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<p>Supplementary Data - Table 1</p>

Data from Sweden1 as well as from the National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) program2 indicate an improvement in relative survival rates (RSRs) for patients diagnosed with both adenocarcinoma and squamous cell esophageal cancer over the last 3 decades. To provide further information on the issue, we considered trends in survival by histotype of esophageal cancer for cases diagnosed between 1974 and 1998 from the cancer registries of Vaud and Neuchâtel in the French-speaking part of Switzerland.3, 4 Information on survival has been published only for the Vaud Cancer Registry until 1993 for all esophageal cancers combined. Overall, 5-year relative survival rates increased in males from 0.08 in 1974–8 to 0.10 in 1989–93, and in females from 0.06 to 0.08.5 We decided therefore to consider trends in survival for both histologic types of esophageal cancer to 1998 for the registries of Vaud and Neuchâtel combined. The data were abstracted from the Vaud and Neuchâtel Cancer Registries files, which include incident cases of malignant neoplasms in the cantons, whose populations, according to the December 2000 census, were about 620,300 and 165,700, respectively. Information collected comprises general demographic characteristics of each case (age, sex, municipality of residence), site and histologic type of the tumor according to standard International Classification of Diseases for Oncology (ICD-O)6 and time of diagnostic confirmation. The present report includes 810 squamous cell carcinomas (ICD-O-1 M codes 8070-8076) and 221 adenocarcinomas (ICD-O-1 M 8140-8570) of the esophagus registered from 1974 to 1998.7 Information on survival is integrated from mortality statistics into the incidence data file and, for patients who are apparently alive, through an active follow-up based on verification of vital status from registries of current residence. The vital status of each case has been verified up to 30 December 2002. Relative survival rates were computed after allowance for the general life tables of the cantons. No information was available on tumor stage or treatment. Table I gives the number of registered cases and 1-, 3- and 5-year RSRs in 5 subsequent calendar periods (from 1974–8 to 1994–8) for squamous cell carcinomas, and in 4 calendar periods for adenocarcinomas, due to small absolute numbers in earlier calendar years. For squamous cell cancer, RSRs steadily increased from 25.1% to 46.7% at 1 year, from 7.6% to 19.7% at 3 years and from 5.2% to 13.9% at 5 years. Due to smaller absolute numbers, the pattern was less consistent for adenocarcinomas, but an improvement over calendar years (from 27.7% to 37.0% at 1 year, from 16.4% to 22.2% at 3 years, from 12.9% to 21.0% at 5 years) was observed for adenocarcinomas, too. Thus, the present analyses confirm the existence of appreciable improvements in RSRs for both histologic types of esophageal cancer over the last 3 decades.1, 2 Possible explanations of these findings include earlier diagnosis and detection through wider adoption of endoscopy for squamous cell and also for adenocarcinomas potentially related to Barrett's esophagus and gastroesophageal reflux,8 as well as potential advancements in (surgical) treatment of the disease.9, 10 Yours sincerely, The contribution of the Vaud and Neuchâtel Cancer Registry's staff is gratefully acknowledged. Fabio Levi, Van-Cong Te, Lalao Randimbison, Carlo La Vecchia

The relationship between social class indicators, body mass index (BMI), selected life-style habits (alcohol, coffee, maté and tea drinking) and colorectal cancer was investigated in a case-control study conducted between 1993 and 1997 in Córdoba, Argentina, a relatively high mortality area of colorectal cancer. Cases were 190 patients below age 80 years with incident, histologically confirmed colorectal adenocarcinomas, and controls were 393 patients admitted to hospital for a wide spectrum of acute, non-neoplastic disorders. Higher social class, based on occupation of the head of the household, was significantly associated with colorectal cancer risk: the odds ratios (OR) and 95% confidence intervals (95% CI) were 1.9 (1.2-2.9) for intermediate and 2.0 (1.2-3.4) for the highest as compared to the lowest social class individuals. When compared with subjects whose BMI was < 25 kg/m2, the OR was 1.1 (0.7-1.6) for those with BMI 25 to 29 kg/m2, and 1.3 (0.7-2.3) for those > or = 30. In comparison with alcohol abstainers, the OR was 2.8 (1.6-5.1) for drinkers, and there was a significant trend in risk with dose. The association was observed with wine (the most common alcoholic beverage in Argentina), as well as for beer and spirits. The consumption of coffee, maté and tea was not significantly related to colorectal cancer, but the ORs were below unity (0.9 (0.7-1.3) for coffee, 0.9 (0.6-1.2) for maté and 0.8 (0.6-1.2) for tea drinkers). The relationship between social class, alcohol drinking and colorectal cancer were consistent across strata of sex and age. This study confirms that colorectal cancer has positive social class correlates. The association with alcohol drinking is apparently stronger than previously reported, and may be due to the role of chance and/or peculiar correlates of alcohol drinking in this Argentinean population.

The FFQ is a reliable and valid instrument for collecting alcohol intake in regular drinkers. Lower validity in irregular drinkers may be due to seasonal variation and/or inadequacy of the FFQ to capture irregular patterns of consumption and/or inadequacy of the average of two 7-DD as a reference method. Furthermore, a considerable degree of misclassification was observed between non-drinkers and moderate drinkers.

Background Folate, also known as vitamin B9, is a water soluble vitamin and is found naturally in green leafy vegetables, cereals, legumes and fruits. There are suggestions of an inverse association between folate intake with the risk of oral cavity and pharyngeal cancers (OPC), but most of the studies are limited in sample size with only few reporting information on the source of dietary folate. Alcohol consumption, one of the main causes of OPC, perturbs the folate metabolism by reducing folate absorption …

We read with interest the paper by Peterson et al.,1 providing information on the role of total alcohol, and different types of alcoholic beverages, on ovarian carcinogenesis. Authors considered data from a population-based case–control study conducted in the USA on 762 ovarian cancer cases and 6,217 controls. A significant increased risk of serous invasive ovarian cancer was found for women drinking at least 1 beer per day at early ages (20–30 years). However, no association with total alcohol, wine, beer, and spirit drinking was found for all ovarian cancers and for drinking in the recent past, confirming findings from a pooled analysis of 10 cohort studies.2 However, a recent cohort from the USA based on 90,371 women and 253 cases with ovarian cancer found no association with total alcohol, beer or spirit intake, but a direct association with wine.3 To provide further information on the issue, we pooled data from 2 large case–control studies of ovarian cancer,4, 5, 6 conducted in Italy, i.e. in a population with frequent and regular consumption of wine by women and relatively limited consumption of beer and spirits.7, 8 The first study, conducted between 1983 and 1991 in the greater Milan area,4, 5 included 971 cases and 2,503 controls; the second one, conducted between 1992 and 1999 in 4 areas of the North, Center and South of Italy,6 included 1,031 cases and 2,411 controls. Overall, cases were 2,002 women with incident, histologically confirmed epithelial ovarian cancer, admitted to major teaching and general hospitals in the areas under surveillance. Controls were 4,914 women admitted to the same hospitals as cases for acute, nonneoplastic, nongynaecological, nonhormone-related conditions, unrelated to alcohol drinking. Among controls, 29% were admitted for nonalcohol-related traumas, 30% for other orthopedic disorders, 15% for surgical conditions and 25% for other miscellaneous illnesses. Less than 5% of both cases and controls refused to participate. Trained interviewers administered questionnaires, including a detailed and validated section on weekly alcohol consumption for different types of alcoholic beverages.9 The section on alcohol drinking of the first study included the number of days per week each alcoholic beverage (wine, beer, and spirits) was consumed, the number of drinks consumed per day and the duration of the habit. The section on alcohol drinking of the second study included questions on the weekly number of drinks of wine, beer, grappa (a typical Italian spirit), amari and digestives (other types of Italian liquors drunk after meals) and spirits (whisky, cognac, brandy). In both studies, 1 drink corresponded approximately to 125 mL of wine, 330 mL of beer and 30 mL of liquors and spirits, i.e. about 13–15 g of ethanol. We estimated the odds ratios (OR) and corresponding 95% confidence intervals (CI) for various measures of alcohol drinking using unconditional multiple logistic regression models, including terms for study, centre, age, education, body mass index, parity, menopausal status, oral contraceptive and hormone replacement therapy use, and family history of breast/ovarian cancer. When considering different types of alcohol, ORs were derived after further allowance for the continuous term of other types of alcoholic beverages. Table I shows the distribution of ovarian cancer cases and controls according to consumption of different types of alcoholic beverages. Compared with abstainers, no association was found with total alcohol, the continuous OR for an increment of 1 drink per day being 1.02 (95% CI: 0.98–1.06). There was no evidence for the risk to increase with dose. The OR for ≥21 vs. <7 drinks per week was 0.86 (95% CI: 0.67–1.10). After allowance for other types of alcoholic beverages, the continuous ORs were 1.02 (95% CI: 0.97–1.07) for wine, 1.01 (95% CI: 0.82–1.23) for beer and 1.01 (95% CI: 0.85–1.21) for spirits. The OR for high vs. moderate consumption of wine was 0.82 (95% CI: 0.63–1.08). Again, we did not find any trend with dose in risk when the 3 separate alcoholic beverages were considered. There was no modification effect of education as an indicator of socioeconomic status, or any of the other covariates considered. When we limited the analysis to the second study, where we could exclude former drinkers from the reference category, the estimates for current drinkers were substantially unchanged. Alcohol drinking is socially accepted in this population. Consequently, the reproducibility (r = 0.81)10 and validity (r = 0.70)9 of alcohol consumption, particularly wine, were satisfactory. Moreover, findings were derived from a uniquely large dataset of southern Europe, participation was almost complete, catchment areas of cases and controls were comparable and we had the possibility to adjust the models for a number of potential confounding factors, including mutual adjustment for different types of alcohol. In conclusion, the present findings, based on uniquely large datasets from a population characterized by regular and frequent wine consumption in women,7, 8 are in broad agreement with previous large cohort2 and case–control studies.1 They provide therefore definite evidence that wine is not materially related to ovarian cancer risk, the continuous estimate for wine being 1.02, based on over 1,300 wine drinking cases and 630 abstainers. It also confirms that none of the other types of alcoholic beverages is associated to ovarian cancer risk.2, 11 Yours sincerely, Silvano Gallus, Lorenza Scotti, Renato Talamini, Silvia Franceschi, Luigino Dal Maso, Eva Negri and Carlo La Vecchia This work was conducted with the support of the Italian Association for Cancer Research, the Italian League Against Cancer and the Italian Ministry of Education (PRIN 2005). The work in this paper was undertaken while CLV was a senior fellow at the International Agency for Research on Cancer. Silvano Gallus*, Lorenza Scotti*, Renato Talamini , Silvia Franceschi , Luigino Dal Maso , Eva Negri*, Carlo La Vecchia* ?, * Istituto di Ricerche Farmacologiche “Mario Negri,” Milano, Italy, Unità di Epidemiologia e Biostatistica, Centro di Riferimento Oncologico, Aviano (PN), Italy, International Agency for Research on Cancer (IARC), Lyon, France, ? Istituto di Statistica Medica e Biometria “Giulio A. Maccacaro,” Università degli Studi di Milano, Milano, Italy.