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Ministry of University and Research - Decree No. 1159 of July 23, 2023 - PROBEN call.

Low levels of acrylamide have been found in several foods cooked at high temperatures. While there is sufficient evidence for the carcinogenicity of acrylamide in experimental animals, the few epidemiologic studies conducted to date on occupational and dietary exposure to acrylamide have found no consistent evidence of association with human cancer risk. Using data from an integrated network of Italian and Swiss hospital-based case-control studies, we analyzed the relation between dietary acrylamide intake and cancers of the oral cavity and pharynx (749 cases, 1,772 controls), esophagus (395 cases, 1,066 controls), large bowel (1,394 cases of colon, 886 cases of rectal cancer, 4,765 controls), larynx (527 cases, 1,297 controls), breast (2,900 cases, 3,122 controls), ovary (1,031 cases, 2,411 controls) and prostate (1,294 cases, 1,451 controls). All the studies included incident, histologically confirmed cancer cases and controls admitted to the same network of hospitals for acute nonneoplastic conditions. We calculated odds ratios (ORs) using multivariate logistic regression models, adjusted for energy intake and other major covariates of interest. The ORs for the highest versus the lowest quintile of acrylamide intake were 1.12 (95% CI = 0.76-1.66) for cancer of the oral cavity/pharynx, 1.10 (95% CI = 0.65-1.86) for esophageal, 0.97 (95% CI = 0.80-1.18) for colorectal, 1.23 (95% CI = 0.80-1.90) for laryngeal, 1.06 (95% CI = 0.88-1.28) for breast, 0.97 (95% CI = 0.73-1.31) for ovarian and 0.92 (95% CI = 0.69-1.23) for prostate cancer. None of the trend in risk was significant. This uniquely large and comprehensive data set does not show any consistent association between intake of acrylamide and the risk of breast and several other common cancers.

Emerging evidence suggests that a metabolic profile associated with obesity may be a more relevant risk factor for some cancers than adiposity per se. Basal metabolic rate (BMR) is an indicator of overall body metabolism and may be a proxy for the impact of a specific metabolic profile on cancer risk. Therefore, we investigated the association of predicted BMR with incidence of 13 obesity-related cancers in the European Prospective Investigation into Cancer and Nutrition (EPIC). BMR at baseline was calculated using the WHO/FAO/UNU equations and the relationships between BMR and cancer risk were investigated using multivariable Cox proportional hazards regression models. A total of 141,295 men and 317,613 women, with a mean follow-up of 14 years were included in the analysis. Overall, higher BMR was associated with a greater risk for most cancers that have been linked with obesity. However, among normal weight participants, higher BMR was associated with elevated risks of esophageal adenocarcinoma (hazard ratio per 1-standard deviation change in BMR [HR_1-SD ]: 2.46; 95% CI 1.20; 5.03) and distal colon cancer (HR_1-SD : 1.33; 95% CI 1.001; 1.77) among men and with proximal colon (HR_1-SD : 1.16; 95% CI 1.01; 1.35), pancreatic (HR_1-SD : 1.37; 95% CI 1.13; 1.66), thyroid (HR_1-SD : 1.65; 95% CI 1.33; 2.05), postmenopausal breast (HR_1-SD : 1.17; 95% CI 1.11; 1.22) and endometrial (HR_1-SD : 1.20; 95% CI 1.03; 1.40) cancers in women. These results indicate that higher BMR may be an indicator of a metabolic phenotype associated with risk of certain cancer types, and may be a useful predictor of cancer risk independent of body fatness.

Since the investigation, at an individual level, of lifetime sun exposure remains difficult, the site distribution of different types of skin cancer can be an important source of aetiological clues. The present report deals with 1,149 cases of cutaneous malignant melanoma (CMM), 7,685 of basal-cell carcinoma (BCC) and 3,049 of squamous-cell carcinoma (SCC) reported between 1976 and 1992 to the Vaud Cancer Registry, in Switzerland. Site-and type-specific age-standardized (on the world population) incidence rates per 100,000 population and per 100,000 unit surface were computed, together with relative age-standardized incidence rates (i.e., rates per 100,000 surface unit in each anatomical site relative to rates for the body as a whole). The highest rates per unit surface were seen for both genders in the face, thus indicating some role of cumulative sun exposure in all skin-cancer types. Relative to the incidence in the whole body, the excess on the face was, however, more than 20-fold for BCC and SCC, but only 4-fold for CMM. The relative incidence in males was very much higher for SCC than for CMM and BCC in the neck, ears and scalp, a heavily sun-exposed area in men but not in women. Conversely, a substantial lack of SCC was seen in the trunk. In conclusion, site distribution of different skin-cancer types suggests that short-duration UV-light exposure is sufficient to increase CMM risk substantially, but has little influence on SCC risk. With the increase of exposure, however, SCC rises more steeply than BCC. Age-related behaviour (i.e., another indirect indicator of duration of exposure to UV light) is consistent with the anatomical distribution of skin cancer. © 1996 Wiley-Liss, Inc.

Readers are invited to submit letters for publication in this department. Submit letters online at http://joem.edmgr.com. Choose “Submit New Manuscript.” A signed copyright assignment and financial disclosure form must be submitted with the letter. Form available at http://www.joem.org under Author and Reviewer information. Reply: The issue of the alleged contamination of talc from Val Chisone was extensively discussed in previous reports on the mortality of the cohort of talc miners and millers,1,2 and we did not address it at length in our new report,3 but the letter by Dr. Finkelstein raises again the hypothesis of contamination and requires a detailed response. This hypothesis was raised in the past, mainly in the framework of litigation, without any published supporting data. Conversely, there is strong evidence that talc from Val Chisone is not contaminated by tremolite or other asbestos fibers. In a 1972 study, Lighfoot et al4 reported the results of the analysis of 57 samples from Val Chisone mine: in none of the talc samples, there was asbestos contamination. Tremolite and anthophyllite were present (sometimes in nonfibrous form) in a few specimens of the foot wall rocks. In particular, they analyzed nine samples of “old powders and shipments” (final products), which were all free of any fibrous contamination. These results were quoted in the first mortality study of the cohort of miners and millers, published in 1976.1 Supporting evidence was provided by a 1982 paper by other authors,5 in which results based on X-ray diffraction and infrared reflection spectrometry showed no contamination by tremolite or other amphiboles. Furthermore, in a 1983 report, Pooley6 stated: “White Pinerolo Talc – this powder was found to be the most pure talc observed. The only impurity was a very small quantity of the mineral chlorite. Electron microscopic examination of this powder did not reveal any fibrous mineral particulates. Grey Pinerolo Talc – the major mineral observed in this sample by X-ray diffraction was chlorite and talc was present at the 25–30% level; a small quantity of dolomite was also observed. Again electrom microscope examination of this sample did not reveal any fibrous mineral particulate.” The results of the first analysis by Lighfoot et al4 were quoted by Gordon et al,7 who mistakenly interpreted the presence of tremolite in some samples of the footwall rocks as evidence of contamination of the talc ore and the final product used to produce the cosmetic talc. It is noteworthy the fact that this last paper includes a coauthor named Fitzgerald, that is, the name of the person quoted by Dr. Finkelestein as a source of unpublished analysis of one sample of talc from Val Chisone. The paper by Gordon et al7 was criticized by Lee and Van Orden8: these authors identified several methodological errors in the study by Gordon et al,7 and a severe amount of misinterpretation of literature. We think that the issue of contamination of Val Chisone talc by tremolite or other asbestos fibers should be finally put to rest. The data of our cohort confirm, with a follow-up extended to a maximum of 66 years,3 our previous observation that occupational exposure to Val Chisone talc is not associated with an increased risk of mesothelioma.1,2 In the new study, we observed no deaths from mesothelioma, and could exclude a two-fold excess risk. Dr. Finkelstein's calculation of the statistical power of our study is purely speculative, given the lack of support to the hypothesis of 4% asbestos exposure (or any other value different from zero) compared with Québec miners.

The study adds data on the protective effect of dietary garlic on CRC risk. Moreover, it supports evidence of a translocation of bacterial material to bloodstream and corroborates the hypothesis of a diet-microbiota axis as a mechanism behind the role of garlic in CRC prevention.

In the pooled analysis of 11 case-control studies in a large consortium (i.e., the Stomach cancer Pooling (StoP) consortium), we found a positive association between GU and risk of GC and no association between DU and GC risk.

In order to quantify the association between use of statins and the risk of all hematological malignancies and of subtypes, we performed a meta-analysis of observational studies. We achieved a MEDLINE/EMBASE comprehensive search for studies published up to August 2014 investigating the association between use of statins and the risk of hematological malignancies, including Hodgkin- and non-Hodgkin lymphoma, leukemia, and myeloma. Fixed- and random-effect models were fitted to estimate the summary relative risk (RR) based on adjusted study-specific results. Between-study heterogeneity was assessed using the Q and I(2) statistics and the sources of heterogeneity were investigated using Deeks' test. Moreover, an influence analysis was performed. Finally, publication bias was evaluated using funnel plot and Egger's regression asymmetry test. Fourteen studies (10 case-control and four cohort studies) contributed to the analysis. Statin use, compared to nonuse of statins, was negatively associated with all hematological malignancies taken together (summary RR 0.86; 95% CI: 0.77-0.96), with leukemia (0.83; 0.74-0.92), and non-Hodgkin lymphoma (0.81; 0.68 to 0.96), but it was not related to the risk of myeloma (0.89; 0.53-1.51). Long-term users of statins showed a statistically significant reduction in the risk of all hematological malignancies taken together (0.78; 0.71-0.87). Statistically significant between-studies heterogeneity was observed for all outcome except for leukemia. Heterogeneity was caused by differences confounding-adjustment level of the included studies only for Myeloma. No significant evidence of publication bias was found.

DEAR EDITOR, We read with interest the letter by Drs Chen and Zhang1 about our recent investigation, ‘Alcohol drinking and cutaneous melanoma risk: a systematic review and dose–risk meta-analysis’, published in the British Journal of Dermatology.2 With reference to the literature search, excluding studies published in languages other than English has generally little effect on summary effect estimates of meta-analyses.3–5 In our meta-analysis, we considered for inclusion only articles published as originals in English up to 30 April 2012. The contribution by Kvaskoff et al.6 was published in French as a conference abstract, and thus it did not satisfy our inclusion criteria. The article by Asgari et al.7 reported the results of the American VITamins And Lifestyle (VITAL) cohort study. It was published in the June 2012 issue of the Journal of Investigative Dermatology, and appeared online ahead of print on 1 March 2012. Unfortunately, our literature search did not retrieve this article, probably because it was fully indexed in Medline only on 18 July 2012. Still, for the sake of completeness, we have updated our meta-analysis by including it. None of the results materially change; in particular, the overall pooled relative risks (RRs) are 1.20 [95% confidence interval (CI) 1.07–1.35], 1.11 (95% CI 0.99–1.25) and 1.20 (95% CI 1.04– 1.38) for any (Fig. 1), light and moderate-to-heavy alcohol drinking, respectively, vs. no/occasional drinking. With the addition of the Asgari et al. study,7 stratified analyses from studies (n = 8) conducted in America showed an RR of 1.34 (95% CI 1.18–1.52), while no differences appeared in the RR of studies that did not adjust for sun exposure (RR 1.27, 95% CI 1.20–1.35), as in the study of Asgari et al.7 We disagree with the existence of a relevant bias by study quality. In fact, large cohort studies such as the U.K. Million Women Study8 and the U.S. Women’s Health Initiative9 reported an increased risk of cutaneous malignant melanoma (CMM) in alcohol drinkers, and the pooled risk estimates of our meta-analysis were similar for case–control and cohort studies. We agree with Drs Chen and Zhang that current evidence is insufficient to conclude for a causal association of CMM with alcohol consumption. As we pointed out in our review,2 caution in interpreting our results is required, as residual confounding by sun ultraviolet exposure cannot be ruled out. Future well designed studies with specific control for this potential confounder are needed to confirm, or not, our findings.