Cause di epidemiologia analitica
Ricerca bibliografica periodo dal 16 agosto 2012 al 31 ottobre 2012
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Stringa: ("italy"[MeSH Terms] OR "italy"[All Fields]) AND ("2012/08/16"[PDat] : "2012/10/31"[PDat]) AND (“Case-Control†[All fields] OR “Cohortâ€[all fileds] OR “Cross-sectionalâ€[All fields]) AND ("risk"[All Fields] OR "association"[all fields] OR "epidemiologic factors"[MeSH Terms]) and (“odds ratiosâ€[all fields] OR “odds ratioâ€[all fields] OR “ORsâ€[all fields] OR “rate ratioâ€[all fileds] OR “rate ratiosâ€[all fileds] OR “RRâ€[all fileds] OR “RRs†[all fileds] OR “risk ratioâ€[all fields] OR “risk ratiosâ€[all fields] OR “prevalence ratio*†[all fields] OR “prevalence ratios†[all fields] OR “hazard ratio†[all fields] OR “hazard ratios†[all fields] OR “HRâ€[all fields] OR “HRsâ€[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]
Ricerca focalizzata sul tema dei “tumoriâ€: [ AND ("neoplasms"[Mesh] OR (neoplasm*[ti/ab]) OR tumor*[ti/ab] OR cancer*[ti/ab])]
1. Piselli P, Serraino D, Segoloni GP, Sandrini S, Piredda GB, Scolari MP, Rigotti P, Busnach G, Messa P, Donati D, Schena FP, Maresca MC, Tisone G, Veroux M, Sparacino V, Pisani F, Citterio F; The Immunosuppression and Cancer Study Group. Risk of de novo cancers after transplantation: Results from a cohort of 7217 kidney transplant recipients, Italy 1997-2009. Eur J Cancer. 2012 Oct 10. pii: S0959-8049(12)00727-7. doi: 10.1016/j.ejca.2012.09.013. [Epub ahead of print]
Department of Epidemiology, INMI "L. Spallanzani", Rome, Italy. Electronic address: pierluca.piselli@inmi.it.
Abstract
To assess incidence and risk factors for de novo cancers (DNCs) after kidney transplant (KT), we carried out a cohort investigation in 15 Italian KT centres. Seven thousand two-hundred seventeen KT recipients (64.2% men), transplanted between 1997 and 2007 and followed-up until 2009, represented the study group. Person years (PY) were computed from 30days after transplant to cancer diagnosis, death, return to dialysis or to study closure. The number of observed DNCs was compared to that expected in the general population of Italy through standardised incidence ratios (SIR) and 95% confidence intervals (CI). To identify risk factors, incidence rate ratios (IRR) were computed. Three-hundred ninety five DNCs were diagnosed during 39.598PYs, with Kaposi's sarcoma (KS), post-transplant lymphoproliferative disorders (PTLD), particularly non-Hodgkin' lymphoma (NHL), lung, kidney and prostate as the most common types. The overall IR was 9.98/1.000PY, with a 1.7-fold augmented SIR (95% CI: 1.6-1.9). SIRs were particularly elevated for KS (135), lip (9.4), kidney carcinoma (4.9), NHL (4.5) and mesothelioma (4.2). KT recipients born in Southern Italy were at reduced risk of kidney cancer and solid tumors, though at a higher KS risk, than those born in Northern Italy. Use of mTOR inhibitors (mTORi) exerted, for all cancers combined, a 46% significantly reduced risk (95% CI: 0.4-0.7). Our study findings confirmed, in Italy, the increased risks for cancer following KT, and they also suggested a possible protective effect of mTORi in reducing the frequency of post transplant cancers.
Abstract
To assess incidence and risk factors for de novo cancers (DNCs) after kidney transplant (KT), we carried out a cohort investigation in 15 Italian KT centres. Seven thousand two-hundred seventeen KT recipients (64.2% men), transplanted between 1997 and 2007 and followed-up until 2009, represented the study group. Person years (PY) were computed from 30days after transplant to cancer diagnosis, death, return to dialysis or to study closure. The number of observed DNCs was compared to that expected in the general population of Italy through standardised incidence ratios (SIR) and 95% confidence intervals (CI). To identify risk factors, incidence rate ratios (IRR) were computed. Three-hundred ninety five DNCs were diagnosed during 39.598PYs, with Kaposi's sarcoma (KS), post-transplant lymphoproliferative disorders (PTLD), particularly non-Hodgkin' lymphoma (NHL), lung, kidney and prostate as the most common types. The overall IR was 9.98/1.000PY, with a 1.7-fold augmented SIR (95% CI: 1.6-1.9). SIRs were particularly elevated for KS (135), lip (9.4), kidney carcinoma (4.9), NHL (4.5) and mesothelioma (4.2). KT recipients born in Southern Italy were at reduced risk of kidney cancer and solid tumors, though at a higher KS risk, than those born in Northern Italy. Use of mTOR inhibitors (mTORi) exerted, for all cancers combined, a 46% significantly reduced risk (95% CI: 0.4-0.7). Our study findings confirmed, in Italy, the increased risks for cancer following KT, and they also suggested a possible protective effect of mTORi in reducing the frequency of post transplant cancers.
Commento a cura di Lorenzo Richiardi: Questo studio valuta l’incidenza ed iI rischio di tumori in più di 7000 pazienti sottoposti a trapianto di rene in diversi centri-trapianto italiani. Si inserisce nel contesto di una letteratura consistente a livello internazionale che indica un aumento di diverse forme tumorali in pazienti immunosoppressi. Lo studio trova incidenze aumentate per il sarcoma di kaposi, il linfoma non-Hodgkin, il tumore del labbro, il tumore della prostata, il tumore del testicolo, il tumore del rene ed il mesotelioma. Un eccesso di rischio in molte di queste sedi tumorali era atteso per i risultati in studi precedenti e per la loro associazione con virus. Per altre sedi, come il mesotelioma o il tumore del testicolo, i dati sono meno consistenti. Bisogna comunque considerare che non erano presenti informazioni su fattori di rischio (ad esempio occupazionali) al momento del trapianto.
2. Pradelli D, Soranna D, Scotti L, Zambon A, Catapano A, Mancia G, La Vecchia C, Corrao G. Statins and primary liver cancer: a meta-analysis of observational studies. Eur J Cancer Prev. 2012 Sep 22. [Epub ahead of print]
Department of Statistics, Units of Biostatistics and Epidemiology bDepartments of Pharmacological Sciences cClinical Medicine and Prevention, University of Milano-Bicocca dClinical Sciences and Public Health, University of Milano eDepartment of Epidemiology, Institute for Pharmacological Research Mario Negri, Milan, Italy.
Abstract
Statins are among the most commonly prescribed drugs used to manage dyslipidemia. Hepatocellular carcinoma is the third leading cause of cancer mortality and its rates have recently been increasing in central and northern Europe and USA. To quantify the association between statin use and risk for HCC, we performed a meta-analysis of published studies. We conducted a MEDLINE search for observational studies reporting the association between exposure to statins and risk for incident liver cancer until March 2012. Fixed-effect and random-effect models were used to estimate summary relative risks (RR) and the corresponding 95% confidence intervals (CIs). Moreover, between-study heterogeneity and publication bias were assessed using adequate statistical tests. Five observational studies (two case-control and three cohort studies) based on 2574 cases of HCC were included. Statin treatment, compared with no treatment, was inversely related to HCC (summary RR=0.58; 95% CI 0.46-0.74). Between-study heterogeneity was significant (P<0.001) and numerically relevant (I=65%). When only longest statin use was considered, the RR was 0.66 (95% CI 0.55-0.80). Influence analysis on the overall estimate showed that heterogeneity was largely because of one study; when omitting it, the I dropped to 27% (P=0.240), whereas the summary RR was only marginally modified (RR=0.52; 95% CI 0.44-0.62). There was no evidence of publication bias. This meta-analysis suggests a favorable effect of statins on HCC, in the absence, however, of a duration-risk relationship.
Abstract
Statins are among the most commonly prescribed drugs used to manage dyslipidemia. Hepatocellular carcinoma is the third leading cause of cancer mortality and its rates have recently been increasing in central and northern Europe and USA. To quantify the association between statin use and risk for HCC, we performed a meta-analysis of published studies. We conducted a MEDLINE search for observational studies reporting the association between exposure to statins and risk for incident liver cancer until March 2012. Fixed-effect and random-effect models were used to estimate summary relative risks (RR) and the corresponding 95% confidence intervals (CIs). Moreover, between-study heterogeneity and publication bias were assessed using adequate statistical tests. Five observational studies (two case-control and three cohort studies) based on 2574 cases of HCC were included. Statin treatment, compared with no treatment, was inversely related to HCC (summary RR=0.58; 95% CI 0.46-0.74). Between-study heterogeneity was significant (P<0.001) and numerically relevant (I=65%). When only longest statin use was considered, the RR was 0.66 (95% CI 0.55-0.80). Influence analysis on the overall estimate showed that heterogeneity was largely because of one study; when omitting it, the I dropped to 27% (P=0.240), whereas the summary RR was only marginally modified (RR=0.52; 95% CI 0.44-0.62). There was no evidence of publication bias. This meta-analysis suggests a favorable effect of statins on HCC, in the absence, however, of a duration-risk relationship.
3. Turati F, Garavello W, Tramacere I, Pelucchi C, Galeone C, Bagnardi V, Corrao G, Islami F, Fedirko V, Boffetta P, La Vecchia C, Negri E. A Meta-analysis of Alcohol Drinking and Oral and Pharyngeal Cancers: Results from Subgroup Analyses. Alcohol Alcohol. 2012 Sep 4. [Epub ahead of print]
Istituto di Ricerche Farmacologiche 'Mario Negri', Via Giuseppe La Masa 19, 20156 Milan, Italy.
Abstract
AIMS: To quantify the magnitude of the association between alcohol and oral and pharyngeal cancer (OPC) by sex, smoking habits, type of alcoholic beverage and other factors.
METHODS: We combined findings from all case-control and cohort studies published until September 2010 and present in this article the results classified by these factors, using a meta-analytic approach. Summary relative risks (RRs) were obtained using random-effects models; heterogeneity was assessed using the χ(2) test.
RESULTS: The association between alcohol and OPC risk was similar in men and women, with similar dose-response relationships. No notable differences were found with respect to geographic area and other factors, both for drinking overall and heavy (≥4 drinks/day) drinking. Among never/non-current smokers, the pooled RRs were 1.32 (95% confidence interval, CI, 1.05-1.67) for drinking, and 2.54 (95% CI, 1.80-3.58) for heavy drinking. The corresponding RRs in smokers were 2.92 (95% CI, 2.31-3.70) and 6.32 (95% CI, 5.05-7.90). The pooled RRs for any drinking irrespective of smoking were 2.12 (95% CI, 1.37-3.29) for wine-, 2.43 (95% CI, 1.92-3.07) for beer- and 2.30 (95% CI, 1.78-2.98) for spirits-only drinking. The corresponding RRs for heavy drinking were 4.92 (95% CI, 2.80-8.65), 4.20 (95% CI, 1.43-12.38) and 5.20 (95% CI, 2.77-9.78).
CONCLUSION: The alcohol-related RRs are similar with respect to sex, geographic area and type of alcoholic beverage. The association between alcohol and OPC is stronger in smokers than in non-smokers.
Abstract
AIMS: To quantify the magnitude of the association between alcohol and oral and pharyngeal cancer (OPC) by sex, smoking habits, type of alcoholic beverage and other factors.
METHODS: We combined findings from all case-control and cohort studies published until September 2010 and present in this article the results classified by these factors, using a meta-analytic approach. Summary relative risks (RRs) were obtained using random-effects models; heterogeneity was assessed using the χ(2) test.
RESULTS: The association between alcohol and OPC risk was similar in men and women, with similar dose-response relationships. No notable differences were found with respect to geographic area and other factors, both for drinking overall and heavy (≥4 drinks/day) drinking. Among never/non-current smokers, the pooled RRs were 1.32 (95% confidence interval, CI, 1.05-1.67) for drinking, and 2.54 (95% CI, 1.80-3.58) for heavy drinking. The corresponding RRs in smokers were 2.92 (95% CI, 2.31-3.70) and 6.32 (95% CI, 5.05-7.90). The pooled RRs for any drinking irrespective of smoking were 2.12 (95% CI, 1.37-3.29) for wine-, 2.43 (95% CI, 1.92-3.07) for beer- and 2.30 (95% CI, 1.78-2.98) for spirits-only drinking. The corresponding RRs for heavy drinking were 4.92 (95% CI, 2.80-8.65), 4.20 (95% CI, 1.43-12.38) and 5.20 (95% CI, 2.77-9.78).
CONCLUSION: The alcohol-related RRs are similar with respect to sex, geographic area and type of alcoholic beverage. The association between alcohol and OPC is stronger in smokers than in non-smokers.
4. Aleksandrova K, Boeing H, Jenab M, Bueno-de-Mesquita HB, Jansen E, van Duijnhoven FJ, Rinaldi S, Fedirko V, Romieu I, Riboli E, Gunter MJ, Westphal S, Overvad K, Tjønneland A, Halkjær J, Racine A, Boutron-Ruault MC, Clavel-Chapelon F, Kaaks R, Lukanova A, Trichopoulou A, Lagiou P, Trichopoulos D, Mattiello A, Pala V, Palli D, Tumino R, Vineis P, Buckland G, Sánchez MJ, Amiano P, Huerta JM, Barricarte A, Menéndez V, Peeters PH, Söderberg S, Palmqvist R, Allen NE, Crowe FL, Khaw KT, Wareham N, Pischon T. Leptin and Soluble Leptin Receptor in Risk of Colorectal Cancer in the European Prospective Investigation into Cancer and Nutrition Cohort. Cancer Res. 2012 Oct 15;72(20):5328-5337. Epub 2012 Aug 27.
Authors' Affiliations: Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany; International Agency for Research on Cancer, Lyon, France; National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands; Department of Gastroenterology and Hepatology, University Medical Center, Utrecht, The Netherlands; Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, the Netherlands; Division of Human Nutrition, Wageningen University, Wageningen, the Netherlands; Division of Epidemiology, Public Health and Primary Care, Imperial College, London, United Kingdom; Institute of Clinical Chemistry, Otto-von-Guericke-University Magdeburg, Magdeburg, Germany; Department of Epidemiology, School of Public Health, Aarhus University, Aarhus, Denmark; Diet, Genes and Environment Danish Cancer Society Research Center, Copenhagen, Denmark; Inserm, Centre for Research in Epidemiology and Population Health, Institut Gustave Roussy, and Paris South University, UMRS, Villejuif, France; Division of Cancer Epidemiology, German Cancer Research Centre, Heidelberg, Germany; WHO Collaborating Center for Food and Nutrition Policies, Department of Hygiene, Epidemiology and Medical Statistics, University of Athens Medical School, Athens, Greece; Hellenic Health Foundation; Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA; Department of Clinical and Experimental Medicine-Federico II University, Naples, Italy; Nutritional Epidemiology Unit, Fondazione IRCCS Istituto Nazionale Tumori, Milano, Italy; Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute-ISPO, Florence, Italy; Cancer Registry and Histopathology Unit, "M.P. Arezzo" Hospital, Ragusa, Italy; HuGeF Foundation, Turin, Italy; Unit of Nutrition, Environment and Cancer, Cancer Epidemiology Research Programme, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain; Andalusian School of Public Health, Granada, Spain; Consortium for Biomedical Research in Epidemiology and Public Health (CIBER EpidemiologÃa y Salud Pública-CIBERESP), Spain; Public Health Division of Gipuzkoa, BIODonostia Research Institute, Department of Health of the regional Government of the Basque Country, San Sebastian, Spain; Department of Epidemiology, Murcia Regional Health Authority, Murcia, Spain; Navarre Public Health Institute, Pamplona, Spain; Public Health Directorate, Asturias, Spain; Department of Pubic Health and Clinical Medicine, Cardiology, UmeÃ¥ University, UmeÃ¥, Sweden, Department of Medical Biosciences, Pathology, UmeÃ¥ University, UmeÃ¥, Sweden; Cancer Epidemiology Unit, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom; Medical Research Council UK and Cancer Research UK, United Kingdom; and Molecular Epidemiology Group, Max Delbrueck Center for Molecular Medicine (MDC), Berlin-Buch, Germany.
Abstract
Leptin, a peptide hormone produced primarily by the adipocytes, is hypothesized to play a role in the pathogenesis of colorectal cancer (CRC). Soluble leptin receptor (sOB-R) may regulate leptin's physiologic functions; however its relation to CRC risk is unknown. This study explored the association of leptin and sOB-R with risk of CRC in a prospective nested case-control study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. A total of 1,129 incident CRC cases (713 colon, 416 rectal) were matched within risk sets to 1,129 controls. Conditional logistic regression was used to calculate relative risks (RR) and 95% confidence intervals (CI). After multivariable adjustment including body mass index (BMI), waist circumference, and baseline leptin concentrations, sOB-R was strongly inversely associated with CRC (RR comparing the highest quintile vs. the lowest, 0.55; 95% CI, 0.40-0.76; P(trend) = 0.0004) and colon cancer (RR, 0.42; 95% CI, 0.28-0.63, P(trend) = 0.0001); whereas no association was seen for rectal cancer (RR adjusted for BMI and waist circumference, 0.83; 95% CI, 0.48-1.44, P(trend) = 0.38). In contrast, leptin was not associated with risk of CRC (RR adjusted for BMI and waist circumference, 0.85; 95% CI, 0.56-1.29, P(trend) = 0.23). Additional adjustments for circulating metabolic biomarkers did not attenuate these results. These novel findings suggest a strong inverse association between circulating sOB-R and CRC risk, independent of obesity measures, leptin concentrations, and other metabolic biomarkers. Further research is needed to confirm the potentially important role of sOB-R in CRC pathogenesis. Cancer Res; 72(20); 5328-37.
Abstract
Leptin, a peptide hormone produced primarily by the adipocytes, is hypothesized to play a role in the pathogenesis of colorectal cancer (CRC). Soluble leptin receptor (sOB-R) may regulate leptin's physiologic functions; however its relation to CRC risk is unknown. This study explored the association of leptin and sOB-R with risk of CRC in a prospective nested case-control study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. A total of 1,129 incident CRC cases (713 colon, 416 rectal) were matched within risk sets to 1,129 controls. Conditional logistic regression was used to calculate relative risks (RR) and 95% confidence intervals (CI). After multivariable adjustment including body mass index (BMI), waist circumference, and baseline leptin concentrations, sOB-R was strongly inversely associated with CRC (RR comparing the highest quintile vs. the lowest, 0.55; 95% CI, 0.40-0.76; P(trend) = 0.0004) and colon cancer (RR, 0.42; 95% CI, 0.28-0.63, P(trend) = 0.0001); whereas no association was seen for rectal cancer (RR adjusted for BMI and waist circumference, 0.83; 95% CI, 0.48-1.44, P(trend) = 0.38). In contrast, leptin was not associated with risk of CRC (RR adjusted for BMI and waist circumference, 0.85; 95% CI, 0.56-1.29, P(trend) = 0.23). Additional adjustments for circulating metabolic biomarkers did not attenuate these results. These novel findings suggest a strong inverse association between circulating sOB-R and CRC risk, independent of obesity measures, leptin concentrations, and other metabolic biomarkers. Further research is needed to confirm the potentially important role of sOB-R in CRC pathogenesis. Cancer Res; 72(20); 5328-37.
5. Tavani A, Malerba S, Pelucchi C, Dal Maso L, Zucchetto A, Serraino D, Levi F, Montella M, Franceschi S, Zambon A, La Vecchia C. Dietary folates and cancer risk in a network of case-control studies. Ann Oncol. 2012 Oct;23(10):2737-42. Epub 2012 Aug 16.
Department of Epidemiology, Istituto di Ricerche Farmacologiche 'Mario Negri', Milan.
Abstract
Background. Folate deficiency leads to DNA damage and inadequate repair, caused by a decreased synthesis of thymidylate and purines. We analyzed the relationship between dietary folate intake and the risk of several cancers.
Patients and Methods. The study is based on a network of case-control studies conducted in Italy and Switzerland in 1991-2009. The odds ratios (ORs) for dietary folate intake were estimated by multiple logistic regression models, adjusted for major identified confounding factors.
Results. For a few cancer sites, we found a significant inverse relation, with ORs for an increment of 100 μg/day of dietary folate of 0.65 for oropharyngeal (1467 cases), 0.58 for esophageal (505 cases), 0.83 for colorectal (2390 cases), 0.72 for pancreatic (326 cases), 0.67 for laryngeal (851 cases) and 0.87 for breast (3034 cases) cancers. The risk estimates were below unity, although not significantly, for cancers of the endometrium (OR = 0.87, 454 cases), ovary (OR = 0.86, 1031 cases), prostate (OR = 0.91, 1468 cases) and kidney (OR = 0.88, 767 cases), and was 1.00 for stomach cancer (230 cases). No material heterogeneity was found in strata of sex, age, smoking and alcohol drinking.
Conclusions. Our data support a real inverse association of dietary folate intake with the risk of several common cancers.
Abstract
Background. Folate deficiency leads to DNA damage and inadequate repair, caused by a decreased synthesis of thymidylate and purines. We analyzed the relationship between dietary folate intake and the risk of several cancers.
Patients and Methods. The study is based on a network of case-control studies conducted in Italy and Switzerland in 1991-2009. The odds ratios (ORs) for dietary folate intake were estimated by multiple logistic regression models, adjusted for major identified confounding factors.
Results. For a few cancer sites, we found a significant inverse relation, with ORs for an increment of 100 μg/day of dietary folate of 0.65 for oropharyngeal (1467 cases), 0.58 for esophageal (505 cases), 0.83 for colorectal (2390 cases), 0.72 for pancreatic (326 cases), 0.67 for laryngeal (851 cases) and 0.87 for breast (3034 cases) cancers. The risk estimates were below unity, although not significantly, for cancers of the endometrium (OR = 0.87, 454 cases), ovary (OR = 0.86, 1031 cases), prostate (OR = 0.91, 1468 cases) and kidney (OR = 0.88, 767 cases), and was 1.00 for stomach cancer (230 cases). No material heterogeneity was found in strata of sex, age, smoking and alcohol drinking.
Conclusions. Our data support a real inverse association of dietary folate intake with the risk of several common cancers.
6. Landi D, Gemignani F, Pardini B, Naccarati A, Garritano S, Vodicka P, Vodickova L, Canzian F, Novotny J, Barale R, Landi S. Identification of candidate genes carrying polymorphisms associated with the risk of colorectal cancer by analyzing the colorectal mutome and microRNAome. Cancer. 2012 Oct 1;118(19):4670-80. doi: 10.1002/cncr.27435. Epub 2012 Jan 26.
Department of Biology, University of Pisa, Pisa, Italy.
Abstract
BACKGROUND: The presence of single-nucleotide polymorphisms (SNPs) within the 3'-untranslated regions of genes could affect the binding between a microRNA (miRNA) and its target, with consequences on gene expression regulation. Considering the important role of miRNAs in carcinogenesis, it is hypothesized here that these SNPs could also affect the individual risk of colorectal cancer (CRC).
METHODS: To test this hypothesis, a list was developed of 140 somatically mutated genes deduced from previous works on the mutome of the CRC. A further selection was conducted of SNPs within target sites for miRNAs that are expressed only in the colorectum (the colorectal microRNAome) and having adequate population frequencies. This yielded 12 SNPs that were genotyped in a case-control association study on 717 colorectal cases and 1171 controls from the Czech Republic.
RESULTS: Statistically significant associations were found between the risk of CRC and the variant alleles of KIAA0182 (rs709805) (odds ratio = 1.57; 95% confidence interval = 1.06-2.78, for the variant homozygotes) and NUP210 genes (rs354476) (odds ratio = 1.36; 95% confidence interval = 1.02-1.82, for the variant homozygotes).
CONCLUSIONS: The results support the study hypothesis and highlight the importance of SNPs within miRNA-dependent regulatory regions. Further studies on the role exerted by NUP210 and KIAA0182 in colorectal carcinogenesis are warranted. Cancer 2012. © 2012 American Cancer Society.
Abstract
BACKGROUND: The presence of single-nucleotide polymorphisms (SNPs) within the 3'-untranslated regions of genes could affect the binding between a microRNA (miRNA) and its target, with consequences on gene expression regulation. Considering the important role of miRNAs in carcinogenesis, it is hypothesized here that these SNPs could also affect the individual risk of colorectal cancer (CRC).
METHODS: To test this hypothesis, a list was developed of 140 somatically mutated genes deduced from previous works on the mutome of the CRC. A further selection was conducted of SNPs within target sites for miRNAs that are expressed only in the colorectum (the colorectal microRNAome) and having adequate population frequencies. This yielded 12 SNPs that were genotyped in a case-control association study on 717 colorectal cases and 1171 controls from the Czech Republic.
RESULTS: Statistically significant associations were found between the risk of CRC and the variant alleles of KIAA0182 (rs709805) (odds ratio = 1.57; 95% confidence interval = 1.06-2.78, for the variant homozygotes) and NUP210 genes (rs354476) (odds ratio = 1.36; 95% confidence interval = 1.02-1.82, for the variant homozygotes).
CONCLUSIONS: The results support the study hypothesis and highlight the importance of SNPs within miRNA-dependent regulatory regions. Further studies on the role exerted by NUP210 and KIAA0182 in colorectal carcinogenesis are warranted. Cancer 2012. © 2012 American Cancer Society.