Figure 2 The relationship between increasing

Figure 2 The relationship between increasing selleck kinase inhibitor amounts of average daily alcohol consumption and the relative risk for cancer, with lifetime abstainers serving as the reference group. A recent meta-analysis also has indicated that alcohol consumption is significantly linked to an increased risk of developing prostate cancer in a dose-dependent manner (Rota et al. 2012); this observation is consistent with previous meta-analyses concluding that alcohol consumption and the risk for prostate cancer are significantly correlated (Dennis 2000; Fillmore et al. 2009). Additional research, however, is required on the biological pathways to prove the role of alcohol consumption in the development of this type of cancer. Evidence also has suggested that stomach cancer may be linked to ethanol consumption (Bagnardi et al.

2001; Tramacere et al. 2012a); however, the findings have not been unequivocal. Thus, two recent meta-analyses found no association between alcohol drinking status (i.e., drinkers compared with non-drinkers) and risk of gastric cardia adenocarcinoma (Tramacere et al. 2012a, d). However, one meta-analysis did find an association between heavy alcohol consumption and the risk of this type of cancer (Tramacere et al. 2012a). For several types of cancer investigators have found a nonsignificant positive association with alcohol consumption, including endometrial (Bagnardi et al. 2001; Rota et al. 2012), ovarian (Bagnardi et al. 2001), and pancreatic cancers (Bagnardi et al. 2001). However, because the relationship at least between alcohol consumption and endometrial and pancreatic cancer is modest (i.

e., the point estimates of RR are low, even at high levels of average daily alcohol consumption), additional studies with large numbers of participants are needed to accurately assess the relationship (Bagnardi et al. 2001). The relationship between alcohol consumption and bladder and lung cancers is even less clear, with one meta-analysis finding that alcohol significantly increases the risk for both types of tumors (Bagnardi et al. 2001), whereas more recent meta-analyses have found no significant association between alcohol consumption and the risk of bladder cancer (Pelucchi et al. 2012) or the risk of lung cancer in individuals who had never smoked (Bagnardi et al. 2001).

These conflicting results may Batimastat stem from the studies in the more recent meta-analyses adjusting for smoking status when assessing the risk relationship between alcohol and these cancers within individual observational studies (Bagnardi et al. 2001; Pelucchi et al. 2012). The biological pathways by which alcohol increases the risk of developing cancer depends on the targeted organ and are not yet fully understood. Factors that seem to play a role include the specific variants of alcohol-metabolizing enzymes (i.e.

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