Cause ed epidemiologia analitica
Ricerca bibliografica periodo fino al 15 ottobre 2010
All’interno dell’area “Cause ed epidemiologia analitica†in questo numero saranno selezionati gli articoli relativi al tema: "Tumori".
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Selezione limitata ai tumori. Come riportato nella stringa di ricerca sono escluse le revisioni. Escludo inoltre eventuali editoriali. Gli studi multicentrici sono inclusi quando vengono rilevati grazie alla stringa di ricerca (che non effettua per limitazioni tecniche la ricerca sulle affiliazioni di tutti gli autori). Ho escluso dai risultati: i) gli studi non condotti in Italia, ii) gli articoli che non riportano stime di associazione e ii) articoli provenienti dallo stesso studio con valutazioni di associazione esposizione-malattia in parte sovrapponibili.
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1. Consonni D, De Matteis S, Lubin JH, Wacholder S, Tucker M, Pesatori AC, Caporaso NE, Bertazzi PA, Landi MT. Lung cancer and occupation in a population-based case-control study. Am J Epidemiol. 2010 Feb 1;171(3):323-33. Epub 2010 Jan 4.
Unit of Epidemiology, Department of Preventive Medicine, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Via San Barnaba, 8, 20122 Milano, Italy. dario.consonni@unimi.it
Abstract
The authors examined the relation between occupation and lung cancer in the large, population-based Environment And Genetics in Lung cancer Etiology (EAGLE) case-control study. In 2002-2005 in the Lombardy region of northern Italy, 2,100 incident lung cancer cases and 2,120 randomly selected population controls were enrolled. Lifetime occupational histories (industry and job title) were coded by using standard international classifications and were translated into occupations known (list A) or suspected (list B) to be associated with lung cancer. Smoking-adjusted odds ratios and 95% confidence intervals were calculated with logistic regression. For men, an increased risk was found for list A (177 exposed cases and 100 controls; odds ratio = 1.74, 95% confidence interval: 1.27, 2.38) and most occupations therein. No overall excess was found for list B with the exception of filling station attendants and bus and truck drivers (men) and launderers and dry cleaners (women). The authors estimated that 4.9% (95% confidence interval: 2.0, 7.8) of lung cancers in men were attributable to occupation. Among those in other occupations, risk excesses were found for metal workers, barbers and hairdressers, and other motor vehicle drivers. These results indicate that past exposure to occupational carcinogens remains an important determinant of lung cancer occurrence.
PMID: 20047975 [PubMed - indexed for MEDLINE]
Abstract
The authors examined the relation between occupation and lung cancer in the large, population-based Environment And Genetics in Lung cancer Etiology (EAGLE) case-control study. In 2002-2005 in the Lombardy region of northern Italy, 2,100 incident lung cancer cases and 2,120 randomly selected population controls were enrolled. Lifetime occupational histories (industry and job title) were coded by using standard international classifications and were translated into occupations known (list A) or suspected (list B) to be associated with lung cancer. Smoking-adjusted odds ratios and 95% confidence intervals were calculated with logistic regression. For men, an increased risk was found for list A (177 exposed cases and 100 controls; odds ratio = 1.74, 95% confidence interval: 1.27, 2.38) and most occupations therein. No overall excess was found for list B with the exception of filling station attendants and bus and truck drivers (men) and launderers and dry cleaners (women). The authors estimated that 4.9% (95% confidence interval: 2.0, 7.8) of lung cancers in men were attributable to occupation. Among those in other occupations, risk excesses were found for metal workers, barbers and hairdressers, and other motor vehicle drivers. These results indicate that past exposure to occupational carcinogens remains an important determinant of lung cancer occurrence.
PMID: 20047975 [PubMed - indexed for MEDLINE]
Breve commento a cura di Lorenzo Richiardi
Lo studio EAGLE è uno studio caso-controllo sul tumore del polmone di grandi dimensioni condotto nella popolazione della Lombardia nella prima metà degli anni 2000. Questo articolo riporta i risultati per occupazioni note (lista A) o sospette (lista B) di comportare esposizione a cancerogeni polmonari. Lo studio riporta un aumento di rischio per tumore del polmone nei lavoratori impiegati in occupazioni della Lista A, con una stima del rischio attribuibile di popolazione (quindi in Lombardia in anni recenti) del 5%.
2. Heck JE, Berthiller J, Vaccarella S, Winn DM, Smith EM, Shan'gina O, Schwartz SM, Purdue MP, Pilarska A, Eluf-Neto J, Menezes A, McClean MD, Matos E, Koifman S, Kelsey KT, Herrero R, Hayes RB, Franceschi S, Wünsch-Filho V, Fernández L, Daudt AW, Curado MP, Chen C, Castellsagué X, Ferro G, Brennan P, Boffetta P, Hashibe M. Sexual behaviours and the risk of head and neck cancers: a pooled analysis in the International Head and Neck Cancer Epidemiology (INHANCE) consortium. Int J Epidemiol. 2010 Feb;39(1):166-81. Epub 2009 Dec 18.
Lifestyle, Environment, and Cancer Group, International Agency for Research on Cancer, Lyon, France.
Abstract
BACKGROUND: Sexual contact may be the means by which head and neck cancer patients are exposed to human papillomavirus (HPV).
METHODS: We undertook a pooled analysis of four population-based and four hospital-based case-control studies from the International Head and Neck Cancer Epidemiology (INHANCE) consortium, with participants from Argentina, Australia, Brazil, Canada, Cuba, India, Italy, Spain, Poland, Puerto Rico, Russia and the USA. The study included 5642 head and neck cancer cases and 6069 controls. We calculated odds ratios (ORs) of associations between cancer and specific sexual behaviours, including practice of oral sex, number of lifetime sexual partners and oral sex partners, age at sexual debut, a history of same-sex contact and a history of oral-anal contact. Findings were stratified by sex and disease subsite.
RESULTS: Cancer of the oropharynx was associated with having a history of six or more lifetime sexual partners [OR = 1.25, 95% confidence interval (CI) 1.01, 1.54] and four or more lifetime oral sex partners (OR = 2.25, 95% CI 1.42, 3.58). Cancer of the tonsil was associated with four or more lifetime oral sex partners (OR = 3.36, 95 % CI 1.32, 8.53), and, among men, with ever having oral sex (OR = 1.59, 95% CI 1.09, 2.33) and with an earlier age at sexual debut (OR = 2.36, 95% CI 1.37, 5.05). Cancer of the base of the tongue was associated with ever having oral sex among women (OR = 4.32, 95% CI 1.06, 17.6), having two sexual partners in comparison with only one (OR = 2.02, 95% CI 1.19, 3.46) and, among men, with a history of same-sex sexual contact (OR = 8.89, 95% CI 2.14, 36.8).
CONCLUSIONS: Sexual behaviours are associated with cancer risk at the head and neck cancer subsites that have previously been associated with HPV infection.
PMID: 20022926 [PubMed - indexed for MEDLINE]
Abstract
BACKGROUND: Sexual contact may be the means by which head and neck cancer patients are exposed to human papillomavirus (HPV).
METHODS: We undertook a pooled analysis of four population-based and four hospital-based case-control studies from the International Head and Neck Cancer Epidemiology (INHANCE) consortium, with participants from Argentina, Australia, Brazil, Canada, Cuba, India, Italy, Spain, Poland, Puerto Rico, Russia and the USA. The study included 5642 head and neck cancer cases and 6069 controls. We calculated odds ratios (ORs) of associations between cancer and specific sexual behaviours, including practice of oral sex, number of lifetime sexual partners and oral sex partners, age at sexual debut, a history of same-sex contact and a history of oral-anal contact. Findings were stratified by sex and disease subsite.
RESULTS: Cancer of the oropharynx was associated with having a history of six or more lifetime sexual partners [OR = 1.25, 95% confidence interval (CI) 1.01, 1.54] and four or more lifetime oral sex partners (OR = 2.25, 95% CI 1.42, 3.58). Cancer of the tonsil was associated with four or more lifetime oral sex partners (OR = 3.36, 95 % CI 1.32, 8.53), and, among men, with ever having oral sex (OR = 1.59, 95% CI 1.09, 2.33) and with an earlier age at sexual debut (OR = 2.36, 95% CI 1.37, 5.05). Cancer of the base of the tongue was associated with ever having oral sex among women (OR = 4.32, 95% CI 1.06, 17.6), having two sexual partners in comparison with only one (OR = 2.02, 95% CI 1.19, 3.46) and, among men, with a history of same-sex sexual contact (OR = 8.89, 95% CI 2.14, 36.8).
CONCLUSIONS: Sexual behaviours are associated with cancer risk at the head and neck cancer subsites that have previously been associated with HPV infection.
PMID: 20022926 [PubMed - indexed for MEDLINE]
Breve commento a cura di Lorenzo Richiardi
Il consorzio INHANCE riunisce insieme numerosi studi sul tumore del capo-collo condotti in diversi paesi del mondo, tra cui l’Italia, per un totale di più di 20.000 casi e controlli. Questo articolo riporta i risultati di un’analisi sugli studi con informazioni sui comportamenti sessuali. Anche se i risultati non sono interamente consistenti, gli eccessi di rischio trovati supportano un ruolo dell’HPV nell’eziologia di alcuni tumori del capo-collo.
3. Willeit P, Willeit J, Mayr A, Weger S, Oberhollenzer F, Brandstätter A, Kronenberg F, Kiechl S. Telomere length and risk of incident cancer and cancer mortality. JAMA. 2010 Jul 7;304(1):69-75.
Department of Neurology, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria.
Abstract
CONTEXT : Telomeres are essential to preserve the integrity of the genome. Critically short telomeres lead to replicative cell senescence and chromosomal instability and may thereby increase cancer risk.
OBJECTIVE: To determine the association between baseline telomere length and incident cancer and cancer mortality.
DESIGN, SETTING, AND PARTICIPANTS : Leukocyte telomere length was measured by quantitative polymerase chain reaction in 787 participants free of cancer at baseline in 1995 from the prospective, population-based Bruneck Study in Italy.
MAIN OUTCOME MEASURES : Incident cancer and cancer mortality over a follow-up period of 10 years (1995-2005 with a follow-up rate of 100%).
RESULTS : A total of 92 of 787 participants (11.7%) developed cancer (incidence rate, 13.3 per 1000 person-years). Short telomere length at baseline was associated with incident cancer independently of standard cancer risk factors (multivariable hazard ratio [HR] per 1-SD decrease in log(e)-transformed telomere length, 1.60; 95% confidence interval [CI], 1.30-1.98; P < .001). Compared with participants in the longest telomere length group, the multivariable HR for incident cancer was 2.15 (95% CI, 1.12-4.14) in the middle length group and 3.11 (95% CI, 1.65-5.84) in the shortest length group (P < .001). Incidence rates were 5.1 (95% CI, 2.9-8.7) per 1000 person-years in the longest telomere length group, 14.2 (95% CI, 10.0-20.1) per 1000 person-years in the middle length group, and 22.5 (95% CI, 16.9-29.9) per 1000 person-years in the shortest length group. The association equally applied to men and women and emerged as robust under a variety of circumstances. Furthermore, short telomere length was associated with cancer mortality (multivariable HR per 1-SD decrease in log(e)-transformed telomere length, 2.13; 95% CI, 1.58-2.86; P < .001) and individual cancer subtypes with a high fatality rate.
CONCLUSION : In this study population, there was a statistically significant inverse relationship between telomere length and both cancer incidence and mortality.
PMID: 20606151 [PubMed - indexed for MEDLINE]
Abstract
CONTEXT : Telomeres are essential to preserve the integrity of the genome. Critically short telomeres lead to replicative cell senescence and chromosomal instability and may thereby increase cancer risk.
OBJECTIVE: To determine the association between baseline telomere length and incident cancer and cancer mortality.
DESIGN, SETTING, AND PARTICIPANTS : Leukocyte telomere length was measured by quantitative polymerase chain reaction in 787 participants free of cancer at baseline in 1995 from the prospective, population-based Bruneck Study in Italy.
MAIN OUTCOME MEASURES : Incident cancer and cancer mortality over a follow-up period of 10 years (1995-2005 with a follow-up rate of 100%).
RESULTS : A total of 92 of 787 participants (11.7%) developed cancer (incidence rate, 13.3 per 1000 person-years). Short telomere length at baseline was associated with incident cancer independently of standard cancer risk factors (multivariable hazard ratio [HR] per 1-SD decrease in log(e)-transformed telomere length, 1.60; 95% confidence interval [CI], 1.30-1.98; P < .001). Compared with participants in the longest telomere length group, the multivariable HR for incident cancer was 2.15 (95% CI, 1.12-4.14) in the middle length group and 3.11 (95% CI, 1.65-5.84) in the shortest length group (P < .001). Incidence rates were 5.1 (95% CI, 2.9-8.7) per 1000 person-years in the longest telomere length group, 14.2 (95% CI, 10.0-20.1) per 1000 person-years in the middle length group, and 22.5 (95% CI, 16.9-29.9) per 1000 person-years in the shortest length group. The association equally applied to men and women and emerged as robust under a variety of circumstances. Furthermore, short telomere length was associated with cancer mortality (multivariable HR per 1-SD decrease in log(e)-transformed telomere length, 2.13; 95% CI, 1.58-2.86; P < .001) and individual cancer subtypes with a high fatality rate.
CONCLUSION : In this study population, there was a statistically significant inverse relationship between telomere length and both cancer incidence and mortality.
PMID: 20606151 [PubMed - indexed for MEDLINE]
4. Rossi M, Lipworth L, Polesel J, Negri E, Bosetti C, Talamini R, McLaughlin JK, La Vecchia C. Dietary glycemic index and glycemic load and risk of pancreatic cancer: a case-control study. Ann Epidemiol. 2010 Jun;20(6):460-5.
Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.
Abstract
PURPOSE : Carbohydrates and dietary glycemic index (GI) influence the secretion of insulin and insulin-related growth factors and may play a role in the development of diabetes and obesity, both of which have been related to pancreatic cancer risk.
METHODS : We examined the association between dietary GI and glycemic load (GL) and pancreatic cancer by conducting a hospital-based case-control study in Italy in 1991-2008 of 326 cases of pancreatic cancer and 652 control patients. Dietary data were obtained with the use of a validated food-frequency questionnaire. Odds ratios (ORs) and corresponding 95% confidence intervals (95% CIs) were computed with the use of multiple logistic regression.
RESULTS : GI was positively associated with pancreatic cancer, with ORs of 1.56 (95% CI, 1.06-2.30) and 1.78 (95% CI, 1.20-2.62) for the second and third tertiles, respectively, compared with the lowest. No significant association was observed between GL and pancreatic cancer. Consumption of sugar, candy, honey, and jam was positively associated with pancreatic cancer, whereas consumption of fruit was inversely associated.
CONCLUSIONS : In conclusion, the positive association with high GI, in the absence of an association with dietary GL, fruit, or total carbohydrates, likely reflects the positive association between sweets or refined carbohydrates and pancreatic cancer in this study population.
PMID: 20470973 [PubMed - indexed for MEDLINE]
Abstract
PURPOSE : Carbohydrates and dietary glycemic index (GI) influence the secretion of insulin and insulin-related growth factors and may play a role in the development of diabetes and obesity, both of which have been related to pancreatic cancer risk.
METHODS : We examined the association between dietary GI and glycemic load (GL) and pancreatic cancer by conducting a hospital-based case-control study in Italy in 1991-2008 of 326 cases of pancreatic cancer and 652 control patients. Dietary data were obtained with the use of a validated food-frequency questionnaire. Odds ratios (ORs) and corresponding 95% confidence intervals (95% CIs) were computed with the use of multiple logistic regression.
RESULTS : GI was positively associated with pancreatic cancer, with ORs of 1.56 (95% CI, 1.06-2.30) and 1.78 (95% CI, 1.20-2.62) for the second and third tertiles, respectively, compared with the lowest. No significant association was observed between GL and pancreatic cancer. Consumption of sugar, candy, honey, and jam was positively associated with pancreatic cancer, whereas consumption of fruit was inversely associated.
CONCLUSIONS : In conclusion, the positive association with high GI, in the absence of an association with dietary GL, fruit, or total carbohydrates, likely reflects the positive association between sweets or refined carbohydrates and pancreatic cancer in this study population.
PMID: 20470973 [PubMed - indexed for MEDLINE]
5. Canova C, Richiardi L, Merletti F, Pentenero M, Gervasio C, Tanturri G, Garzino-Demo P, Pecorari G, Talamini R, Barzan L, Sulfaro S, Franchini G, Muzzolini C, Bordin S, Pugliese GN, Macrì E, Simonato L. Alcohol, tobacco and genetic susceptibility in relation to cancers of the upper aerodigestive tract in northern Italy. Tumori. 2010 Jan-Feb;96(1):1-10.
Department of Environmental Medicine and Public Health, University of Padua, Italy. cristina.canova@unipd.it
Abstract
AIMS AND BACKGROUND: Each year in Italy there are approximately 14,000 new cases and 7,000 deaths from cancer of the upper aerodigestive tract, which includes malignant tumors originating from the oral cavity, pharynx, larynx and esophagus. Established etiological factors include tobacco consumption and heavy alcohol drinking. The study of single nucleotide polymorphisms in upper aerodigestive tract cancer etiology may help to identify high-risk subgroups and to better understand the pathways leading to the development of these cancers.
METHODS: Italian results on about 500 cases and 500 controls from a large case-control study (ARCAGE) conducted in 10 European countries are presented with the major objectives of updating results on the effects of alcohol and tobacco consumptions in northern Italy, investigating the role of genetic variation with regard to the metabolism of alcohol and carcinogens from tobacco smoke, and evaluating possible interactions of these single nucleotide polymorphisms with these carcinogens.
RESULTS: The present study confirmed the importance of tobacco smoking and alcohol drinking as the main risk factors for upper aerodigestive tract cancers, indicating that about 68% of cancers among populations in northern Italy can be attributed to the combination of these risk factors. Significant associations between metabolizing phase I genes (CYP1A1 and CYP2A6), phase II genes (GSTA2) and upper aerodigestive tract cancers were found. A polymorphism of ADH1C has been associated with an increased risk of upper aerodigestive tract cancers, suggesting that the less rapid alcohol metabolizers are more susceptible to upper aerodigestive tract cancer risk.
CONCLUSIONS: Our results suggest that the ADH1C allele modifies the carcinogenic dose response for alcohol in the upper aerodigestive tract, giving rise to a gene-environment interaction. The role of genes as possible modifiers of life-style risks seems the most reliable.
PMID: 20437850 [PubMed - indexed for MEDLINE]
Abstract
AIMS AND BACKGROUND: Each year in Italy there are approximately 14,000 new cases and 7,000 deaths from cancer of the upper aerodigestive tract, which includes malignant tumors originating from the oral cavity, pharynx, larynx and esophagus. Established etiological factors include tobacco consumption and heavy alcohol drinking. The study of single nucleotide polymorphisms in upper aerodigestive tract cancer etiology may help to identify high-risk subgroups and to better understand the pathways leading to the development of these cancers.
METHODS: Italian results on about 500 cases and 500 controls from a large case-control study (ARCAGE) conducted in 10 European countries are presented with the major objectives of updating results on the effects of alcohol and tobacco consumptions in northern Italy, investigating the role of genetic variation with regard to the metabolism of alcohol and carcinogens from tobacco smoke, and evaluating possible interactions of these single nucleotide polymorphisms with these carcinogens.
RESULTS: The present study confirmed the importance of tobacco smoking and alcohol drinking as the main risk factors for upper aerodigestive tract cancers, indicating that about 68% of cancers among populations in northern Italy can be attributed to the combination of these risk factors. Significant associations between metabolizing phase I genes (CYP1A1 and CYP2A6), phase II genes (GSTA2) and upper aerodigestive tract cancers were found. A polymorphism of ADH1C has been associated with an increased risk of upper aerodigestive tract cancers, suggesting that the less rapid alcohol metabolizers are more susceptible to upper aerodigestive tract cancer risk.
CONCLUSIONS: Our results suggest that the ADH1C allele modifies the carcinogenic dose response for alcohol in the upper aerodigestive tract, giving rise to a gene-environment interaction. The role of genes as possible modifiers of life-style risks seems the most reliable.
PMID: 20437850 [PubMed - indexed for MEDLINE]
6. Price AJ, Allen NE, Appleby PN, Crowe FL, Jenab M, Rinaldi S, Slimani N, Kaaks R, Rohrmann S, Boeing H, Pischon T, Benetou V, Naska A, Trichopoulou A, Palli D, Sieri S, Tumino R, Vineis P, Bueno-de-Mesquita HB, Donate I, González CA, Sánchez MJ, Chirlaque MD, Ardanaz E, Larrañaga N, Khaw KT, Rodwell S, Gallo V, Michaud DS, Riboli E, Key TJ. Plasma phytanic acid concentration and risk of prostate cancer: results from the European Prospective Investigation into Cancer and Nutrition. Am J Clin Nutr. 2010 Jun;91(6):1769-76. Epub 2010 Apr 28.
Nuffield Department of Clinical Medicine, University of Oxford, United Kingdom. alison.price@ceu.ox.ac.uk
Abstract
BACKGROUND: Phytanic acid, a fatty acid predominantly obtained from foods high in ruminant fat, may have a biological role in the up-regulation of the protein alpha-methylacyl-coenzyme A racemase, which is overexpressed in prostate cancer tissue.
OBJECTIVE: This study aimed to examine the association between plasma concentrations of phytanic acid and subsequent risk of prostate cancer.
DESIGN: Within the European Prospective Investigation into Cancer and Nutrition cohort, 566 incident prostate cancer cases from Germany, Greece, Italy, the Netherlands, Spain, and the United Kingdom were individually matched to 566 controls by study center, age at recruitment, and time of day and duration of fasting at blood collection. Phytanic acid concentrations were measured by using a gas chromatography-mass spectrometry assay.
RESULTS: In controls, plasma phytanic acid concentration was strongly correlated with dairy fat intake (r = 0.49, P < 0.0001), varied significantly by country (P for heterogeneity < 0.0001), and decreased with age (P for trend = 0.02) and duration of fasting at blood collection (P for trend = 0.002). There was no significant association of phytanic acid with prostate cancer risk overall (odds ratio for a doubling in concentration: 1.05; 95% CI: 0.91, 1.21; P for trend = 0.53) or by stage or grade of disease. However, in men who had fasted (>3 h) at blood collection, the odds ratio for prostate cancer was 1.27 (95% CI: 1.01, 1.60; P for trend = 0.04).
CONCLUSION: Plasma phytanic acid concentration is significantly associated with intake of dairy fat but not with overall risk of prostate cancer in this European population.
PMID: 20427733 [PubMed - indexed for MEDLINE]
Abstract
BACKGROUND: Phytanic acid, a fatty acid predominantly obtained from foods high in ruminant fat, may have a biological role in the up-regulation of the protein alpha-methylacyl-coenzyme A racemase, which is overexpressed in prostate cancer tissue.
OBJECTIVE: This study aimed to examine the association between plasma concentrations of phytanic acid and subsequent risk of prostate cancer.
DESIGN: Within the European Prospective Investigation into Cancer and Nutrition cohort, 566 incident prostate cancer cases from Germany, Greece, Italy, the Netherlands, Spain, and the United Kingdom were individually matched to 566 controls by study center, age at recruitment, and time of day and duration of fasting at blood collection. Phytanic acid concentrations were measured by using a gas chromatography-mass spectrometry assay.
RESULTS: In controls, plasma phytanic acid concentration was strongly correlated with dairy fat intake (r = 0.49, P < 0.0001), varied significantly by country (P for heterogeneity < 0.0001), and decreased with age (P for trend = 0.02) and duration of fasting at blood collection (P for trend = 0.002). There was no significant association of phytanic acid with prostate cancer risk overall (odds ratio for a doubling in concentration: 1.05; 95% CI: 0.91, 1.21; P for trend = 0.53) or by stage or grade of disease. However, in men who had fasted (>3 h) at blood collection, the odds ratio for prostate cancer was 1.27 (95% CI: 1.01, 1.60; P for trend = 0.04).
CONCLUSION: Plasma phytanic acid concentration is significantly associated with intake of dairy fat but not with overall risk of prostate cancer in this European population.
PMID: 20427733 [PubMed - indexed for MEDLINE]
7. Malagoli C, Fabbi S, Teggi S, Calzari M, Poli M, Ballotti E, Notari B, Bruni M, Palazzi G, Paolucci P, Vinceti M. Risk of hematological malignancies associated with magnetic fields exposure from power lines: a case-control study in two municipalities of northern Italy. Environ Health. 2010 Mar 30;9:16.
CREAGEN-Environmental, Genetic and Nutritional Epidemiology Research Center, Department of Public Health Sciences, University of Modena and Reggio Emilia, via Campi 287, 41125 Modena, Italy.
Abstract
BACKGROUND: Some epidemiologic studies have suggested an association between electromagnetic field exposure induced by high voltage power lines and childhood leukemia, but null results have also been yielded and the possibility of bias due to unmeasured confounders has been suggested.
METHODS: We studied this relation in the Modena and Reggio Emilia municipalities of northern Italy, identifying the corridors along high voltage power lines with calculated magnetic field intensity in the 0.1-<0.2, 0.2-<0.4, and > or = 0.4 microTesla ranges. We identified 64 cases of newly-diagnosed hematological malignancies in children aged <14 within these municipalities from 1986 to 2007, and we sampled four matched controls for each case, collecting information on historical residence and parental socioeconomic status of these subjects.
RESULTS: Relative risk of leukemia associated with antecedent residence in the area with exposure > or = 0.1 microTesla was 3.2 (6.7 adjusting for socioeconomic status), but this estimate was statistically very unstable, its 95% confidence interval being 0.4-23.4, and no indication of a dose-response relation emerged. Relative risk for acute lymphoblastic leukemia was 5.3 (95% confidence interval 0.7-43.5), while there was no increased risk for the other hematological malignancies.
CONCLUSIONS: Though the number of exposed children in this study was too low to allow firm conclusions, results were more suggestive of an excess risk of leukemia among exposed children than of a null relation.
PMID: 20353586 [PubMed - indexed for MEDLINE]
Abstract
BACKGROUND: Some epidemiologic studies have suggested an association between electromagnetic field exposure induced by high voltage power lines and childhood leukemia, but null results have also been yielded and the possibility of bias due to unmeasured confounders has been suggested.
METHODS: We studied this relation in the Modena and Reggio Emilia municipalities of northern Italy, identifying the corridors along high voltage power lines with calculated magnetic field intensity in the 0.1-<0.2, 0.2-<0.4, and > or = 0.4 microTesla ranges. We identified 64 cases of newly-diagnosed hematological malignancies in children aged <14 within these municipalities from 1986 to 2007, and we sampled four matched controls for each case, collecting information on historical residence and parental socioeconomic status of these subjects.
RESULTS: Relative risk of leukemia associated with antecedent residence in the area with exposure > or = 0.1 microTesla was 3.2 (6.7 adjusting for socioeconomic status), but this estimate was statistically very unstable, its 95% confidence interval being 0.4-23.4, and no indication of a dose-response relation emerged. Relative risk for acute lymphoblastic leukemia was 5.3 (95% confidence interval 0.7-43.5), while there was no increased risk for the other hematological malignancies.
CONCLUSIONS: Though the number of exposed children in this study was too low to allow firm conclusions, results were more suggestive of an excess risk of leukemia among exposed children than of a null relation.
PMID: 20353586 [PubMed - indexed for MEDLINE]
8. Agodi A, Barchitta M, Cipresso R, Marzagalli R, La Rosa N, Caruso M, Castiglione MG, Travali S. Distribution of p53, GST, and MTHFR polymorphisms and risk of cervical intraepithelial lesions in Sicily. Int J Gynecol Cancer. 2010 Jan;20(1):141-6.
Department of Biomedical Sciences, University of Catania, Catania, Italy, Via S. Sofia n. 87, 95123 Catania, Italy. agodia@unict.it
Abstract
OBJECTIVES: Host factors, including genetic polymorphisms, may explain some of the individual differences in cervical cancer occurrence, and susceptibility information may be useful to address effective and specific preventive strategies for different countries. The purpose of the present study was to investigate the role of p53 codon 72, glutathione S-transferase class mu (GSTM1), glutathione S-transferase class theta (GSTT1), and methylenetetrahydrofolate reductase (MTHFR) C677T polymorphisms on the risk for infection and/or of cervical intraepithelial lesions in women attending a colposcopy service in Catania, Sicily, with an already reported high prevalence of human papillomavirus.
METHODS: To identify the association among individual genetic polymorphisms, human papillomavirus infection, and histological findings, a case-control study was designed. Furthermore, to assess the combined effects of these polymorphisms on cervical cancer risk, combined genotype frequencies were compared among case patients and controls.
RESULTS: Women homozygous for the p53 codon 72 Arg genotype were at a 5.6-fold higher risk for developing cervical intraepithelial neoplasia (CIN) 2 or 3 compared with those showing homozygosity for the Pro genotype or heterozygosity for the Pro/Arg genotype. The GSTM1 and GSTT1 null genotypes were overrepresented in infected patients and in women with CIN 2 or 3, although without any significant associations. A decreased risk for CIN of individuals homozygous for the MTHFR T allele was shown.
CONCLUSIONS: After multiple logistic analyses, the presence of the allele 677T of the MTHFR gene was the best explaining protective factor against cervical carcinogenesis, and the allelic distribution in the control group followed the Hardy-Weinberg equilibrium expectations. However, the findings of our study still remain to be confirmed by additional and larger population-based surveys.
PMID: 20130515 [PubMed - indexed for MEDLINE]
Abstract
OBJECTIVES: Host factors, including genetic polymorphisms, may explain some of the individual differences in cervical cancer occurrence, and susceptibility information may be useful to address effective and specific preventive strategies for different countries. The purpose of the present study was to investigate the role of p53 codon 72, glutathione S-transferase class mu (GSTM1), glutathione S-transferase class theta (GSTT1), and methylenetetrahydrofolate reductase (MTHFR) C677T polymorphisms on the risk for infection and/or of cervical intraepithelial lesions in women attending a colposcopy service in Catania, Sicily, with an already reported high prevalence of human papillomavirus.
METHODS: To identify the association among individual genetic polymorphisms, human papillomavirus infection, and histological findings, a case-control study was designed. Furthermore, to assess the combined effects of these polymorphisms on cervical cancer risk, combined genotype frequencies were compared among case patients and controls.
RESULTS: Women homozygous for the p53 codon 72 Arg genotype were at a 5.6-fold higher risk for developing cervical intraepithelial neoplasia (CIN) 2 or 3 compared with those showing homozygosity for the Pro genotype or heterozygosity for the Pro/Arg genotype. The GSTM1 and GSTT1 null genotypes were overrepresented in infected patients and in women with CIN 2 or 3, although without any significant associations. A decreased risk for CIN of individuals homozygous for the MTHFR T allele was shown.
CONCLUSIONS: After multiple logistic analyses, the presence of the allele 677T of the MTHFR gene was the best explaining protective factor against cervical carcinogenesis, and the allelic distribution in the control group followed the Hardy-Weinberg equilibrium expectations. However, the findings of our study still remain to be confirmed by additional and larger population-based surveys.
PMID: 20130515 [PubMed - indexed for MEDLINE]
9. Lumachi F, Frigo AC, Basso U, Tombolan V, Ermani M. Estrogen therapy and risk of breast cancer in postmenopausal women: a case-control study and results of a multivariate analysis. Menopause. 2010 May-Jun;17(3):524-8.
Department of Surgical and Gastroenterological Sciences, School of Medicine, University of Padua, 35128 Padova, Italy. flumachi@unipd
Abstract
OBJECTIVE: Several randomized trials and observational studies show that the use of hormone therapy (HT) increases the risk of breast cancer (BC). The aim of this study was to assess the effects of exposure to both HT and oral contraceptives (OCs) on BC risk in postmenopausal women, all residing in the same metropolitan area.
METHODS: Data regarding a series of 238 consecutive postmenopausal women with infiltrating ductal carcinoma (cases) and 255 randomly selected age-matched healthy women (controls) were reviewed. Odds ratios for no breast-feeding and HT and OC use were 1.82 (95% CI, 1.20-2.77), 2.49 (95% CI, 1.73-3.58), and 2.06 (95% CI 1.14-3.70), respectively.
RESULTS: Four independent variables (years between menarche and menopause, breast-feeding, OC use, and HT use) were included in the final multivariate analysis using logistic regression. The cumulative odds ratio calculated from the observed versus predicted values, obtained using the logistic regression function, was 4.55 (95% CI, 2.13-9.71), whereas the cumulative risk of common exposure to both OCs and HT was 2.77 (95% CI, 1.44-5.32). The logistic model correctly classified 67.5% (95% CI, 63.2-71.5) of cases. The receiver operating characteristic (ROC) curve of the complete logistic function showed a fair area of accuracy (0.77; 95% CI, 0.72-0.81).
CONCLUSIONS: Our results show that the risk of common exposure to both OCs and HT increases in women with other risk factors. However, several parameters traditionally considered in epidemiological studies do not have the same weight in each local community, suggesting the need to create different models to correctly select the high-risk population.
PMID: 20130492 [PubMed - indexed for MEDLINE]
Abstract
OBJECTIVE: Several randomized trials and observational studies show that the use of hormone therapy (HT) increases the risk of breast cancer (BC). The aim of this study was to assess the effects of exposure to both HT and oral contraceptives (OCs) on BC risk in postmenopausal women, all residing in the same metropolitan area.
METHODS: Data regarding a series of 238 consecutive postmenopausal women with infiltrating ductal carcinoma (cases) and 255 randomly selected age-matched healthy women (controls) were reviewed. Odds ratios for no breast-feeding and HT and OC use were 1.82 (95% CI, 1.20-2.77), 2.49 (95% CI, 1.73-3.58), and 2.06 (95% CI 1.14-3.70), respectively.
RESULTS: Four independent variables (years between menarche and menopause, breast-feeding, OC use, and HT use) were included in the final multivariate analysis using logistic regression. The cumulative odds ratio calculated from the observed versus predicted values, obtained using the logistic regression function, was 4.55 (95% CI, 2.13-9.71), whereas the cumulative risk of common exposure to both OCs and HT was 2.77 (95% CI, 1.44-5.32). The logistic model correctly classified 67.5% (95% CI, 63.2-71.5) of cases. The receiver operating characteristic (ROC) curve of the complete logistic function showed a fair area of accuracy (0.77; 95% CI, 0.72-0.81).
CONCLUSIONS: Our results show that the risk of common exposure to both OCs and HT increases in women with other risk factors. However, several parameters traditionally considered in epidemiological studies do not have the same weight in each local community, suggesting the need to create different models to correctly select the high-risk population.
PMID: 20130492 [PubMed - indexed for MEDLINE]
10. Seidler A, Becker N, Nieters A, Arhelger R, Mester B, Rossnagel K, Deeg E, Elsner G, Melis M, Sesler S, Avataneo G, Meloni M, Cocco P. Asbestos exposure and malignant lymphoma: a multicenter case-control study in Germany and Italy. Int Arch Occup Environ Health. 2010 Jun;83(5):563-70. Epub 2009 Dec 25.
Federal Institute of Occupational Safety and Health (BAuA), Nöldnerstr. 40-42, 10317, Berlin, Germany. seidler.andreas@baua.bund.de
Abstract
AIMS : To analyze the relationship between asbestos exposure and malignant lymphoma in a multicenter case-control study conducted in Germany and Italy according to a common core protocol.
METHODS : Male and female patients with malignant lymphoma (n = 1,034) between 18 and 80 years of age were prospectively recruited in six study areas in Germany (Ludwigshafen/Upper Palatinate, Heidelberg/Rhine-Neckar-County, Würzburg/Lower Frankonia, Hamburg, Bielefeld/East Westphalia, and Munich) and in two study areas in Sardinia, Italy (Cagliari and Nuoro provinces). A total of 1,173 population control subjects were drawn from population registers. In a structured personal interview, we elicited a complete occupational history, including every occupational period that lasted at least 1 year. On the basis of job task-specific supplementary questionnaires, trained experts assessed the exposure to asbestos. As a measure of cumulative asbestos exposure on a time by intensity scale, fiber-years were calculated. 12 cases (1.2%) and 12 control subjects (1.0%) had a cumulative asbestos exposure of more than 2.6 fiber-years (highest exposure category according to the 90th percentile of exposed control subjects). Odds ratios (OR) and 95% confidence intervals (CI) were calculated using unconditional logistic regression analysis adjusted for age, sex and study region. Patients with specific lymphoma sub-entities were additionally compared with the entire control group.
RESULTS : We observed no statistically significant association between cumulative asbestos exposure and the risk of any lymphoma subtype. An elevated risk was found for the association between exposure to more than 2.6 fiber-years and multiple myeloma (OR = 6.0; 95% CI 1.4-25.1); however, numbers were small (n = 3 cases, all of them from Italy; n = 12 control subjects).
CONCLUSIONS : Our study does not support an association between asbestos exposure and risk of malignant lymphoma.
PMID: 20035432 [PubMed - indexed for MEDLINE]
Abstract
AIMS : To analyze the relationship between asbestos exposure and malignant lymphoma in a multicenter case-control study conducted in Germany and Italy according to a common core protocol.
METHODS : Male and female patients with malignant lymphoma (n = 1,034) between 18 and 80 years of age were prospectively recruited in six study areas in Germany (Ludwigshafen/Upper Palatinate, Heidelberg/Rhine-Neckar-County, Würzburg/Lower Frankonia, Hamburg, Bielefeld/East Westphalia, and Munich) and in two study areas in Sardinia, Italy (Cagliari and Nuoro provinces). A total of 1,173 population control subjects were drawn from population registers. In a structured personal interview, we elicited a complete occupational history, including every occupational period that lasted at least 1 year. On the basis of job task-specific supplementary questionnaires, trained experts assessed the exposure to asbestos. As a measure of cumulative asbestos exposure on a time by intensity scale, fiber-years were calculated. 12 cases (1.2%) and 12 control subjects (1.0%) had a cumulative asbestos exposure of more than 2.6 fiber-years (highest exposure category according to the 90th percentile of exposed control subjects). Odds ratios (OR) and 95% confidence intervals (CI) were calculated using unconditional logistic regression analysis adjusted for age, sex and study region. Patients with specific lymphoma sub-entities were additionally compared with the entire control group.
RESULTS : We observed no statistically significant association between cumulative asbestos exposure and the risk of any lymphoma subtype. An elevated risk was found for the association between exposure to more than 2.6 fiber-years and multiple myeloma (OR = 6.0; 95% CI 1.4-25.1); however, numbers were small (n = 3 cases, all of them from Italy; n = 12 control subjects).
CONCLUSIONS : Our study does not support an association between asbestos exposure and risk of malignant lymphoma.
PMID: 20035432 [PubMed - indexed for MEDLINE]
11. Galvan A, Falvella FS, Frullanti E, Spinola M, Incarbone M, Nosotti M, Santambrogio L, Conti B, Pastorino U, Gonzalez-Neira A, Dragani TA. Genome-wide association study in discordant sibships identifies multiple inherited susceptibility alleles linked to lung cancer. Carcinogenesis. 2010 Mar;31(3):462-5. Epub 2009 Dec 18.
Fondazione IRCCS, Istituto Nazionale Tumori, 20133 Milan, Italy.
Abstract
We analyzed a series of young (median age = 52 years) non-smoker lung cancer patients and their unaffected siblings as controls, using a genome-wide 620 901 single-nucleotide polymorphism (SNP) array analysis and a case-control DNA pooling approach. We identified 82 putatively associated SNPs that were retested by individual genotyping followed by use of the sib transmission disequilibrium test, pointing to 36 SNPs associated with lung cancer risk in the discordant sibs series. Analysis of these 36 SNPs in a polygenic model characterized by additive and interchangeable effects of rare alleles revealed a highly statistically significant dosage-dependent association between risk allele carrier status and proportion of cancer cases. Replication of the same 36 SNPs in a population-based series confirmed the association with lung cancer for three SNPs, suggesting that phenocopies and genetic heterogeneity can play a major role in the complex genetics of lung cancer risk in the general population.
PMID: 20022890 [PubMed - indexed for MEDLINE]
Abstract
We analyzed a series of young (median age = 52 years) non-smoker lung cancer patients and their unaffected siblings as controls, using a genome-wide 620 901 single-nucleotide polymorphism (SNP) array analysis and a case-control DNA pooling approach. We identified 82 putatively associated SNPs that were retested by individual genotyping followed by use of the sib transmission disequilibrium test, pointing to 36 SNPs associated with lung cancer risk in the discordant sibs series. Analysis of these 36 SNPs in a polygenic model characterized by additive and interchangeable effects of rare alleles revealed a highly statistically significant dosage-dependent association between risk allele carrier status and proportion of cancer cases. Replication of the same 36 SNPs in a population-based series confirmed the association with lung cancer for three SNPs, suggesting that phenocopies and genetic heterogeneity can play a major role in the complex genetics of lung cancer risk in the general population.
PMID: 20022890 [PubMed - indexed for MEDLINE]
12. Bagnardi V, Randi G, Lubin J, Consonni D, Lam TK, Subar AF, Goldstein AM, Wacholder S, Bergen AW, Tucker MA, Decarli A, Caporaso NE, Bertazzi PA, Landi MT. Alcohol consumption and lung cancer risk in the Environment and Genetics in Lung Cancer Etiology (EAGLE) study. Am J Epidemiol. 2010 Jan 1;171(1):36-44. Epub 2009 Nov 22. Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd., EPS 7114, Bethesda, MD 20892-7236, USA.
Abstract
The authors investigated the relation between alcohol consumption and lung cancer risk in the Environment and Genetics in Lung Cancer Etiology (EAGLE) Study, a population-based case-control study. Between 2002 and 2005, 2,100 patients with primary lung cancer were recruited from 13 hospitals within the Lombardy region of Italy and were frequency-matched on sex, area of residence, and age to 2,120 randomly selected controls. Alcohol consumption during adulthood was assessed in 1,855 cases and 2,065 controls. Data on lifetime tobacco smoking, diet, education, and anthropometric measures were collected. Adjusted odds ratios and 95% confidence intervals for categories of mean daily ethanol intake were calculated using unconditional logistic regression. Overall, both nondrinkers (odds ratio = 1.42, 95% confidence interval: 1.03, 2.01) and very heavy drinkers (>/=60 g/day; odds ratio = 1.44, 95% confidence interval: 1.01, 2.07) were at significantly greater risk than very light drinkers (0.1-4.9 g/day). The alcohol effect was modified by smoking behavior, with no excess risk being observed in never smokers. In summary, heavy alcohol consumption was a risk factor for lung cancer among smokers in this study. Although residual confounding by tobacco smoking cannot be ruled out, this finding may reflect interplay between alcohol and smoking, emphasizing the need for preventive measures.
PMID: 19933698 [PubMed - indexed for MEDLINE]
Abstract
The authors investigated the relation between alcohol consumption and lung cancer risk in the Environment and Genetics in Lung Cancer Etiology (EAGLE) Study, a population-based case-control study. Between 2002 and 2005, 2,100 patients with primary lung cancer were recruited from 13 hospitals within the Lombardy region of Italy and were frequency-matched on sex, area of residence, and age to 2,120 randomly selected controls. Alcohol consumption during adulthood was assessed in 1,855 cases and 2,065 controls. Data on lifetime tobacco smoking, diet, education, and anthropometric measures were collected. Adjusted odds ratios and 95% confidence intervals for categories of mean daily ethanol intake were calculated using unconditional logistic regression. Overall, both nondrinkers (odds ratio = 1.42, 95% confidence interval: 1.03, 2.01) and very heavy drinkers (>/=60 g/day; odds ratio = 1.44, 95% confidence interval: 1.01, 2.07) were at significantly greater risk than very light drinkers (0.1-4.9 g/day). The alcohol effect was modified by smoking behavior, with no excess risk being observed in never smokers. In summary, heavy alcohol consumption was a risk factor for lung cancer among smokers in this study. Although residual confounding by tobacco smoking cannot be ruled out, this finding may reflect interplay between alcohol and smoking, emphasizing the need for preventive measures.
PMID: 19933698 [PubMed - indexed for MEDLINE]
13. Deandrea S, Foschi R, Galeone C, La Vecchia C, Negri E, Hu J. Is temperature an effect modifier of the association between green tea intake and gastric cancer risk? Eur J Cancer Prev. 2010 Jan;19(1):18-22.
Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy.
Abstract
We considered the relationship between green tea and gastric cancer risk in Harbin, Heilongjiang province, Northeast China, an area with high baseline risk of stomach cancer. We used data from a case-control study conducted from 1987 to 1989 among 266 incident cases of stomach cancer and 533 controls admitted to the same hospitals as cases, with non-neoplastic and non-gastric diseases. No association emerged when tea consumption alone was considered: the odds ratio (OR) for green tea consumption was 0.87 (95% CI: 0.60-1.25) for green tea intake > or = 750 g/year versus no intake and 0.99 (95% CI: 0.97-1.02) for an increment of 500 g of tea per year. When tea consumption was classified according to the temperature, however, the OR was 0.19 (95% CI: 0.07-0.49) for lukewarm tea intake > or = 750 g/year and 1.27 (95% CI: 0.85-1.90) for hot tea intake (P value for interaction <0.001) as compared with non-drinkers. The corresponding ORs for an increment of 500 g of tea per year were 0.61 (95% CI: 0.45-0.82) and 1.03 (95% CI: 0.99-1.07) for lukewarm and hot tea, respectively (P value for interaction <0.001). We found an inverse relationship between green tea drinking and gastric cancer risk limited to the intake of lukewarm tea.
PMID: 19864955 [PubMed - indexed for MEDLINE]
Abstract
We considered the relationship between green tea and gastric cancer risk in Harbin, Heilongjiang province, Northeast China, an area with high baseline risk of stomach cancer. We used data from a case-control study conducted from 1987 to 1989 among 266 incident cases of stomach cancer and 533 controls admitted to the same hospitals as cases, with non-neoplastic and non-gastric diseases. No association emerged when tea consumption alone was considered: the odds ratio (OR) for green tea consumption was 0.87 (95% CI: 0.60-1.25) for green tea intake > or = 750 g/year versus no intake and 0.99 (95% CI: 0.97-1.02) for an increment of 500 g of tea per year. When tea consumption was classified according to the temperature, however, the OR was 0.19 (95% CI: 0.07-0.49) for lukewarm tea intake > or = 750 g/year and 1.27 (95% CI: 0.85-1.90) for hot tea intake (P value for interaction <0.001) as compared with non-drinkers. The corresponding ORs for an increment of 500 g of tea per year were 0.61 (95% CI: 0.45-0.82) and 1.03 (95% CI: 0.99-1.07) for lukewarm and hot tea, respectively (P value for interaction <0.001). We found an inverse relationship between green tea drinking and gastric cancer risk limited to the intake of lukewarm tea.
PMID: 19864955 [PubMed - indexed for MEDLINE]
14. Lucenteforte E, Talamini R, Bosetti C, Polesel J, Franceschi S, Serraino D, Negri E, La Vecchia C. Macronutrients, fatty acids, cholesterol and pancreatic cancer. Eur J Cancer. 2010 Feb;46(3):581-7. Epub 2009 Oct 21.
Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. ersilia.lucenteforte@marionegri.it
Abstract
A role of diet and nutrition in pancreatic carcinogenesis has been suggested, but the association between selected macronutrients, fatty acids, cholesterol and pancreatic cancer remains controversial. We analysed data from a hospital-based case-control study conducted in Italy between 1991 and 2008, including 326 cases (174 men and 152 women) with incident pancreatic cancer, and 652 controls (348 men and 304 women) frequency-matched to cases by sex, age and study centre. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multiple logistic regression models conditioned on age, sex and study centre, and adjusted for year of interview, education, tobacco smoking, history of diabetes and energy intake. A positive association was found for animal proteins (OR=1.85 for the highest versus the lowest quintile of intake; 95% CI: 1.15-2.96; p for trend=0.039), whereas a negative association was observed for sugars (OR=0.52; 95% CI: 0.31-0.86; p for trend=0.003). Non-significant negative associations emerged for vegetable proteins (OR=0.69) and polyunsaturated fatty acids (OR=0.67). In conclusion, a diet poor in animal proteins and rich in sugars (mainly derived from fruit) appears to have a beneficial effect on pancreatic cancer risk.
PMID: 19850469 [PubMed - indexed for MEDLINE]
Abstract
A role of diet and nutrition in pancreatic carcinogenesis has been suggested, but the association between selected macronutrients, fatty acids, cholesterol and pancreatic cancer remains controversial. We analysed data from a hospital-based case-control study conducted in Italy between 1991 and 2008, including 326 cases (174 men and 152 women) with incident pancreatic cancer, and 652 controls (348 men and 304 women) frequency-matched to cases by sex, age and study centre. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multiple logistic regression models conditioned on age, sex and study centre, and adjusted for year of interview, education, tobacco smoking, history of diabetes and energy intake. A positive association was found for animal proteins (OR=1.85 for the highest versus the lowest quintile of intake; 95% CI: 1.15-2.96; p for trend=0.039), whereas a negative association was observed for sugars (OR=0.52; 95% CI: 0.31-0.86; p for trend=0.003). Non-significant negative associations emerged for vegetable proteins (OR=0.69) and polyunsaturated fatty acids (OR=0.67). In conclusion, a diet poor in animal proteins and rich in sugars (mainly derived from fruit) appears to have a beneficial effect on pancreatic cancer risk.
PMID: 19850469 [PubMed - indexed for MEDLINE]
15. Talamini R, Polesel J, Gallus S, Dal Maso L, Zucchetto A, Negri E, Bosetti C, Lucenteforte E, Boz G, Franceschi S, Serraino D, La Vecchia C. Tobacco smoking, alcohol consumption and pancreatic cancer risk: a case-control study in Italy. Eur J Cancer. 2010 Jan;46(2):370-6. Epub 2009 Sep 24.
SOC Epidemiologia e Biostatistica, Centro di Riferimento Oncologico, IRCCS, Via Franco Gallini, 2, 33081 Aviano, Italy. talaminir@cro.it
Abstract
In Italy, pancreatic cancer accounts for approximately 5% of cancer-related deaths. Tobacco smoking is the major established risk factor for this cancer, whereas the role of alcohol consumption is open to debate. Between 1991 and 2008, we conducted a hospital-based case-control study on pancreatic cancer in northern Italy. Cases were 326 patients (median age 63 years) with incident pancreatic cancer admitted to major general hospitals. Controls were 652 patients (median age 63 years) with acute non-neoplastic conditions admitted to the same hospital network of cases. Multiple logistic regression was used to estimate the odds ratios (OR) and the corresponding 95% confidence intervals (CI). Pancreatic cancer was associated to current smoking (OR=1.68; 95% CI: 1.13-2.48), and the risk rose with increasing number of cigarettes/day (OR=2.04; 95% CI: 1.14-3.66 for > or = 20 cigarettes/day). No association emerged for former smokers (OR=0.98; 95% CI: 0.66-1.45). Alcohol consumption was associated to increased pancreatic cancer risk, but ORs were significant only among heavy drinkers (ORs: 2.03 and 3.42 for 21-34 and > or = 35 drinks/week, respectively). Pancreatic cancer risk was 4.3-fold higher in heavy smokers (> or = 20 cigarettes/day) and heavy drinkers (> or = 21 drinks/week) in comparison with never smokers who drunk < 7 drinks/week, which is compatible with an additive effect of these exposures. In conclusion, we found that tobacco smoking and alcohol drinking are two independent risk factors for pancreatic cancer which may be responsible for approximately one third of these cancers in our population.
PMID: 19782561 [PubMed - indexed for MEDLINE]
Abstract
In Italy, pancreatic cancer accounts for approximately 5% of cancer-related deaths. Tobacco smoking is the major established risk factor for this cancer, whereas the role of alcohol consumption is open to debate. Between 1991 and 2008, we conducted a hospital-based case-control study on pancreatic cancer in northern Italy. Cases were 326 patients (median age 63 years) with incident pancreatic cancer admitted to major general hospitals. Controls were 652 patients (median age 63 years) with acute non-neoplastic conditions admitted to the same hospital network of cases. Multiple logistic regression was used to estimate the odds ratios (OR) and the corresponding 95% confidence intervals (CI). Pancreatic cancer was associated to current smoking (OR=1.68; 95% CI: 1.13-2.48), and the risk rose with increasing number of cigarettes/day (OR=2.04; 95% CI: 1.14-3.66 for > or = 20 cigarettes/day). No association emerged for former smokers (OR=0.98; 95% CI: 0.66-1.45). Alcohol consumption was associated to increased pancreatic cancer risk, but ORs were significant only among heavy drinkers (ORs: 2.03 and 3.42 for 21-34 and > or = 35 drinks/week, respectively). Pancreatic cancer risk was 4.3-fold higher in heavy smokers (> or = 20 cigarettes/day) and heavy drinkers (> or = 21 drinks/week) in comparison with never smokers who drunk < 7 drinks/week, which is compatible with an additive effect of these exposures. In conclusion, we found that tobacco smoking and alcohol drinking are two independent risk factors for pancreatic cancer which may be responsible for approximately one third of these cancers in our population.
PMID: 19782561 [PubMed - indexed for MEDLINE]