06 May 2014 In Cancer

 

 

 

PURPOSE OF REVIEW: The data indicating that alcohol is an important factor increasing the risk to develop gastrointestinal cancer are consolidating. The purpose of this review is to summarize current evidence.

RECENT FINDINGS: Acetaldehyde is the first metabolite of ethanol metabolism and has direct carcinogenic and mutagenic effects by modifying DNA via generation of DNA adducts. Oxidative stress has a prominent role in triggering chronic inflammation and carcinogenesis through formation of reactive oxygen species. Recently published large prospective cohort studies with sufficient statistical power and meta-analyses could refine the knowledge regarding the impact of alcohol on gastrointestinal cancer. Functional genetic variants of alcohol-metabolizing enzymes proved to be associated with increased risk for esophageal and gastric cancer.The highest risk increase for malignancy was observed in the upper aerodigestive tract (oral cavity, pharynx, larynx) and esophagus (squamous cell carcinoma), weaker correlations were established regarding gastric, pancreatic, and colorectal neoplasias.

SUMMARY: Alcohol overconsumption is a serious avoidable risk factor for the development of gastrointestinal tract cancer, both alone but even more in combination with other risk factors such as tobacco and obesity.

 

 

 

06 May 2014 In Cancer

 

 

 

Using a mailed questionnaire, we investigated the risk of renal cell cancer in relation to different types of alcoholic beverages, and to total ethanol in a large population-based case-control study among Swedish adults, including 855 cases and 1204 controls. Compared to non-drinkers, a total ethanol intake of >620 g month(-1) was significantly related to a decreased risk of renal cell cancer (odds ratio (OR) 0.6, 95% confidence interval (CI) 0.4-0.9; P-value for trend=0.03). The risk decreased 30-40% with drinking more than two glasses per week of red wine (OR 0.6, 95% CI 0.4-0.9), white wine (OR 0.7, 95% CI 0.4-1.0), or strong beer (OR 0.6, 95% CI 0.4-1.0); there was a clear linear trend of decreasing risk with increasing consumption of these beverages (P-values for trends <0.05).

 

 

 

06 May 2014 In Cancer

Several recent studies have evaluated the association between dietary flavonoid intake and ovarian cancer risk, and all reported significant or suggestive inverse associations with certain flavonoids or flavonoid subclasses; however, most of these studies were small to moderate in size. We, therefore, examined this association in a large, population-based case-control study. We calculated intake of 5 common dietary flavonoids (myricetin, kaempferol, quercetin, luteolin, and apigenin), as well as total intake of these flavonoids, for 1,141 cases and 1,183 frequency-matched controls. We used unconditional logistic regression to estimate the relative risk (RR) of ovarian cancer for each quintile of flavonoid intake when compared with the lowest quintile. We did not observe an association between total flavonoid intake and ovarian cancer risk. The multivariable-adjusted RR for the highest versus lowest quintile of total flavonoid intake was 1.06 (95% confidence interval [CI] = 0.78-1.45). In analyses of each individual flavonoid, only intake of apigenin was associated with a borderline significant decrease in risk (RR, highest vs. lowest quintile = 0.79, 95% CI = 0.59-1.06; p-trend = 0.26), and this association was significant after adjustment for intake of the other 4 individual flavonoids (comparable RR = 0.72, 95% CI = 0.53-0.98; p-trend = 0.09). These results provide limited support for an association between flavonoid intake and ovarian cancer risk. However, given the findings of previous studies and the biologic plausibility of this association, additional studies are warranted.

06 May 2014 In Cancer

 

 

 

Alcohol consumption has been hypothesized to increase the risk of endometrial cancer. We used data from the prospective population-based Swedish Mammography Cohort including 61,226 women to examine the association between alcohol and endometrial cancer incidence. Alcohol consumption was assessed with validated food frequency questionnaires at baseline 1987 to 1990 and at follow-up in 1997. During a mean follow-up of 17.6 years, 687 endometrial cancer cases were identified in the Swedish cancer registries. We found no association between alcohol consumption and endometrial cancer risk after adjustment for age, body mass index, and smoking. The multivariable rate ratios (95% confidence intervals) for the three upper categories of long-term alcohol consumption as compared with no consumption were 1.01 (0.84-1.22) for <3.4 g/d, 1.01 (0.80-1.27) for 3.4 to 9.9 g/d, and 1.09 (0.71-1.67) for >or=10 g/d, respectively. The association did not differ by age, body mass index, folic acid intake, or postmenopausal hormone use in stratified analysis. In conclusion, our results suggest that low alcohol consumption (up to one drink per day) is unlikely to substantially influence risk of endometrial cancer.

 

 

 

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