumptions, the burden of alcohol-associated cancer appears to be substantial and needs to be considered when making public health recommendations on alcohol drinking
Interaction between cigarette smoking and hepatitis B and C virus infection on the risk of liver cancer: A meta-analysis
No full textIntroduction: Chronic infection with hepatitis B (HBV) and C viruses (HCV) as well as cigarette smoking are established risk factors of hepatocellular carcinoma (HCC), but it is unclear whether an interaction exists between these factors in causing hepatocellular carcinogenesis. We conducted a meta-analysis to evaluate the interaction of HBV and HCV infection and cigarette smoking on the risk of HCC. Methods: We systematically searched the PUBMED and the China National Knowledge Infrastructure databases. A total of 16 eligible publications were identified. Cigarette smoking and chronic HBV and HCV infections were dichotomized into present or absent. Additive (S) and multiplicative interaction indexes (V) between smoking and each of the two infections and their 95% confidence intervals (95% CI) were calculated for each study and then combined in a meta-analysis. Results:We found a more than additive interaction between HBV infection and cigarette smoking (S = 1.44; 95% CI, 1.00-2.06; nine studies) and a more than multiplicative interaction (V = 1.60; 95% CI, 1.16-2.20; six studies) between HCV infection and cigarette smoking. No publication bias was detected. Conclusion: Smoking seems to interact with both HBV and HCV in determining HCC risk. A pooled analysis of individual subject data, with appropriate adjustment with other risk factors, is warranted to confirm these results. Impact: The results of this study imply the evidence of a synergistic effect between smoking and HBV or HCVinfection on the risk of HCC. Thus, chronic carriers of HBVor HCV are recommended to avoid smoking. ©2010 AACR
Indoor air pollution from solid fuels and risk of hypopharyngeal/ laryngeal and lung cancers: A multicentric case - Control study from India
No full textBackground: A recent monograph by the International Agency for Research on Cancer (IARC) has identified indoor air pollution from coal usage as a known human carcinogen, while that from biomass as a probable human carcinogen. Although as much as 74% of the Indian population relies on solid fuels for cooking, very little information is available on cancer risk associated with these fuels in India. Methods: Using data from a multicentric case-control study of 799 lung and 1062 hypopharyngeal/laryngeal cancer cases, and 718 controls, we investigated indoor air pollution from various solid fuels as risk factors for these cancers in India. Results: Compared with never users, individuals who always used coal had an increased risk of lung cancer [odds ratio (OR) 3.76, 95% confidence interval (CI) 1.64-8.63]. Long duration of coal usage (>50 years) was a risk factor for hypopharyngeal (OR 3.47, CI 0.95-12.69) and laryngeal (OR 3.65, CI 1.11-11.93) cancers. An increased risk of hypopharyngeal cancer was observed among lifelong users of wood (OR 1.62, CI 1.14-2.32), however this was less apparent among never-smokers. Increasing level of smokiness inside the home was associated with an increasing risk of hypopharyngeal and lung cancer (Ptrend< 0.05). Conclusion: This study showed differential risks associated with indoor air pollution from wood and coal burning, and provides novel evidence on cancer risks associated with solid fuel usage in India. Our findings suggest that reducing indoor air pollution from solid fuels may contribute to prevention of these cancers in India, in addition to tobacco and alcohol control programs. © The Author 2008; all rights reserved
Alcohol consumption and cancer of the oral cavity and pharynx from 1988 to 2009 : an update
No full textEvidence for the human carcinogenic effects of alcohol consumption on the risk of cancers of the oral cavity and pharynx has been considered sufficient in the International Agency for Research on Cancer Monograph 44 on alcohol and cancer in 1988. We evaluated human carcinogenic evidence related to the risk of oral and pharyngeal cancers based on cohort and case-control studies published from 1988 to 2009. A large body of evidence from epidemiological studies of different designs and conducted in different populations has consistently supported the fact that alcohol consumption is strongly associated with an increase in the risk of oral and pharyngeal cancers. The relative risks are 3.2-9.2 for more than 60 g/day (or more than four drinks/day) when adjusted for tobacco smoking and other potential confounders. A strong dose-response effect on the intensity of alcohol use is reported in most of the studies. However, no apparent association is observed for the duration of alcohol use. Compared with current alcoholics, a decreased risk of approximately 10 to 15 years is associated with alcohol cessation. Similar associations have been observed among nonsmokers in over 20 studies. In general, the dominant type of alcohol consumption in each population is associated with the greatest increase in risk. A large number of studies on joint exposure to alcohol and tobacco consumption show a greater than multiplicative synergistic effect
NAD(P)H:quinone oxidoreductase 1 (NQO1) Pro187Ser polymorphism and the risk of lung, bladder, and colorectal cancers: A meta-analysis
No full textNAD(P)H:quinone oxidoreductase 1 (NQO1) is a cytosolic enzyme that catalyzes the two-electron reduction of quinoid compounds into hydroquinones, their less toxic form. A sequence variant at position 609 (C ? T) in the NQO1 gene encodes an enzyme with reduced quinone reductase activity in vitro and thus was hypothesized to affect cancer susceptibility. We conducted meta-analyses focusing on three cancer sites (lung, bladder, and colorectum) to summarize the findings from the current literature and to explore sources of heterogeneity. Results: There is no clear association between the NQO1 Pro187Ser polymorphism and lung cancer risk in the three ethnic groups examined: odds ratio (ORWhite) C/T + T/T versus C/C = 1.04 [95% confidence interval (95% CI), 0.96-1.13], ORAsian = 0.99 (95% CI, 0.72-1.34), and OR Blacks = 0.95 (95% CI, 0.66-1.36). However, a modestly increased risk was suggested for the variant homozygotes in whites (OR T/T versus C/C, 1.19; 95% CI, 0.94-1.50). Analysis excluding one outlier study suggested the variant allele may be associated with reduced lung cancer risk in Asians. Meta-analyses for bladder and colorectal cancer suggested a statistically significant association with the variant genotypes in whites. In stratified analyses, the NQO1 Pro187Ser variant genotypes were associated with slightly increased lung cancer risk in white ever smokers but not in white never smokers and were mainly associated with a reduced risk of lung adenocarcinoma but not squamous cell carcinoma in Asians. Conclusions: Results from our meta-analyses suggest that the variant NQO1 Pro187Ser genotype may affect individual susceptibility to lung, bladder, and colorectal cancer. Such effects of the NQO1 polymorphism seem to be modified by ethnicity and smoking status. Copyright © 2006 American Association for Cancer Research
Cancer incidence and mortality attributable to alcohol consumption
No full textAlcohol consumption is a major cause of disease and death. In a previous study, we reported that in 2002, 3.6% of all cases of cancer and a similar proportion of cancer deaths were attributable to the consumption of alcohol. We aimed to update these figures to 2012 using global estimates of cancer cases and cancer deaths, data on the prevalence of drinkers from the World Health Organization (WHO) global survey on alcohol and health, and relative risks for alcohol-related neoplasms from a recent meta-analysis. Over the 10-year period considered, the total number of alcohol-attributable cancer cases increased to approximately 770,000 worldwide (5.5% of the total number of cancer cases)-540,000 men (7.2%) and 230,000 women (3.5%). Corresponding figures for cancer deaths attributable to alcohol consumption increased to approximately 480,000 (5.8% of the total number of cancer deaths) in both sexes combined-360,000 (7.8%) men and 120,000 (3.3%) women. These proportions were particularly high in the WHO Western Pacific region, the WHO European region and the WHO South-East Asia region. A high burden of cancer mortality and morbidity is attributable to alcohol, and public health measures should be adopted in order to limit excessive alcohol consumption
A meta-analysis of coffee and tea consumption and the risk of glioma in adults
No full textBACKGROUND: Coffee contains many compounds, including antioxidants, which could prevent cancerogenesis, and coffee has been related with lower incidence of cancer at several sites. Tea is also rich in antioxidants, mainly polyphenols. To provide a quantitative overall estimate on the relation between coffee and tea consumption and glioma, we combined all published data, using a meta-analytic approach. METHODS: In September 2012, a bibliography search was carried out in both PubMed and Embase to identify observational studies providing quantitative estimates on the issue. Pooled estimates of the relative risks (RR) and the corresponding 95 % confidence intervals (CI) were calculated using random-effects models. RESULTS: Six studies (four cohort and two case-control studies) were available for meta-analysis, for a total of about 2100 cases. The summary RRs and 95 % CIs of glioma for drinkers versus non/occasional drinkers were 0.96 (95 % CI: 0.81-1.13) for coffee and 0.86 (95 % CI: 0.78-0.94) for tea, with no heterogeneity between studies. When we compared the highest versus the lowest categories of consumption, the RRs were 1.01 (95 % CI: 0.83-1.22) for coffee, 0.88 (95 % CI: 0.69-1.12) for tea, and 0.75 (95 % CI: 0.54-1.05) for coffee plus tea. CONCLUSIONS: This meta-analysis, although based on few studies, suggests a lack of association between coffee intake and glioma risk, and a tendency, if any, to a lower risk for tea and coffee plus tea drinker
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