Background: The magnitude of risk conferred by the interaction between tobacco and alcohol use on the risk of head and neck cancers is not clear because studies have used various methods to quantify the excess head and neck cancer burden. Methods: We analyzed individual-level pooled data from 17 European and American case-control studies (11,221 cases and 16,168 controls) participating in the International Head and Neck Cancer Epidemiology consortium. We estimated the multiplicative interaction parameter (y) and population attributable risks (PAR). Results: A greater than multiplicative joint effect between ever tobacco and alcohol use was observed for head and neck cancer risk (y = 2.15; 95% confidence interval, 1.53-3.04). The PAR for tobacco or alcohol was 72% (95% confidence interval, 61-79%) for head and

Sexual behaviours are associated with cancer risk at the head and neck cancer subsites that have previously been associated with HPV infection.

The global increase in lung cancer burden, together with its poor survival and resistance to classical chemotherapy, underscores the need for identification of critical molecular events involved in lung carcinogenesis. Here, we have applied quantitative profiling of DNA methylation states in a panel of five cancer-associated genes (CDH1, CDKN2A, GSTP1, MTHFR , and RASSF1A) to a large case-control study of lung cancer. Our analyses revealed a high frequency of aberrant hypermethylation of MTHFR, RASSF1A, and CDKN2A in lung tumors as compared with control blood samples, whereas no significant increase in methylation levels of GSTP1 and CDH1 was observed, consistent with the notion that aberrant DNA methylation occurs in a tumor-specific and gene-specific manner. Importantly, we found that tobacco smoking, sex, and alcohol intake had a strong influence on the methylation levels of distinct genes (RASSF1A and MTHFR), whereas folate intake, age, and histologic subtype had no significant influence on methylation states. We observed a strong association between MTHFR hypermethylation in lung cancer and tobacco smoking, whereas methylation levels of CDH1, CDKN2A, GSTP1, and RASSF1A were not associated with smoking, indicating that tobacco smoke targets specific genes for hypermethylation. We also found that methylation levels in RASSF1A, but not the other genes under study, were influenced by sex, with males showing higher levels of methylation. Together, this study identifies aberrant DNA methylation patterns in lung cancer and thus exemplifies the mechanism by which environmental factors may interact with key genes involved in tumor suppression and contribute to lung cancer.

Our results indicate no association between childhood exposure to ETS and lung cancer risk. We did find weak evidence of a dose-response relationship between risk of lung cancer and exposure to spousal and workplace ETS. There was no detectable risk after cessation of exposure.

A multisite case-control study on factor analysis and several cancer sites (mouth and pharynx, esophagus, stomach, colon, rectum, larynx, lung, breast, prostate, bladder, kidney) was conducted in Uruguay. The study included 3,528 cases and 2,532 controls. Factor analysis (principal components) was modeled among controls. This patterning method retained 4 factors per sex, labeled as prudent, drinker, traditional and Western. Odds ratios for these cancer sites, stratified by sex, were estimated using polytomous regression. Whereas the prudent pattern was mainly negatively associated with cancers of the upper aerodigestive tract, the Western pattern showed a strong increase in breast, lung and colon cancers. The study allowed for the reproducibility of the prudent, drinker and Western patterns, whereas the traditional pattern appears to be country specific. ' 2008 Wiley-Liss, Inc.Key words: dietary patterns; factor analysis; principal components; polytomous regression Uruguay is a developing country with high rates of cancer, showing age-adjusted incidence rates of 386.0 per 100,000 men and 303.2 per 100,000 women for all sites. 1 The most frequent sites are female breast (age standardized rate 114.9 per 100,000 women) and lung (Age standardized rate 76.5 per 100,000 men). Smoking and alcohol drinking are the major risk factors for frequent cancers like lung cancer and cancers of the upper aerodigestive tract in the Uruguayan population. Also, a diet low in vegetables and fruits and high in beef consumption are risk factors for digestive tract cancers. 2 Since foods are consumed together it could be suggested that the true effect of the diet may only be observed when all components are analyzed simultaneously. In fact, foods could act in synergism or be metabolized jointly. [3][4][5] Patterning methodologies, including factor analysis, may turn the analytical difficulties into an advantage. Factor analysis is used to reduce a large number of foods or nutrients to smaller number of factors for modeling purposes. 6 This analytic method was originated in the pioneer paper of Spearman in 1904. 7 Since then it has grown explosively mainly in psychology and social sciences. In 1992, Randall et al. 8 firstly applied this method in the study of food patterns and colon cancer. Since then, numerous studies on dietary patterns and diverse cancers have been published all over the World.On the basis of a large dataset of cases and controls, we decided to conduct a multisite study using factor analysis in a high-risk country such as Uruguay. The main objective was to estimate odds ratios (ORs) of several cancer sites by means of the application of the principal components method and multinomial regression. Material and methodsA large scale study was designed jointly by the