Lung cancer mortality in young women in the European Union (EU) has steadily increased until the mid 1990 s and has levelled off thereafter, but trends have been heterogeneous in various countries. We analyzed therefore age-standardized trends in lung cancer mortality in young women (20-44) for the 6 major European countries, using joinpoint regression. In the early 1970s the highest lung cancer mortality in young women was in the UK (2.1/100,000). UK rates, however, steadily declined and in 2000-2004 they were the lowest of all 6 major EU countries (1.2/100,000). The second lowest rate in 2000-2002 was in Italy, whose rates remained around 1.1/100,000 between 1970 and 1994, and increased to 1.4 thereafter. In Germany and Poland, lung cancer rates in young women rose from 0.8-1.0/100,000 in the early 1970s to 1.7-1.9 in the mid 1990 s and levelled off during the last decade. Major rises over recent years were observed in France (from 0.8/100,000 in 1985-1989 to 2.2 in 2000-2003) and in Spain (from 0.8 in the 1985-1989 to 1.7 in 2000-2004). Thus, France showed both the highest rate observed over the last 3 decades and the largest rise over the last 2 decades. Since recent trends in the young give relevant information to the likely future trends in middle age, the female lung cancer epidemic is likely to expand in southern Europe from the current rates of 5.0/100,000 in Spain and 7.7 in France to approach 20/100,000 within the next 2-3 decades. Urgent interventions for smoking cessation in women are therefore required.

Folate consumption is inversely associated with the risk of oral and pharyngeal cancer (OPC) and potentially interacts with alcohol drinking in the risk of OPC. Aldehyde dehydrogenase 2 (ALDH2) gene polymorphism is known to interact with alcohol consumption. The aim of this study was to investigate potential interaction between folate, alcohol drinking, and ALDH2 polymorphism in the risk of OPC in a Japanese population. The study group comprised 409 head and neck cancer cases and 1227 age-matched and sex-matched noncancer controls; of these, 251 cases and 759 controls were evaluated for ALDH rs671 polymorphism. Associations were assessed by odds ratios and 95% confidence intervals in multiple logistic regression models. We observed an inverse association between folate consumption and OPC risk. The odds ratio for high folate intake was 0.53 (95% confidence interval: 0.36-0.77) relative to low intake (P trend=0.003). This association was consistent across strata of sex, age, smoking, and ALDH2 genotypes. Interaction between folate consumption, drinking, and ALDH2 genotype was remarkable (three-way interaction, P<0.001). We observed significant interaction among folate, drinking, and ALDH2 genotype in the Japanese population.

Evidence 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.

Aspirin and nonsteroidal anti-inflammatory drugs have been related to decreased risk of several cancers, but studies on the relation with the risk of renal cell cancer (RCC) are inconsistent. A case-control study of RCC was conducted in Italy between 1992 and 2004. Cases were 755 patients with incident, histologically confirmed RCC, and controls were 1297 patients in hospital for acute non-neoplastic conditions. Odds ratios (OR) and 95% confidence intervals (CI) for RCC were conditioned on center, sex, age, and year of interview, and adjusted for education, smoking, alcohol consumption, diabetes, and hypertension. Regular use of aspirin for at least 6 months was reported by 67 cases and 99 controls, corresponding to an OR of 0.98 (95% CI 0.69-1.38). The ORs were 0.91 (95% CI 0.55-1.50) in regular users for less than 3 years, and 1.04 (95% CI 0.67-1.63) in users for 3 years or longer; 0.47 (95% CI 0.20-1.12) when aspirin was used as analgesic and 1.10 (95% CI 0.75-1.62) when it was used for cardiovascular disease prevention. No significant heterogeneity was found for regular use of aspirin across strata of age and sex. This study, based on a large dataset, suggests that regular use of aspirin did not increase RCC risk.

This meta-analysis suggests that binge and heavy irregular drinking modify the favourable effect of alcohol intake on the CHD risk. However, this conclusion should be taken with caution because of the small number of studies considered.

There is no consistent evidence from epidemiological studies, although a modest excess risk emerged in case-control studies, that added sugars, dietary glycemic index and glycemic load are associated with increased risk of colon cancer, independently from their effect on energy intake, overweight, obesity and diabetes, which are related to excess colon cancer risk.

Diabetes has been associated to the risk of a few cancer sites, though quantification of this association in various populations remains open to discussion. We analyzed the relation between diabetes and the risk of various cancers in an integrated series of case-control studies conducted in Italy and Switzerland between 1991 and 2009. The studies included 1,468 oral and pharyngeal, 505 esophageal, 230 gastric, 2,390 colorectal, 185 liver, 326 pancreatic, 852 laryngeal, 3,034 breast, 607 endometrial, 1,031 ovarian, 1,294 prostate, and 767 renal cell cancer cases and 12,060 hospital controls. The multivariate odds ratios (OR) for subjects with diabetes as compared to those without-adjusted for major identified confounding factors for the cancers considered through logistic regression models-were significantly elevated for cancers of the oral cavity/pharynx (OR = 1.58), esophagus (OR = 2.52), colorectum (OR = 1.23), liver (OR = 3.52), pancreas (OR = 3.32), postmenopausal breast (OR = 1.76), and endometrium (OR = 1.70). For cancers of the oral cavity, esophagus, colorectum, liver, and postmenopausal breast, the excess risk persisted over 10 yr since diagnosis of diabetes. Our data confirm and further quantify the association of diabetes with colorectal, liver, pancreatic, postmenopausal breast, and endometrial cancer and suggest forthe first time that diabetes may also increase the risk of oral/pharyngeal and esophageal cancer.

This study supports the hypothesis that alcohol is more strongly related to ER+ than to ER- breast tumors.