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Cause ed epidemiologia analitica

  • Lorenzo Richiardi1

  1. 1. Università di Torino

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Ricerca bibliografica periodo dal 16 ottobre 2011 al 1 gennaio 2012

All’interno dell’area “Cause ed epidemiologia analitica” in questo numero saranno selezionati gli articoli relativi al tema: "Tumori".

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Stringa: ("italy"[MeSH Terms] OR "italy"[All Fields]) AND ("2011/10/16"[PDat] : "2012/01/01"[PDat]) AND (“Case-Control” [All fields] OR “Cohort”[all fileds] OR “Cross-sectional”[All fields]) AND ("risk"[All Fields] OR "association"[all fields] OR "epidemiologic factors"[MeSH Terms]) and (“odds ratios”[all fields] OR “odds ratio”[all fields] OR “ORs”[all fields] OR “rate ratio”[all fileds] OR “rate ratios”[all fileds] OR “RR”[all fileds] OR “RRs” [all fileds] OR “risk ratio”[all fields] OR “risk ratios”[all fields] OR “prevalence ratio*” [all fields] OR “prevalence ratios” [all fields] OR “hazard ratio” [all fields] OR “hazard ratios” [all fields] OR “HR”[all fields] OR “HRs”[all fields]) NOT "Clinical Trials as Topic"[Mesh] NOT "Sensitivity and Specificity"[Mesh] NOT "Comorbidity"[Mesh] NOT "Predictive Value of Tests"[Mesh] NOT "Prognosis"[Mesh] NOT "Review"[publication type] NOT "Population Surveillance"[Mesh]
1. Edefonti V, Hashibe M, Ambrogi F, Parpinel M, Bravi F, Talamini R, Levi F, Yu G, Morgenstern H, Kelsey K, McClean M, Schantz S, Zhang Z, Chuang S, Boffetta P, La Vecchia C, Decarli A. Nutrient-based dietary patterns and the risk of head and neck cancer: a pooled analysis in the International Head and Neck Cancer Epidemiology consortium. Ann Oncol. 2011 Nov 28. [Epub ahead of print]
Section of Medical Statistics and Biometry 'Giulio A. Maccacaro', Department of Occupational and Environmental Health, University of Milan, Milan, Italy.

Abstract
BACKGROUND: The association between dietary patterns and head and neck cancer has rarely been addressed.
PATIENTS AND METHODS: We used individual-level pooled data from five case-control studies (2452 cases and 5013 controls) participating in the International Head and Neck Cancer Epidemiology consortium. A posteriori dietary patterns were identified through a principal component factor analysis carried out on 24 nutrients derived from study-specific food-frequency questionnaires. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were estimated using unconditional logistic regression models on quintiles of factor scores.
RESULTS: We identified three major dietary patterns named 'animal products and cereals', 'antioxidant vitamins and fiber', and 'fats'. The 'antioxidant vitamins and fiber' pattern was inversely related to oral and pharyngeal cancer (OR = 0.57, 95% CI 0.43-0.76 for the highest versus the lowest score quintile). The 'animal products and cereals' pattern was positively associated with laryngeal cancer (OR = 1.54, 95% CI 1.12-2.11), whereas the 'fats' pattern was inversely associated with oral and pharyngeal cancer (OR = 0.78, 95% CI 0.63-0.97) and positively associated with laryngeal cancer (OR = 1.69, 95% CI 1.22-2.34).
CONCLUSIONS: These findings suggest that diets rich in animal products, cereals, and fats are positively related to laryngeal cancer, and those rich in fruit and vegetables inversely related to oral and pharyngeal cancer.

2. Polesel J, Gheit T, Talamini R, Shahzad N, Lenardon O, Sylla B, La Vecchia C, Serraino D, Tommasino M, Franceschi S. Urinary human polyomavirus and papillomavirus infection and bladder cancer risk. Br J Cancer. 2012 Jan 3;106(1):222-6. doi: 10.1038/bjc.2011.519. Epub 2011 Nov 24.
Unit of Epidemiology and Biostatistics, IRCCS Centro di Riferimento Oncologico, 33081 Aviano (PN), Italy.

Abstract
Background:The association of transitional cell carcinomas of the bladder (TCB) with Schistosoma haematobium suggested a possible role of infections in the aetiology of TCB. Methods:In all, 114 TCB cases and 140 hospital controls from Pordenone Province were enrolled within an Italian multi-centric case-control study. Urine samples were screened for DNA from five human polyomaviruses (HPyV) (JCV, BKV, MCV, WUV, and KIV); SV40; and 22 mucosal human papillomaviruses (HPV) using highly sensitive PCR assays. Odds ratios (ORs) and corresponding confidence intervals (CIs) were computed for risk of TCB by HPyV- or HPV-positivity using unconditional logistic regression. Results:Human polyomavirus prevalence was similar in TCB cases (71.7%) and controls (77.7%) (OR for TCB=0.85; 95% CI: 0.45-1.61). JCV was the most frequently detected HPyV type. No individual HPyV showed a significant association. Among cases, HPyV-positivity was not associated with tumour characteristics, but it was significantly lower in women than men and among current and former smokers than never smokers. Human papillomavirus was detected in seven cases and five controls (OR=1.52; 95% CI: 0.42-5.45). Conclusion:The present small study does not support an involvement of HPyV or HPV infection in TCB aetiology in immunocompetent individuals. Differences in HPyV-positivity by sex and smoking may derive from differences in either acquisition or persistence of the infection.

3. Bosetti C, Lucenteforte E, Silverman DT, Petersen G, Bracci PM, Ji BT, Negri E, Li D, Risch HA, Olson SH, Gallinger S, Miller AB, Bueno-de-Mesquita HB, Talamini R, Polesel J, Ghadirian P, Baghurst PA, Zatonski W, Fontham E, Bamlet WR, Holly EA, Bertuccio P, Gao YT, Hassan M, Yu H, Kurtz RC, Cotterchio M, Su J, Maisonneuve P, Duell EJ, Boffetta P, La Vecchia C. Cigarette smoking and pancreatic cancer: an analysis from the International Pancreatic Cancer Case-Control Consortium (Panc4). Ann Oncol. 2011 Nov 21. [Epub ahead of print]
Department of Epidemiology, Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy.

Abstract
BACKGROUND: To evaluate the dose-response relationship between cigarette smoking and pancreatic cancer and to examine the effects of temporal variables. METHODS: We analyzed data from 12 case-control studies within the International Pancreatic Cancer Case-Control Consortium (PanC4), including 6507 pancreatic cases and 12 890 controls. We estimated summary odds ratios (ORs) by pooling study-specific ORs using random-effects models. RESULTS: Compared with never smokers, the OR was 1.2 (95% confidence interval [CI] 1.0-1.3) for former smokers and 2.2 (95% CI 1.7-2.8) for current cigarette smokers, with a significant increasing trend in risk with increasing number of cigarettes among current smokers (OR = 3.4 for ≥35 cigarettes per day, P for trend <0.0001). Risk increased in relation to duration of cigarette smoking up to 40 years of smoking (OR = 2.4). No trend in risk was observed for age at starting cigarette smoking, whereas risk decreased with increasing time since cigarette cessation, the OR being 0.98 after 20 years. CONCLUSIONS: This uniquely large pooled analysis confirms that current cigarette smoking is associated with a twofold increased risk of pancreatic cancer and that the risk increases with the number of cigarettes smoked and duration of smoking. Risk of pancreatic cancer reaches the level of never smokers ∼20 years after quitting.

4. Turati F, Edefonti V, Talamini R, Ferraroni M, Malvezzi M, Bravi F, Franceschi S, Montella M, Polesel J, Zucchetto A, La Vecchia C, Negri E, Decarli A. Family history of liver cancer and hepatocellular carcinoma. Hepatology. 2011 Nov 16. doi: 10.1002/hep.24794. [Epub ahead of print]
Dipartimento di Epidemiologia, Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy; Dipartimento di Medicina del Lavoro, Università degli Studi di Milano, Milan, Italy.

Abstract
Familial clustering of hepatocellular carcinoma (HCC) has been reported frequently among eastern Asiatic countries, where hepatitis B infection is common. Little is known about the relationship between family history of liver cancer and HCC in Western populations. We carried out a case-control study in Italy, involving 229 HCC cases and 431 hospital controls. Data on family history were summarized through a binary indicator (yes/no) and a family history score (FHscore), considering selected family characteristics. Odds ratios (OR) and the corresponding 95% confidence intervals (CI) were obtained from unconditional multiple logistic regression models including terms for age, sex, study center, education, tobacco smoking, alcohol drinking, hepatitis B surface antigen and/or anti-hepatitis C virus positivity. We also performed a meta-analysis on family history and liver cancer updated to April 2011 using random-effects models. After adjustment for chronic infection with hepatitis B/C viruses, family history of liver cancer was associated to HCC risk, when using both the binary indicator (OR=2.38, 95% CI, 1.01-5.58) and the FHscore, with increasing ORs for successive score categories. Compared to subjects without family history and no chronic infection with hepatitis B/C viruses, the OR for those exposed to both risk factors was 72.48 (95% CI, 21.92-239.73). In the meta-analysis, based on 9 case-control and 4 cohort studies, for a total of about 3600 liver cancer cases, the pooled relative risk for family history of liver cancer was 2.50 (95% CI, 2.06-3.03). CONCLUSION: A family history of liver cancer increases HCC risk, independently of hepatitis. The combination of family history of liver cancer and hepatitis B/C serum markers is associated to an over 70-fold elevated HCC risk.

5. Guglielmini P, Rubagotti A, Boccardo F. Serum enterolactone levels and mortality outcome in women with early breast cancer: a retrospective cohort study. Breast Cancer Res Treat. 2011 Nov 18. [Epub ahead of print]
Department of Oncology, Biology and Genetics, University of Genoa, Genoa, Italy.

Abstract
We previously demonstrated that high serum enterolactone levels are associated with a reduced incidence of breast cancer in healthy women. The present study was aimed at investigating whether a similar association might be found between serum enterolactone levels and the mortality of women with early breast cancer. The levels of enterolactone in cryopreserved serum aliquots obtained from 300 patients, operated on for breast cancer, were measured using a time-resolved fluoro-immunoassay. Levels were analyzed in respect to the risk of mortality following surgery. Cox proportional hazard regression models were used to check for prognostic features, to estimate hazard ratios for group comparisons and to test for the interaction on mortality hazards between the variables and enterolactone concentrations. The Fine and Gray competing risk proportional hazard regression model was used to predict the probabilities of breast cancer-related and breast cancer-unrelated mortalities. At a median follow-up time of 23 years (range 0.6-26.1), 180 patients died, 112 of whom died due to breast cancer-related events. An association between a decreased mortality risk and enterolactone levels ≥10 nmol/l was found in respect to both all-cause and breast cancer-specific mortality. The difference in mortality hazards was statistically significant, but it appeared to decrease and to lose significance after the first 10 years, though competing risk analysis showed that breast cancer-related mortality risk remained constantly lower in those patients with higher enterolactone levels. Our findings are consistent with those of most recent literature and provide further evidence that mammalian lignans might play an important role in reducing all-cause and cancer-specific mortality of the patients operated on for breast cancer.

6. Rossi M, Lugo A, Lagiou P, Zucchetto A, Polesel J, Serraino D, Negri E, Trichopoulos D, La Vecchia C. Proanthocyanidins and other flavonoids in relation to pancreatic cancer: a case-control study in Italy. Ann Oncol. 2011 Nov 2. [Epub ahead of print]
Department of Epidemiology, "Mario Negri" Institute for Pharmacological Research, Milan.

Abstract
BACKGROUND: Four cohort studies have examined the relation between flavonoids and pancreatic cancer risk providing inconsistent results. PATIENTS AND METHODS: We conducted a case-control study between 1991 and 2008 in Northern Italy. Subjects were 326 cases with incident pancreatic cancer and 652 frequency-matched controls (admitted to the same hospitals as cases for acute non-neoplastic conditions) who answered a reproducible and valid food-frequency questionnaire. We computed odds ratios (ORs) using logistic regression models conditioned on gender, age and study center, and adjusted for education, history of diabetes, tobacco smoking, alcohol drinking and energy intake. RESULTS: Proanthocyanidins with three or more mers were inversely related to pancreatic cancer risk. The ORs were similar in all classes of polymers with three or more mers and in their combination (OR for the highest versus the lowest quintile of intake, 0.41; 95% confidence interval 0.24-0.69), and did not substantially change after adjustment for fruit and vegetable consumption, and for vitamin C and folate intakes. Eating an additional portion of fruits rich in proanthocyanidins every day reduced the risk of pancreatic cancer by 25%. CONCLUSION: Dietary proanthocyanidins-mostly present in apples, pears and pulses-may convey some protection against pancreatic cancer risk.

7. Pelucchi C, Serraino D, Negri E, Montella M, Dellanoce C, Talamini R, La Vecchia C. The metabolic syndrome and risk of prostate cancer in Italy. Ann Epidemiol. 2011 Nov;21(11):835-41. doi: 10.1016/j.annepidem.2011.07.007.
Dipartimento di Epidemiologia, Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy. claudio.pelucchi@marionegri.it

Abstract
PURPOSE: To provide information on the role of the metabolic syndrome on prostate cancer risk. METHODS: We examined data from a multicentric Italian case-control study. Cases were 1294 patients with incident, histologically confirmed prostate cancer. Controls were 1451 men hospitalized with acute, non-neoplastic conditions. All subjects were younger than 75 years. The metabolic syndrome was defined according to selected indicators of abdominal obesity, hypercholesterolemia, hypertension, and diabetes. We computed multivariate odds ratios (OR) and 95% confidence intervals (CI) using unconditional logistic regression. RESULTS: Considering separate components of the metabolic syndrome, the ORs were 0.98 (95% CI, 0.72-1.34) for diabetes, 1.14 (95% CI, 0.96-1.36) for hypertension, 1.54 (95% CI, 1.26-1.89) for hypercholesterolemia, and 1.02 (95% CI, 0.86-1.21) for abdominal obesity. The OR of prostate cancer was 1.66 (95% CI, 1.22-2.28) in men with metabolic syndrome compared with those without. We found ORs of 1.02 (95% CI, 0.83-1.26) for men with one component of the metabolic syndrome, 1.12 (95% CI, 0.89-1.42) for two, 1.65 (95% CI, 1.15-2.36) for three, and 3.99 (95% CI, 1.03-15.4) for four compared with no components. CONCLUSIONS: The metabolic syndrome was associated with the risk of prostate cancer in this population.

8. Giannandrea F, Gandini L, Paoli D, Turci R, Figà-Talamanca I. Pesticide exposure and serum organochlorine residuals among testicular cancer patients and healthy controls. J Environ Sci Health B. 2011 Nov-Dec;46(8):780-7.
Department of Public Health and Infectious Diseases, University of Rome Sapienza, Rome, Italy.

Abstract
The incidence of testicular cancer (TC) has been increasing worldwide during the last decades. The reasons of the increase remains unknown, but recent findings suggest that organochlorine pesticides (OPs) could influence the development of TC. A hospital-based case-control study of 50 cases and 48 controls was conducted to determine whether environmental exposure to OPs is associated with the risk of TC, and by measuring serum concentrations of OPs, including p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) isomer and hexachlorobenzene (HCB) in participants. A significant association was observed between TC and household insecticide use (odds ratio [OR] = 3.01, 95 % CI: 1.11-8.14; OR(adjusted) = 3.23, 95 % CI: 1.15-9.11). Crude and adjusted ORs for TC were also significantly associated with higher serum concentrations of total OPs (OR = 3.15, 95 % CI: 1.00-9.91; OR(adjusted) = 3.34, 95 % CI: 1.09-10.17) in cases compared with controls. These findings give additional support to the results of previous research that suggest that some environmental exposures to OPs may be implicated in the pathogenesis of TC.

Breve commento a cura di L. Richiardi
I risultati sul rischio di tumore del testicolo negli utilizzatori di pesticidi, e in generale per esposizioni occupazionali e non-occupazionali a composti organoclorurati, sono di forte interesse; anche se spesso non consistenti, in generale indicano la possibilità di un aumento di rischio per tumore del testicolo. Questo studio caso-controll oospedaliero, anche se di dimensioni limiate e su un campione selzionato, riporta i risultati di un’analisi su esposizioni ambientali a pesticidi organoclorurati e rischio di tumore del testicolo.
I risultati indicano un aumento di rischio per tumore del testicolo associato con livelli di p,p_-dichlorodiphenyldichloroethylene (p,p’-DDE) misurati su campioni di sangue raccolti al momento della diagnosi o reclutamento nei controlli.

9. Prandoni P, Casiglia E, Tikhonoff V, Leizorovicz A, Decousus H; Calisto Investigators. The risk of subsequent cancer and arterial cardiovascular events in patients with superficial vein thrombosis in the legs. Blood. 2011 Oct 27;118(17):4719-22. Epub 2011 Aug 31.
Collaborators: Shvalb P, Kalinin R, Kachinskiy A, Pshennikov AS, Gerasimov AA, Novikov AN, Apartsin K, Chizhova E, Zubareva N, Gusev V, Mineev D, Chumakov A, Smirnov G, Krasavin V, Chernyatina M, Belikov L, Gladchenko M, Rodionov O, Scherbakov A, Sokolenko N, Alfyerova E, Belentsov S, Matyas L, Szentesi S, Simon G, Juhasz K, Hajdu L, Varga M, Mietaschk A, Kunze S, von Bilderling P, Betzl G, Gudz I, Voloshyna M, Syerna A, Giannoukas A, Saleptsis V, Koutsias S, Lazarides M, Nikolopoulos ES, Filis K, Krievins D, Gedins M, Kisis K, Camporese G, Verlato F, Andreozzi G, Davì G, Lessiani G, Pesavento R, Minotto I, Parisi R, Ambrosio G, Prisco D, Acín Garcia F, Canibano C, Trujillo J, Hirmerova SJ, Krcova E, Stanek F, Maasalu K, Gaastra M, Jeanneret CC, Mazzolai L, Banyai M, Heidemann M.

Department of Cardiothoracic and Vascular Sciences, Clinica Medica 2, University of Padua, Padua, Italy. paoloprandoni@tin.it

Abstract
Although it has been clearly demonstrated that venous thromboembolism is associated with an increased risk of subsequent overt cancer and arterial cardiovascular events in comparison with control populations, whether this association also applies to patients with isolated (ie, without concomitant involvement of the deep vein system) superficial vein thrombosis (SVT) in the legs is unknown. In 737 consecutive patients with isolated SVT not involving the sapheno-femoral junction, we conducted a retrospective investigation to assess the rate of cancer and that of arterial cardiovascular events occurring during follow-up. The event rates were compared with those occurring in 1438 controls having comparable characteristics. Both cases and controls were followed-up for an average period of 26 ± 8 months (range, 3-45). Malignancy was diagnosed in 26 cases (3.5%) and 56 controls (3.9%), leading to a hazard ratio of 0.86 (95% confidence interval, 0.55%-1.35%). Arterial cardiovascular events occurred in 32 cases (4.3%) and 63 controls (4.4%), leading to a hazard ratio of 0.97 (95% confidence interval, 0.63%-1.50%). We conclude that the occurrence of isolated SVT in the legs does not place patients at an increased risk of malignancies or arterial cardiovascular events. Whether this conclusion also applies to patients whose thrombosis involves the sapheno-femoral junction remains to be demonstrated.

10. Bo S, Ciccone G, Rosato R, Villois P, Appendino G, Ghigo E, Grassi G. Cancer mortality reduction and metformin: a retrospective cohort study in type 2 diabetic patients. Diabetes Obes Metab. 2012 Jan;14(1):23-9. doi: 10.1111/j.1463-1326.2011.01480.x. Epub 2011 Nov 21.
Department of Internal Medicine, University of Torino, Turin, Italy Unit of Cancer Epidemiology CPO, S. Giovanni Battista Hospital, University of Torino, Turin, Italy.

Abstract
Aims: Few studies suggest that metformin decreases cancer mortality in type-2 diabetic patients (T2DP). We explored the association between the type and duration of antidiabetic therapies and cancer and other-than-cancer mortality in a T2DP cohort, taking into account the competing risks between different causes of death and multiple potential confounding effects. The mortality rates were compared with the general population from the same area. Methods: In 1995, all T2DP (n = 3685) at our diabetes clinic in Turin (∼12% of all T2DP in the city), without cancer at baseline, were identified. Vital status was assessed after a mean 4.5-year follow-up. Results: Metformin users had greater adiposity, while insulin users had more co-morbidities. All-cause- and cancer-related deaths occurred in: 9.2 and 1.6% of metformin users, 13.1 and 3.0% of sulfonylureas users and 26.8 and 4.8% of insulin users, respectively. In a Cox regression model for competing risks, adjusted for propensity score, metformin users showed a lower cancer mortality risk [hazard ratio (HR) = 0.56; 95% confidence interval (CI) 0.34-0.94], while insulin was positively associated with other-than-cancer mortality (HR = 1.56; 95%CI 1.22-1.99). Each 5-year metformin exposure was associated with a reduction in cancer death by 0.73, whereas every 5-year insulin exposure was associated with 1.25-fold increase in other-than-cancer death. Standardized mortality ratios for cancer and other-than-cancer mortality in metformin users were 43.6 (95%CI 25.8-69.0) and 99.1 (95%CI 79.3-122.5), respectively, in comparison with the general population. Conclusions: Metformin users showed a lower risk of cancer-related mortality than not users or patients on diet only; this may represent another reason to choose metformin as a first-line therapy in T2DP.

11. Warner M, Mocarelli P, Samuels S, Needham L, Brambilla P, Eskenazi B. Dioxin exposure and cancer risk in the Seveso Women's Health Study. Environ Health Perspect. 2011 Dec;119(12):1700-5. Epub 2011 Aug 2.
Center for Environmental Research and Children's Health, School of Public Health, University of California at Berkeley, Berkeley, California 94720, USA. mwarner@berkeley.edu

Abstract
BACKGROUND: 2,3,7,8-Tetrachlorodibenzo-para-dioxin (TCDD), a widespread environmental contaminant, disrupts multiple endocrine pathways. The International Agency for Research on Cancer classified TCDD as a known human carcinogen, based on predominantly male occupational studies of increased mortality from all cancers combined. OBJECTIVES: After a chemical explosion on 10 July 1976 in Seveso, Italy, residents experienced some of the highest levels of TCDD exposure in a human population. In 1996, we initiated the Seveso Women's Health Study (SWHS), a retrospective cohort study of the reproductive health of the women. We previously reported a significant increased risk for breast cancer and a nonsignificant increased risk for all cancers combined with individual serum TCDD, but the cohort averaged only 40 years of age in 1996. Herein we report results for risk of cancer from a subsequent follow-up of the cohort in 2008. METHODS: In 1996, we enrolled 981 women who were 0-40 years of age in 1976, lived in the most contaminated areas, and had archived sera collected near the explosion. Individual TCDD concentration was measured in archived serum by high-resolution mass spectrometry. A total of 833 women participated in the 2008 follow-up study. We examined the relation of serum TCDD with cancer incidence using Cox proportional hazards models. RESULTS: In total, 66 (6.7%) women had been diagnosed with cancer. The adjusted hazard ratio (HR) associated with a 10-fold increase in serum TCDD for all cancers combined was significantly increased [adjusted HR = 1.80; 95% confidence interval (CI): 1.29, 2.52]. For breast cancer, the HR was increased, but not significantly (adjusted HR = 1.44; 95% CI: 0.89, 2.33). CONCLUSIONS: Individual serum TCDD is significantly positively related with all cancer incidence in the SWHS cohort, more than 30 years later. This all-female study adds to the epidemiologic evidence that TCDD is a multisite carcinogen.

12. Turati F, Edefonti V, Bravi F, Ferraroni M, Franceschi S, La Vecchia C, Montella M, Talamini R, Decarli A. Nutrient-based dietary patterns, family history, and colorectal cancer. Eur J Cancer Prev. 2011 Nov;20(6):456-61.
Sezione di Statistica Medica e Biometria G. A. Maccacaro, Dipartimento di Medicina del Lavoro Clinica del Lavoro Luigi Devoto, Università degli Studi di Milano, Italy.

Abstract
The effect of dietary habits on colorectal cancer (CRC) risk may be modified by a family history of CRC. We analyzed data from an Italian case-control study, including 1953 CRC cases and 4154 controls. Odds ratios (OR) and 95% confidence intervals (CI) for combined categories of family history and tertiles of two a posteriori dietary patterns were derived using multiple logistic regression models. Compared with individuals without family history and in the lowest tertile category of the 'starch-rich' pattern, the ORs of CRC were 1.38 (95% CI: 1.19-1.61) for the group without family history and in the highest tertile, 2.89 (95% CI: 2.30-3.64) for the one with family history and in the lowest tertile, and 4.00 (95% CI: 3.03-5.27) for the one with family history and in the highest tertile. Compared with individuals without family history and in the highest tertile of the 'vitamins and fiber' pattern, the ORs were 1.29 (95% CI: 1.12-1.48) for the group without family history and in the lowest tertile, 2.89 (95% CI: 2.30-3.64) for the one with family history and in the highest tertile, and 3.74 (95% CI: 2.85-4.91) for the one with family history and in the lowest tertile. Family history of CRC and 'starch-rich' or 'vitamins and fiber' patterns has an independent effect on CRC risk in our population. However, as having a family history plausibly implies shared environmental and/or genetic risk factors, our results could not exclude that dietary habits can modify genetic susceptibility to CRC.

13. Cancemi L, Romei C, Bertocchi S, Tarrini G, Spitaleri I, Cipollini M, Landi D, Garritano S, Pellegrini G, Cristaudo A, Pinchera A, Barale R, Elisei R, Landi S, Gemignani F. Evidences that the polymorphism Pro-282-Ala within the tumor suppressor gene WWOX is a new risk factor for differentiated thyroid carcinoma. Int J Cancer. 2011 Dec 15;129(12):2816-24. doi: 10.1002/ijc.25937. Epub 2011 Apr 25.
Department of Biology, University of Pisa, Pisa, Italy.

Abstract
We report a hypothesis-driven study aimed to detect genetic markers of susceptibility to differentiated thyroid carcinomas (DTC). A large number of candidate genes were first selected through literature search (genome-wide studies were also included). To restrict the analysis to single nucleotide polymorphisms (SNPs) with a high likelihood to be associated with increased risk, each SNP must comply with several a priori hypotheses. Only one SNP, the rs3764340 encoding for the aminoacidic substitution proline-to-alanine at codon 282 of the tumor suppressor gene WWOX, passed the selection. A case-control association study was carried out, involving a total of 1,741 cases and 1,042 controls. The logistic regression analysis revealed an increased risk of DTC for the carriers of the G-allele (crude odds ratio, OR = 1.53; 95% confidence interval, CI = 1.18-1.99; p = 1.38 × 10(-3) ). When we controlled for covariates, the adjusted OR was 1.48 with a 95% CI of 1.08-2.03 (p = 8.0 × 10(-3) ). The association was confirmed after stratification for histology (for papillary thyroid carcinoma the adjusted OR was 1.43; 95% CI 1.02-2.00; p = 0.037), incident cases and smokers, but was also at the limit of statistical significance in all the other categories considered. In silico analyses showed that when alanine substitutes proline, subtle changes of the proteic structure can be predicted. These findings together with other observations from literature on human cancers and the fact that the proline at codon 282 is extremely conserved in phylogenetically distant organisms (including Drosophila) suggest that the variant allele-282 could affect the biological function of WWOX, thereby predisposing individuals to thyroid cancer.

14. Bidoli E, Pelucchi C, Zucchetto A, Negri E, Dal Maso L, Polesel J, Boz G, Montella M, Franceschi S, Serraino D, La Vecchia C, Talamini R. Fiber intake and pancreatic cancer risk: a case-control study. Ann Oncol. 2012 Jan;23(1):264-8. Epub 2011 Apr 2.
Unit of Epidemiology and Biostatistics, Centro di Riferimento Oncologico, Aviano.

Abstract
BACKGROUND: Scanty and inconsistent studies are available on the relation between dietary fiber intake and pancreatic cancer. A case-control study was carried out in northern Italy to further investigate the role of various types of dietary fibers in the etiology of pancreatic cancer. PATIENTS AND METHODS: Cases were 326 patients with incident pancreatic cancer, excluding neuroendocrine tumors, admitted to major teaching and general hospitals during 1991-2008. Controls were 652 patients admitted for acute, nonneoplastic conditions to the same hospital network of cases. Information was elicited using a validated food frequency questionnaire. Odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) were estimated for intake quintiles of different types of fiber after allowance for total energy intake and other potential confounding factors. RESULTS: Total fiber intake was inversely related to risk of pancreatic cancer (OR = 0.4 for highest versus lowest quintile of intake; 95% CI 0.2-0.7). An inverse association emerged between pancreatic cancer and both soluble (OR = 0.4; 95% CI 0.2-0.7) and total insoluble fiber (OR = 0.5; 95% CI 0.3-0.8), particularly cellulose (OR = 0.4; 95% CI 0.3-0.7) and lignin (OR = 0.5; 95% CI 0.3-0.9). Fruit fiber intake was inversely associated with pancreatic cancer (OR = 0.5; 95% CI 0.3-0.8), whereas grain fiber was not (OR = 1.2; 95% CI 0.7-2.0). CONCLUSIONS: This study suggests that selected types of fiber and total fiber are inversely related to pancreatic cancer.

15. Rosato V, Bosetti C, Talamini R, Levi F, Montella M, Giacosa A, Negri E, La Vecchia C. Metabolic syndrome and the risk of breast cancer in postmenopausal women. Ann Oncol. 2011 Dec;22(12):2687-92. Epub 2011 Mar 17.
Department of Epidemiology, Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.

Abstract
BACKGROUND: Only a few small studies investigated the association between postmenopausal breast cancer and metabolic syndrome (MetS) as a single entity. MATERIALS AND METHODS: We analyzed the data of two Italian and Swiss case-control studies conducted between 1983 and 2007, including 3869 postmenopausal women with incident breast cancer and 4082 postmenopausal controls admitted to the same hospitals as cases for acute conditions. MetS was defined as the presence of at least three components among diabetes, drug-treated hypertension, drug-treated hyperlipidemia, and obesity. RESULTS: The odds ratios (ORs) of postmenopausal breast cancer were 1.33 [95% confidence interval (CI) 1.09-1.62] for diabetes, 1.19 (95% CI 1.07-1.33) for hypertension, 1.08 (95% CI 0.95-1.22) for hyperlipidemia, 1.26 (95% CI 1.11-1.44) for body mass index ≥30 kg/m(2), and 1.22 (95% CI 1.09-1.36) for waist circumference ≥88 cm. The risk of postmenopausal breast cancer was significantly increased for women with MetS (OR = 1.75, 95% CI 1.37-2.22, for three or more MetS components, P for trend for increasing number of components < 0.0001) and the risk was higher at older age (OR = 3.04, 95% CI 1.75-5.29, at age ≥70 years for three or more MetS components). CONCLUSIONS: This study supports a direct association between MetS and postmenopausal breast cancer risk.

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