Folate may be inversely related to colorectal cancer risk, possibly in combination with low methionine and high alcohol consumption. We considered, therefore, the relation between folate and colorectal cancer in a multicentric case-control study of 1,953 cases and 4,154 controls from Italy, i.e., a population with frequent regular alcohol drinking. In the overall data set, the odds ratio (OR) was 0.72 for the highest quintile of folate, and the continuous OR per 100 microg was 0.86. The inverse relation was similar in men and women and somewhat stronger for the rectum (OR = 0.59 for the highest quintile) compared to the colon (OR = 0.81). It was also somewhat stronger in the highest tertile of alcohol drinking (OR = 0.65), though trends were not heterogeneous across strata of alcohol, whereas no appreciable difference was observed across strata of methionine intake. Compared to subjects reporting low alcohol, high methionine and high folate intake, the OR was 1.83 for those reporting high alcohol, low methionine and low folate intake. The present findings support a favorable role of folate in colorectal carcinogenesis.

The report by Kyle et al.1 updates trends in multiple myeloma incidence in Olmsted County, Minnesota, and indicates that the incidence of multiple myeloma has remained stable over the 56-year period considered (1945–2001). Likewise, in Malmö, Sweden, the incidence of multiple myeloma remained stable between 1950 and 1979.2 However, in several other cancer registration areas, trends in the incidence of multiple myeloma have been rising over the last few decades. Furthermore, mortality from myeloma has tended to rise steadily over the last few decades in the United States and across Europe. In the European Union, age-standardized (world standard) mortality from myeloma increased for men from 0.9 per 100,000 in 1960 to 2.2 per 100,000 in 2000 and from 0.7 per 100,000 to 1.5 per 100,000 for women.3 However, the upward trends were larger in the elderly4 and were not observed in several countries that originally had high mortality rates, such as Sweden, Denmark, the Netherlands, and Norway.3 The Swiss canton of Vaud is another population that can contribute toward addressing the issue of trends in multiple myeloma, because it long has been covered with optimal and uniform surveillance for lymphohemopoietic conditions.5 We analyzed trends in myeloma incidence over the period from 1978 to 1987 and found no appreciable change in rates.5 Here, we update incidence rates in the Vaud population to the year 2001. The Vaud cancer registry includes information concerning incident cases of malignant neoplasms occurring in the resident population of the Canton (≈ 640,000 inhabitants in 2000). The current series includes 674 patients who were diagnosed with multiple myeloma (341 males and 333 females) from 1978 to 2001. For men, the overall, age-standardized rates (world standard) were 3.6 per 100,000 in 1978–1982 (95% confidence interval [CI], 2.7–4.5 per 100,000) and 2.4 per 100,000 (95%CI, 1.7–3.1 per 100,000) in 1998–2001. The corresponding rates for women were 1.9 per 100,000 (95%CI, 1.3–2.4 per 100,000) and 2.1 per 100,000 (95%CI, 1.5–2.7 per 100,000). Among the population aged ≥ 65 years, multiple myeloma incidence rates for men were 27.7 per 100,000 in 1978–1982 and 18.8 per 100,000 in 1998–2001. For women, the corresponding rates were 15.4 per 100,000 and 18.0 per 100,000. The current data, together with those from Olmsted County,1 provide conclusive evidence that the incidence of multiple myeloma in well surveilled populations from different areas of the world has been constant for several decades. Therefore, the apparent upward trends in incidence in several other populations and the rises in mortality rates from most countries are artifactual and attributable to improved diagnosis and certification of the disease.1-3

During the clinical validation of a new drug there are several clinical phases. Once phase II studies have defined the efficacy of a new drug, clinical research is used to evaluate its significance in clinical practice, comparing it with other drugs or treatments in use for similar clinical conditions. The group of patients undergoing standard treatment (either untreated or treated with placebo) is thus used as a control; these phase III studies are termed 'controlled clinical studies'. The general condition for comparing patients treated with the new drug is that they do not have characteristics (relevant to the study) that are systematically different from those in the control group. Randomization guarantees comparability between treated and untreated (or otherwise treated) patients. The comparability of the observations of the studied events are guaranteed by blinding and placebo. The fundamental question when designing a controlled clinical study to evaluate whether there are differences between two or more treatments is how many patients are needed. Generally, the smaller the clinically relevant differences in efficacy between treatments, the more patients are required, to provide sufficient statistical power and meaningful clinical results. A group of randomized patients represents the final point of sequential steps. Also of importance is to what kind of 'population' the results from the studied sample can be applied (qualitatively, not necessarily quantitatively), i.e. the general applicability of a study, or whether the findings can be used to treat future patients with the same or similar characteristics as those randomized, or to all patients with the same pathology. Answers to these questions depend on many aspects of the randomized selection mechanisms, the disease characteristics, and knowledge of the biological effects of the drug to be tested.

To investigate the role of a wide range of foods and beverages on the risk of stomach cancer, we analyzed data from a case-control study carried out in Italy between 1997 and 2007 on 230 subjects with incident histologically confirmed stomach cancer (143 men and 87 women, age range 22-80 yr) and 547 controls (286 men and 261 women, age range 22-80 yr) admitted to hospital for acute, non-neoplastic diseases. Odds ratios (OR) of stomach cancer and their corresponding 95% confidence intervals (CI) were estimated using unconditional multiple logistic regression models, adjusted for age, sex, energy intake, and other selected variables. A direct association with stomach cancer risk was observed for cereals (OR = 2.07, 95% CI = 1.01-4.24, for the highest compared to the lowest quintile of intake, P for trend = 0.03), soups (OR = 1.94, 95% CI = 1.10-3.42, P for trend = 0.05), and potatoes (OR = 2.04, 95% CI = 1.05-3.98, P for trend = 0.04). Conversely, inverse trends in risk were observed with vegetables (OR = 0.47, 95% CI = 0.27-0.81, P for trend = 0.01) and fruit intake (OR = 0.53, 95% CI = 0.30-0.93, P for trend = 0.08). The results of this study confirm a protective role of vegetables and fruit against stomach cancer and suggest a detrimental effect of (refined) cereals on this neoplasm.

The inverse relations between trunk, but not face and neck BCC, and obesity, diabetes mellitus and asthma may indirectly reflect the different role of past sunlight exposure to different body locations and variable etiologic pathways for BCCs according to body areas.

European epidemiological studies on ambient air pollution and cancer published before December 2006 are reviewed, with focus on five analytic studies providing data on the association between various measures of particulate matter (PM) and lung cancer. A case-control study of 755 men who died from lung cancer in Trieste, Italy, reported that, compared with less than 0.18 g/m/day of deposition of particulate, the relative risk (RR) was 1.1 [95% confidence interval (CI): 0.8-1.5] for 0.18-0.30 and 1.4 (95% CI: 1.1-1.8) for more than 0.30 g/m/day. In the Netherlands Cohort Study on Diet and Cancer with 60 deaths from lung cancer, the RR was 1.06 (95% CI: 0.43-2.63) for an increase of 10 mug/m in black smoke. In the French Pollution Atmospherique et Affections Respiratoires Chroniques study cohort based on 178 deaths from lung cancer, the RR associated with an increase in exposure to 10 mug/m of total suspended particulate was 0.97 (95% CI: 0.94-1.01). A nested case-control study within the European Prospective Investigation on Cancer and Nutrition included 113 nonsmokers or exsmokers diagnosed with lung cancer and 312 controls. The RRs were 0.91 (95% CI: 0.70-1.18) for an increase in PM with diameter </=10 mum (PM10) of 10 mug/m, and 0.98 (95% CI: 0.66-1.45) for exposure over 27 mug/m compared with less than 27 mug/m. In a Norwegian record linkage study, based on 1453 lung cancer deaths, no significant excess risk was found for men, and a modest association was observed for women. European studies of PM exposure and lung cancer do not show a clear association, but uncertainties remain for the measurement of exposure and latency.