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2. Diabetes, antidiabetic medications, and pancreatic cancer risk: an analysis from the International Pancreatic Cancer Case-Control Consortium

Author

Bosetti, C., Rosato, V., Li, D., Silverman, D., Petersen, G.M., Bracci, P.M., Neale, R.E., Muscat, J., Anderson, K., Gallinger, S., Olson, S.H., Miller, A.B., Bas Bueno-de-Mesquita, H., Scelo, G., Janout, V., Holcatova, I., Lagiou, P., Serraino, D., Lucenteforte, E., Fabianova, E., Baghurst, P.A., Zatonski, W., Foretova, L., Fontham, E., Bamlet, W.R., Holly, E.A., Negri, E., Hassan, M., Prizment, A., Cotterchio, M., Cleary, S., Kurtz, R.C., Maisonneuve, P., Trichopoulos, D., Polesel, J., Duell, E.J., Boffetta, P., La Vecchia, C., and Ghadirian, P.

Published
2014
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3. Cigarette smoking and pancreatic cancer: an analysis from the International Pancreatic Cancer Case-Control Consortium (Panc4)

Author

Bosetti, C., Lucenteforte, E., Silverman, D.T., Petersen, G., Bracci, P.M., Ji, B.T., Negri, E., Li, D., Risch, H.A., Olson, S.H., Gallinger, S., Miller, A.B., Bueno-de-Mesquita, H.B., Talamini, R., Polesel, J., Ghadirian, P., Baghurst, P.A., Zatonski, W., Fontham, E., Bamlet, W.R., Holly, E.A., Bertuccio, P., Gao, Y.T., Hassan, M., Yu, H., Kurtz, R.C., Cotterchio, M., Su, J., Maisonneuve, P., Duell, E.J., Boffetta, P., and La Vecchia, C.

Published
2012
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4. Cigar and pipe smoking, smokeless tobacco use and pancreatic cancer: an analysis from the International Pancreatic Cancer Case-Control Consortium (PanC4)

Author

Bertuccio, P., La Vecchia, C., Silverman, D.T., Petersen, G.M., Bracci, P.M., Negri, E., Li, D., Risch, H.A., Olson, S.H., Gallinger, S., Miller, A.B., Bueno-de-Mesquita, H.B., Talamini, R., Polesel, J., Ghadirian, P., Baghurst, P.A., Zatonski, W., Fontham, E.T., Bamlet, W.R., Holly, E.A., Lucenteforte, E., Hassan, M., Yu, H., Kurtz, R.C., Cotterchio, M., Su, J., Maisonneuve, P., Duell, E.J., Bosetti, C., and Boffetta, P.

Published
2011
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5. Mendelian randomization analysis of n-6 polyunsaturated fatty acid levels and pancreatic cancer risk.

Author

Ghoneim D.H., Zhu J., Zheng W., Long J., Murff H.J., Ye F., Setiawan V.W., Wilkens L.R., Khankari N.K., Haycock P., Antwi S.O., Yang Y., Arslan A.A., Freeman L.E.B., Bracci P.M., Canzian F., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Marchand L.L., Neale R.E., Scelo G., Visvanathan K., White E., Albane D., Amiano P., Andreott G., Babic A., Bamlet W.R., Berndt S.I., Brais L.K., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Rabe K.G., Chanock S.J., Duggal P., Fuchs C.S., Gaziano J.M., Goggins M.G., Hackert T., Hassan M.M., Helzlsouer K.J., Holly E.A., Hoover R.N., Katske V., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Oberg A.L., Porta M., Rothman N., Sesso H.D., Silverman D.T., Ian T., Wactawski-Wende J., Wang X., Wentzensen N., Yu H., Zeleniuch-Jacquotte A., Yu K., Wolpin B.M., Jacobs E.J., Duell E.J., Risch H.A., Petersen G.M., Amundadottir L.T., Kraft P., Klein A.P., Stolzenberg-Solomon R.Z., Shu X.-O., Wu L., Ghoneim D.H., Zhu J., Zheng W., Long J., Murff H.J., Ye F., Setiawan V.W., Wilkens L.R., Khankari N.K., Haycock P., Antwi S.O., Yang Y., Arslan A.A., Freeman L.E.B., Bracci P.M., Canzian F., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Marchand L.L., Neale R.E., Scelo G., Visvanathan K., White E., Albane D., Amiano P., Andreott G., Babic A., Bamlet W.R., Berndt S.I., Brais L.K., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Rabe K.G., Chanock S.J., Duggal P., Fuchs C.S., Gaziano J.M., Goggins M.G., Hackert T., Hassan M.M., Helzlsouer K.J., Holly E.A., Hoover R.N., Katske V., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Oberg A.L., Porta M., Rothman N., Sesso H.D., Silverman D.T., Ian T., Wactawski-Wende J., Wang X., Wentzensen N., Yu H., Zeleniuch-Jacquotte A., Yu K., Wolpin B.M., Jacobs E.J., Duell E.J., Risch H.A., Petersen G.M., Amundadottir L.T., Kraft P., Klein A.P., Stolzenberg-Solomon R.Z., Shu X.-O., and Wu L.

Abstract

Background: Whether circulating polyunsaturated fatty acid (PUFA) levels are associated with pancreatic cancer risk is uncertain. Mendelian randomization (MR) represents a study design using genetic instruments to better characterize the relationship between exposure and outcome. Method(s): We utilized data from genome-wide association studies within the Pancreatic Cancer Cohort Consortium and Pancreatic Cancer Case-Control Consortium, involving approximately 9,269 cases and 12,530 controls of European descent, to evaluate associations between pancreatic cancer risk and genetically predicted plasma n-6 PUFA levels. Conventional MR analyses were performed using individual-level and summary-level data. Result(s): Using genetic instruments, we did not find evidence of associations between genetically predicted plasma n-6 PUFA levels and pancreatic cancer risk [estimates per one SD increase in each PUFA-specific weighted genetic score using summary statistics: Linoleic acid odds ratio (OR)1.00, 95% confidence interval (CI) 0.98-1.02; arachidonic acid OR 1.00, 95% CI 0.99-1.01; and dihomo-gamma-linolenic acid OR 0.95, 95% CI 0.87-1.02]. The OR estimates remained virtually unchanged after adjustment for covariates, using individual-level data or summary statistics, or stratification by age and sex. Conclusion(s): Our results suggest that variations of genetically determined plasma n-6 PUFA levels are not associated with pancreatic cancer risk. Impact: These results suggest that modifying n-6 PUFA levels through food sources or supplementation may not influence risk of pancreatic cancer.Copyright © 2020 American Association for Cancer Research Inc.. All rights reserved.

Published
2021

6. Genome-wide genediabetes and geneobesity interaction scan in 8,255 cases and 11,900 controls from panscan and PanC4 consortia.

Author

Campa D., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Blackford A., Bueno-De-Mesquita B., Buring J.E., Chanock S.J., Childs E., Duell E.J., Fuchs C., Michael Gaziano J., Goggins M., Hartge P., Hassam M.H., Holly E.A., Hoover R.N., Hung R.J., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Ng K., Oberg A.L., Orlow I., Peters U., Porta M., Rabe K.G., Rothman N., Scelo G., Sesso H.D., Silverman D.T., Thompson I.M., Tjonneland A., Trichopoulou A., Wactawski-Wende J., Wentzensen N., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Amundadottir L.T., Jacobs E.J., Petersen G.M., Wolpin B.M., Risch H.A., Chatterjee N., Klein A.P., Li D., Kraft P., Wei P., Tang H., Jiang L., Stolzenberg-Solomon R.Z., Arslan A.A., Beane Freeman L.E., Bracci P.M., Brennan P., Canzian F., Du M., Gallinger S., Giles G.G., Campa D., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Blackford A., Bueno-De-Mesquita B., Buring J.E., Chanock S.J., Childs E., Duell E.J., Fuchs C., Michael Gaziano J., Goggins M., Hartge P., Hassam M.H., Holly E.A., Hoover R.N., Hung R.J., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Ng K., Oberg A.L., Orlow I., Peters U., Porta M., Rabe K.G., Rothman N., Scelo G., Sesso H.D., Silverman D.T., Thompson I.M., Tjonneland A., Trichopoulou A., Wactawski-Wende J., Wentzensen N., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Amundadottir L.T., Jacobs E.J., Petersen G.M., Wolpin B.M., Risch H.A., Chatterjee N., Klein A.P., Li D., Kraft P., Wei P., Tang H., Jiang L., Stolzenberg-Solomon R.Z., Arslan A.A., Beane Freeman L.E., Bracci P.M., Brennan P., Canzian F., Du M., Gallinger S., and Giles G.G.

Abstract

Background: Obesity and diabetes are major modifiable risk factors for pancreatic cancer. Interactions between genetic variants and diabetes/obesity have not previously been comprehensively investigated in pancreatic cancer at the genome-wide level. Method(s): We conducted a gene-environment interaction (GxE) analysis including 8,255 cases and 11,900 controls from four pancreatic cancer genome-wide association study (GWAS) datasets (Pancreatic Cancer Cohort Consortium I-III and Pancreatic Cancer Case Control Consortium). Obesity (body mass index >=30 kg/m2) and diabetes (duration >=3 years) were the environmental variables of interest. Approximately 870,000 SNPs (minor allele frequency >=0.005, genotyped in at least one dataset) were analyzed. Case-control (CC), case-only (CO), and joint-effect test methods were used for SNP-level GxE analysis. As a complementary approach, gene-based GxE analysis was also performed. Age, sex, study site, and principal components accounting for population substructure were included as covariates. Meta-analysis was applied to combine individual GWAS summary statistics. Result(s): No genome-wide significant interactions (departures from a log-additive odds model) with diabetes or obesity were detected at the SNP level by the CC or CO approaches. The joint-effect test detected numerous genome-wide significant GxE signals in the GWAS main effects top hit regions, but the significance diminished after adjusting for the GWAS top hits. In the gene-based analysis, a significant interaction of diabetes with variants in the FAM63A (family with sequence similarity 63 member A) gene (significance threshold P < 1.25 106) was observed in the meta-analysis (PGxE 1/4 1.2 106, PJoint 1/4 4.2 107). Conclusion(s): This analysis did not find significant GxE interactions at the SNP level but found one significant interaction with diabetes at the gene level. A larger sample size might unveil additional genetic factors via GxE scans. Impact: This study may

Published
2021

7. Smoking modifies pancreatic cancer risk loci on 2q21.3.

Author

Mocci E., Kundu P., Wheeler W., Arslan A.A., Beane-Freeman L.E., Bracci P.M., Brennan P., Canzian F., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Blackford A.L., Bueno-De-Mesquita B., Buring J.E., Campa D., Chanock S.J., Childs E.J., Duell E.J., Fuchs C.S., Gaziano J.M., Giovannucci E.L., Goggins M.G., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Hung R.J., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Ng K., Oberg A.L., Panico S., Peters U., Porta M., Rabe K.G., Riboli E., Rothman N., Scelo G., Sesso H.D., Silverman D.T., Stevens V.L., Strobel O., Thompson I.M., Tjonneland A., Trichopoulou A., van Den Eeden S.K., Wactawski-Wende J., Wentzensen N., Wilkens L.R., Yu H., Yuan F., Zeleniuch-Jacquotte A., Amundadottir L.T., Li D., Jacobs E.J., Petersen G.M., Wolpin B.M., Risch H.A., Kraft P., Chatterjee N., Klein A.P., Stolzenberg-Solomon R., Mocci E., Kundu P., Wheeler W., Arslan A.A., Beane-Freeman L.E., Bracci P.M., Brennan P., Canzian F., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Blackford A.L., Bueno-De-Mesquita B., Buring J.E., Campa D., Chanock S.J., Childs E.J., Duell E.J., Fuchs C.S., Gaziano J.M., Giovannucci E.L., Goggins M.G., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Hung R.J., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Ng K., Oberg A.L., Panico S., Peters U., Porta M., Rabe K.G., Riboli E., Rothman N., Scelo G., Sesso H.D., Silverman D.T., Stevens V.L., Strobel O., Thompson I.M., Tjonneland A., Trichopoulou A., van Den Eeden S.K., Wactawski-Wende J., Wentzensen N., Wilkens L.R., Yu H., Yuan F., Zeleniuch-Jacquotte A., Amundadottir L.T., Li D., Jacobs E.J., Petersen G.M., Wolpin B.M., Risch H.A., Kraft P., Chatterjee N., Klein A.P., and Stolzenberg-Solomon R.

Abstract

Germline variation and smoking are independently associated with pancreatic ductal adenocarcinoma (PDAC). We conducted genome-wide smoking interaction analysis of PDAC using genotype data from four previous genome-wide association studies in individuals of European ancestry (7,937 cases and 11,774 controls). Examination of expression quantitative trait loci data from the Genotype-Tissue Expression Project followed by colocalization analysis was conducted to determine whether there was support for common SNP(s) underlying the observed associations. Statistical tests were two sided and P < 5 10-8 was considered statistically significant. Genome-wide significant evidence of qualitative interaction was identified on chr2q21.3 in intron 5 of the transmembrane protein 163 (TMEM163) and upstream of the cyclin T2 (CCNT2). The most significant SNP using the Empirical Bayes method, in this region that included 45 significantly associated SNPs, was rs1818613 [per allele OR in never smokers 0.87, 95% confidence interval (CI), 0.82-0.93; former smokers 1.00, 95% CI, 0.91-1.07; current smokers 1.25, 95% CI 1.12-1.40, Pinteraction 1/4 3.08 10-9). Examination of the Genotype-Tissue Expression Project data demonstrated an expression quantitative trait locus in this region for TMEM163 and CCNT2 in several tissue types. Colocalization analysis supported a shared SNP, rs842357, in high linkage disequilibrium with rs1818613 (r2 1/4 0. 94) driving both the observed interaction and the expression quantitative trait loci signals. Future studies are needed to confirm and understand the differential biologic mechanisms by smoking status that contribute to our PDAC findings.Copyright © 2021 American Association for Cancer Research.

Published
2021

8. Genome-wide association study data reveal genetic susceptibility to chronic inflammatory intestinal diseases and pancreatic ductal adenocarcinoma risk.

Author

Wang X., Yuan F., Hung R.J., Walsh N., Zhang H., Platz E.A., Wheeler W., Song L., Arslan A.A., Beane Freeman L.E., Bracci P., Canzian F., Du M., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Shi J., Duell E.J., Amundadottir L.T., Li D., Petersen G.M., Wolpin B.M., Risch H.A., Yu K., Klein A.P., Stolzenberg-Solomon R., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Rosendahl J., Scelo G., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Amiano P., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Chanock S.J., Fuchs C.S., Michael Gaziano J., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Katzke V., Kirsten H., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Ng K., Oberg A.L., Porta M., Rabe K.G., Real F.X., Rothman N., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., Wentzensen N., Wang X., Yuan F., Hung R.J., Walsh N., Zhang H., Platz E.A., Wheeler W., Song L., Arslan A.A., Beane Freeman L.E., Bracci P., Canzian F., Du M., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Shi J., Duell E.J., Amundadottir L.T., Li D., Petersen G.M., Wolpin B.M., Risch H.A., Yu K., Klein A.P., Stolzenberg-Solomon R., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Rosendahl J., Scelo G., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Amiano P., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Chanock S.J., Fuchs C.S., Michael Gaziano J., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Katzke V., Kirsten H., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Ng K., Oberg A.L., Porta M., Rabe K.G., Real F.X., Rothman N., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., and Wentzensen N.

Abstract

Registry-based epidemiologic studies suggest associations between chronic inflammatory intestinal diseases and pancreatic ductal adenocarcinoma (PDAC). As genetic susceptibility contributes to a large proportion of chronic inflammatory intestinal diseases, we hypothesize that the genomic regions surrounding established genome-wide associated variants for these chronic inflammatory diseases are associated with PDAC. We examined the association between PDAC and genomic regions (+500 kb) surrounding established common susceptibility variants for ulcerative colitis, Crohn's disease, inflammatory bowel disease, celiac disease, chronic pancreatitis, and primary sclerosing cholangitis. We analyzed summary statistics from genome-wide association studies data for 8,384 cases and 11,955 controls of European descent from two large consortium studies using the summary data-based adaptive rank truncated product method to examine the overall association of combined genomic regions for each inflammatory disease group. Combined genomic susceptibility regions for ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis were associated with PDAC at P values < 0.05 (0.0040, 0.0057, 0.011, and 3.4 x 10-6, respectively). After excluding the 20 PDAC susceptibility regions (+500 kb) previously identified by GWAS, the genomic regions for ulcerative colitis, Crohn disease, and inflammatory bowel disease remained associated with PDAC (P 1/4 0.0029, 0.0057, and 0.0098, respectively). Genomic regions for celiac disease (P 1/4 0.22) and primary sclerosing cholangitis (P 1/4 0.078) were not associated with PDAC. Our results support the hypothesis that genomic regions surrounding variants associated with inflammatory intestinal diseases, particularly, ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis are associated with PDAC.Copyright © 2020 American Association for Cancer Research.

Published
2021

9. A transcriptome-wide association study identifies novel candidate susceptibility genes for pancreatic cancer.

Author

Hasan M., Zhang T., Xiao W., Albanes D., Andreotti G., Arslan A.A., Babic A., Bamlet W.R., Beane-Freeman L., Berndt S., Borgida A., Bracci P.M., Brais L., Brennan P., Bueno-De-Mesquita B., Buring J., Canzian F., Childs E.J., Cotterchio M., Du M., Duell E.J., Fuchs C., Gallinger S., Michael Gaziano J., Giles G.G., Giovannucci E., Goggins M., Goodman G.E., Goodman P.J., Haiman C., Hartge P., Helzlsouer K.J., Holly E.A., Klein E.A., Kogevinas M., Kurtz R.J., LeMarchand L., Malats N., Mannisto S., Milne R., Neale R.E., Ng K., Obazee O., Oberg A.L., Orlow I., Patel A.V., Peters U., Porta M., Rothman N., Scelo G., Sesso H.D., Severi G., Sieri S., Silverman D., Sund M., Tjonneland A., Thornquist M.D., Tobias G.S., Trichopoulou A., van Den Eeden S.K., Visvanathan K., Wactawski-Wende J., Wentzensen N., White E., Yu H., Yuan C., Zeleniuch-Jacquotte A., Hoover R., Brown K., Kooperberg C., Risch H.A., Jacobs E.J., Li D., Yu K., Shu X.-O., Chanock S.J., Wolpin B.M., Stolzenberg-Solomon R.Z., Chatterjee N., Klein A.P., Smith J.P., Kraft P., Shi J., Petersen G.M., Zheng W., Amundadottir L.T., Zhong J., Jermusyk A., Wu L., Hoskins J.W., Collins I., Mocci E., Zhang M., Song L., Chung C.C., Hasan M., Zhang T., Xiao W., Albanes D., Andreotti G., Arslan A.A., Babic A., Bamlet W.R., Beane-Freeman L., Berndt S., Borgida A., Bracci P.M., Brais L., Brennan P., Bueno-De-Mesquita B., Buring J., Canzian F., Childs E.J., Cotterchio M., Du M., Duell E.J., Fuchs C., Gallinger S., Michael Gaziano J., Giles G.G., Giovannucci E., Goggins M., Goodman G.E., Goodman P.J., Haiman C., Hartge P., Helzlsouer K.J., Holly E.A., Klein E.A., Kogevinas M., Kurtz R.J., LeMarchand L., Malats N., Mannisto S., Milne R., Neale R.E., Ng K., Obazee O., Oberg A.L., Orlow I., Patel A.V., Peters U., Porta M., Rothman N., Scelo G., Sesso H.D., Severi G., Sieri S., Silverman D., Sund M., Tjonneland A., Thornquist M.D., Tobias G.S., Trichopoulou A., van Den Eeden S.K., Visvanathan K., Wactawski-Wende J., Wentzensen N., White E., Yu H., Yuan C., Zeleniuch-Jacquotte A., Hoover R., Brown K., Kooperberg C., Risch H.A., Jacobs E.J., Li D., Yu K., Shu X.-O., Chanock S.J., Wolpin B.M., Stolzenberg-Solomon R.Z., Chatterjee N., Klein A.P., Smith J.P., Kraft P., Shi J., Petersen G.M., Zheng W., Amundadottir L.T., Zhong J., Jermusyk A., Wu L., Hoskins J.W., Collins I., Mocci E., Zhang M., Song L., and Chung C.C.

Abstract

Background: Although 20 pancreatic cancer susceptibility loci have been identified through genome-wide association studies in individuals of European ancestry, much of its heritability remains unexplained and the genes responsible largely unknown. Method(s): To discover novel pancreatic cancer risk loci and possible causal genes, we performed a pancreatic cancer transcriptome-wide association study in Europeans using three approaches: FUSION, MetaXcan, and Summary-MulTiXcan. We integrated genome-wide association studies summary statistics from 9040 pancreatic cancer cases and 12 496 controls, with gene expression prediction models built using transcriptome data from histologically normal pancreatic tissue samples (NCI Laboratory of Translational Genomics [n = 95] and Genotype-Tissue Expression v7 [n = 174] datasets) and data from 48 different tissues (Genotype-Tissue Expression v7, n = 74-421 samples). Result(s): We identified 25 genes whose genetically predicted expression was statistically significantly associated with pancreatic cancer risk (false discovery rate <.05), including 14 candidate genes at 11 novel loci (1p36.12: CELA3B; 9q31.1: SMC2, SMC2-AS1; 10q23.31: RP11-80H5.9; 12q13.13: SMUG1; 14q32.33: BTBD6; 15q23: HEXA; 15q26.1: RCCD1; 17q12: PNMT, CDK12, PGAP3; 17q22: SUPT4H1; 18q11.22:RP11-888D10.3; and 19p13.11: PGPEP1) and 11 at six known risk loci (5p15.33: TERT, CLPTM1L, ZDHHC11B; 7p14.1: INHBA; 9q34.2: ABO; 13q12.2: PDX1; 13q22.1: KLF5; and 16q23.1: WDR59, CFDP1, BCAR1, TMEM170A). The association for 12 of these genes (CELA3B, SMC2, and PNMT at novel risk loci and TERT, CLPTM1L, INHBA, ABO, PDX1, KLF5, WDR59, CFDP1, and BCAR1 at known loci) remained statistically significant after Bonferroni correction. Conclusion(s): By integrating gene expression and genotype data, we identified novel pancreatic cancer risk loci and candidate functional genes that warrant further investigation.Copyright © 2020 Oxford University Press. All rights reserved.

Published
2021

10. Genome-wide gene⇓diabetes and gene⇓obesity interaction scan in 8,255 cases and 11,900 controls from panscan and PanC4 consortia

Author

Tang, H. Jiang, L. Stolzenberg-Solomon, R.Z. Arslan, A.A. Beane Freeman, L.E. Bracci, P.M. Brennan, P. Canzian, F. Du, M. Gallinger, S. Giles, G.G. Goodman, P.J. Kooperberg, C. Le Marchand, L. Neale, R.E. Shu, X.-O. Visvanathan, K. White, E. Zheng, W. Albanes, D. Andreotti, G. Babic, A. Bamlet, W.R. Berndt, S.I. Blackford, A. Bueno-De-Mesquita, B. Buring, J.E. Campa, D. Chanock, S.J. Childs, E. Duell, E.J. Fuchs, C. Michael Gaziano, J. Goggins, M. Hartge, P. Hassam, M.H. Holly, E.A. Hoover, R.N. Hung, R.J. Kurtz, R.C. Lee, I.-M. Malats, N. Milne, R.L. Ng, K. Oberg, A.L. Orlow, I. Peters, U. Porta, M. Rabe, K.G. Rothman, N. Scelo, G. Sesso, H.D. Silverman, D.T. Thompson, I.M. Tjønneland, A. Trichopoulou, A. Wactawski-Wende, J. Wentzensen, N. Wilkens, L.R. Yu, H. Zeleniuch-Jacquotte, A. Amundadottir, L.T. Jacobs, E.J. Petersen, G.M. Wolpin, B.M. Risch, H.A. Chatterjee, N. Klein, A.P. Li, D. Kraft, P. Wei, P.

Abstract

Background: Obesity and diabetes are major modifiable risk factors for pancreatic cancer. Interactions between genetic variants and diabetes/obesity have not previously been comprehensively investigated in pancreatic cancer at the genome-wide level. Methods: We conducted a gene–environment interaction (GxE) analysis including 8,255 cases and 11,900 controls from four pancreatic cancer genome-wide association study (GWAS) datasets (Pancreatic Cancer Cohort Consortium I–III and Pancreatic Cancer Case Control Consortium). Obesity (body mass index ≥30 kg/m2) and diabetes (duration ≥3 years) were the environmental variables of interest. Approximately 870,000 SNPs (minor allele frequency ≥0.005, genotyped in at least one dataset) were analyzed. Case–control (CC), case-only (CO), and joint-effect test methods were used for SNP-level GxE analysis. As a complementary approach, gene-based GxE analysis was also performed. Age, sex, study site, and principal components accounting for population substructure were included as covariates. Meta-analysis was applied to combine individual GWAS summary statistics. Results: No genome-wide significant interactions (departures from a log-additive odds model) with diabetes or obesity were detected at the SNP level by the CC or CO approaches. The joint-effect test detected numerous genome-wide significant GxE signals in the GWAS main effects top hit regions, but the significance diminished after adjusting for the GWAS top hits. In the gene-based analysis, a significant interaction of diabetes with variants in the FAM63A (family with sequence similarity 63 member A) gene (significance threshold P < 1.25 106) was observed in the meta-analysis (PGxE ¼ 1.2 106, PJoint ¼ 4.2 107). Conclusions: This analysis did not find significant GxE interactions at the SNP level but found one significant interaction with diabetes at the gene level. A larger sample size might unveil additional genetic factors via GxE scans. Impact: This study may contribute to discovering the mechanism of diabetes-associated pancreatic cancer. © 2020 American Association for Cancer Research.

Published
2020

11. SMAD4 as a Predictive Biomarker For Locally Aggressive Phenotype In Resected Pancreas Cancer

Author

Gits, H.C., primary, Tang, A.H., additional, Harmsen, W.S., additional, Bamlet, W.R., additional, Graham, R.P., additional, Mahipal, A., additional, Ashman, J.B., additional, Rule, W.G., additional, Owen, D., additional, Neben-Wittich, M.A., additional, Ma, W.W., additional, Truty, M., additional, Sio, T.T.W., additional, Haddock, M.G., additional, Hallemeier, C.L., additional, and Merrell, K.W., additional

Published
2020
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13. Genome-wide meta-analysis identifies five new susceptibility loci for pancreatic cancer

Author

Klein, A.P. Wolpin, B.M. Risch, H.A. Stolzenberg-Solomon, R.Z. Mocci, E. Zhang, M. Canzian, F. Childs, E.J. Hoskins, J.W. Jermusyk, A. Zhong, J. Chen, F. Albanes, D. Andreotti, G. Arslan, A.A. Babic, A. Bamlet, W.R. Beane-Freeman, L. Berndt, S.I. Blackford, A. Borges, M. Borgida, A. Bracci, P.M. Brais, L. Brennan, P. Brenner, H. Bueno-De-Mesquita, B. Buring, J. Campa, D. Capurso, G. Cavestro, G.M. Chaffee, K.G. Chung, C.C. Cleary, S. Cotterchio, M. Dijk, F. Duell, E.J. Foretova, L. Fuchs, C. Funel, N. Gallinger, S. Gaziano, J.M.M. Gazouli, M. Giles, G.G. Giovannucci, E. Goggins, M. Goodman, G.E. Goodman, P.J. Hackert, T. Haiman, C. Hartge, P. Hasan, M. Hegyi, P. Helzlsouer, K.J. Herman, J. Holcatova, I. Holly, E.A. Hoover, R. Hung, R.J. Jacobs, E.J. Jamroziak, K. Janout, V. Kaaks, R. Khaw, K.-T. Klein, E.A. Kogevinas, M. Kooperberg, C. Kulke, M.H. Kupcinskas, J. Kurtz, R.J. Laheru, D. Landi, S. Lawlor, R.T. Lee, I.-M. Lemarchand, L. Lu, L. Malats, N. Mambrini, A. Mannisto, S. Milne, R.L. Mohelníková-Duchoňová, B. Neale, R.E. Neoptolemos, J.P. Oberg, A.L. Olson, S.H. Orlow, I. Pasquali, C. Patel, A.V. Peters, U. Pezzilli, R. Porta, M. Real, F.X. Rothman, N. Scelo, G. Sesso, H.D. Severi, G. Shu, X.-O. Silverman, D. Smith, J.P. Soucek, P. Sund, M. Talar-Wojnarowska, R. Tavano, F. Thornquist, M.D. Tobias, G.S. Van Den Eeden, S.K. Vashist, Y. Visvanathan, K. Vodicka, P. Wactawski-Wende, J. Wang, Z. Wentzensen, N. White, E. Yu, H. Yu, K. Zeleniuch-Jacquotte, A. Zheng, W. Kraft, P. Li, D. Chanock, S. Obazee, O. Petersen, G.M. Amundadottir, L.T.

Abstract

In 2020, 146,063 deaths due to pancreatic cancer are estimated to occur in Europe and the United States combined. To identify common susceptibility alleles, we performed the largest pancreatic cancer GWAS to date, including 9040 patients and 12,496 controls of European ancestry from the Pancreatic Cancer Cohort Consortium (PanScan) and the Pancreatic Cancer Case-Control Consortium (PanC4). Here, we find significant evidence of a novel association at rs78417682 (7p12/TNS3, P = 4.35 × 10-8). Replication of 10 promising signals in up to 2737 patients and 4752 controls from the PANcreatic Disease ReseArch (PANDoRA) consortium yields new genome-wide significant loci: Rs13303010 at 1p36.33 (NOC2L, P = 8.36 × 10-14), rs2941471 at 8q21.11 (HNF4G, P = 6.60 × 10-10), rs4795218 at 17q12 (HNF1B, P = 1.32 × 10-8), and rs1517037 at 18q21.32 (GRP, P = 3.28 × 10-8). rs78417682 is not statistically significantly associated with pancreatic cancer in PANDoRA. Expression quantitative trait locus analysis in three independent pancreatic data sets provides molecular support of NOC2L as a pancreatic cancer susceptibility gene. © 2018 The Author(s).

Published
2018

14. Common variation at 2p13.3, 3q29, 7p13 and 17q25.1 associated with susceptibility to pancreatic cancer

Author

Childs, E.J. Mocci, E. Campa, D. Bracci, P.M. Gallinger, S. Goggins, M. Li, D. Neale, R.E. Olson, S.H. Scelo, G. Amundadottir, L.T. Bamlet, W.R. Bijlsma, M.F. Blackford, A. Borges, M. Brennan, P. Brenner, H. Bueno-De-Mesquita, H.B. Canzian, F. Capurso, G. Cavestro, G.M. Chaffee, K.G. Chanock, S.J. Cleary, S.P. Cotterchio, M. Foretova, L. Fuchs, C. Funel, N. Gazouli, M. Hassan, M. Herman, J.M. Holcatova, I. Holly, E.A. Hoover, R.N. Hung, R.J. Janout, V. Key, T.J. Kupcinskas, J. Kurtz, R.C. Landi, S. Lu, L. Malecka-Panas, E. Mambrini, A. Mohelnikova-Duchonova, B. Neoptolemos, J.P. Oberg, A.L. Orlow, I. Pasquali, C. Pezzilli, R. Rizzato, C. Saldia, A. Scarpa, A. Stolzenberg-Solomon, R.Z. Strobel, O. Tavano, F. Vashist, Y.K. Vodicka, P. Wolpin, B.M. Yu, H. Petersen, G.M. Risch, H.A. Klein, A.P.

Abstract

Pancreatic cancer is the fourth leading cause of cancer death in the developed world. Both inherited high-penetrance mutations in BRCA2 (ref. 2), ATM, PALB2 (ref. 4), BRCA1 (ref. 5), STK11 (ref. 6), CDKN2A and mismatch-repair genes and low-penetrance loci are associated with increased risk. To identify new risk loci, we performed a genome-wide association study on 9,925 pancreatic cancer cases and 11,569 controls, including 4,164 newly genotyped cases and 3,792 controls in 9 studies from North America, Central Europe and Australia. We identified three newly associated regions: 17q25.1 (LINC00673, rs11655237, odds ratio (OR) = 1.26, 95% confidence interval (CI) = 1.19-1.34, P = 1.42 × 10-14), 7p13 (SUGCT, rs17688601, OR = 0.88, 95% CI = 0.84-0.92, P = 1.41 × 10-8) and 3q29 (TP63, rs9854771, OR = 0.89, 95% CI = 0.85-0.93, P = 2.35 × 10-8). We detected significant association at 2p13.3 (ETAA1, rs1486134, OR = 1.14, 95% CI = 1.09-1.19, P = 3.36 × 10-9), a region with previous suggestive evidence in Han Chinese. We replicated previously reported associations at 9q34.2 (ABO), 13q22.1 (KLF5), 5p15.33 (TERT and CLPTM1), 13q12.2 (PDX1), 1q32.1 (NR5A2), 7q32.3 (LINC-PINT), 16q23.1 (BCAR1) and 22q12.1 (ZNRF3). Our study identifies new loci associated with pancreatic cancer risk. © 2015 Nature America, Inc. All rights reserved.

Published
2015

15. Diabetes, antidiabetic medications, and pancreatic cancer risk: an analysis from the International Pancreatic Cancer Case-Control Consortium

Author

Bosetti, C. Rosato, V. Li, D. Silverman, D. Petersen, G.M. Bracci, P.M. Neale, R.E. Muscat, J. Anderson, K. Gallinger, S. Olson, S.H. Miller, A.B. Bas Bueno-de-Mesquita, H. Scelo, G. Janout, V. Holcatova, I. Lagiou, P. Serraino, D. Lucenteforte, E. Fabianova, E. Baghurst, P.A. Zatonski, W. Foretova, L. Fontham, E. Bamlet, W.R. Holly, E.A. Negri, E. Hassan, M. Prizment, A. Cotterchio, M. Cleary, S. Kurtz, R.C. Maisonneuve, P. Trichopoulos, D. Polesel, J. Duell, E.J. Boffetta, P. La Vecchia, C. Ghadirian, P.

Abstract

Background: Type 2 diabetes mellitus has been associated with an excess risk of pancreatic cancer, but the magnitude of the risk and the time–risk relationship are unclear, and there is limited information on the role of antidiabetic medications. Patients and methods: We analyzed individual-level data from 15 case–control studies within the Pancreatic Cancer Case-Control Consortium, including 8305 cases and 13 987 controls. Pooled odds ratios (ORs) were estimated from multiple logistic regression models, adjusted for relevant covariates. Results: Overall, 1155 (15%) cases and 1087 (8%) controls reported a diagnosis of diabetes 2 or more years before cancer diagnosis (or interview, for controls), corresponding to an OR of 1.90 (95% confidence interval, CI, 1.72–2.09). Consistent risk estimates were observed across strata of selected covariates, including body mass index and tobacco smoking. Pancreatic cancer risk decreased with duration of diabetes, but a significant excess risk was still evident 20 or more years after diabetes diagnosis (OR 1.30, 95% CI 1.03–1.63). Among diabetics, long duration of oral antidiabetic use was associated with a decreased pancreatic cancer risk (OR 0.31, 95% CI 0.14–0.69, for ≥15 years). Conversely, insulin use was associated with a pancreatic cancer risk in the short term (OR 5.60, 95% CI 3.75–8.35, for

Published
2014

16. Correction to: Vitamin D and pancreatic cancer: a pooled analysis from the Pancreatic Cancer Case–Control Consortium

Author

Waterhouse, M., primary, Risch, H.A., additional, Bosetti, C., additional, Anderson, K.E., additional, Petersen, G.M., additional, Bamlet, W.R., additional, Cotterchio, M., additional, Cleary, S.P., additional, Ibiebele, T.I., additional, La Vecchia, C., additional, Skinner, H.G., additional, Strayer, L., additional, Bracci, P.M., additional, Maisonneuve, P., additional, Bueno-de-Mesquita, H.B., additional, Zatoński, W., additional, Lu, L., additional, Yu, H., additional, Janik-Koncewicz, K., additional, Polesel, J., additional, Serraino, D., additional, and Neale, R.E., additional

Published
2016
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17. Risk of ovarian cancer and the NF-kappaB pathway: genetic association with IL1A and TNFSF10

Author

Charbonneau, B., Block, M.S., Bamlet, W.R., Vierkant, R.A., Kalli, K.R., Fogarty, Z., Rider, D.N., Sellers, T.A., Tworoger, S.S., Poole, E., Risch, H.A., Salvesen, H.B., Kiemeney, B., Baglietto, L., Giles, G.G., Severi, G., Trabert, B., Wentzensen, N., Chenevix-Trench, G., Whittemore, A.S., Sieh, W., Chang-Claude, J., Bandera, E.V., Orlow, I., Terry, K., Goodman, M.T., Thompson, P.J., Cook, L.S., Rossing, M.A., Ness, R.B., Narod, S.A., Kupryjanczyk, J., Lu, K., Butzow, R., Dork, T., Pejovic, T., Campbell, I., Le, N.D., Bunker, C.H., Bogdanova, N., Runnebaum, I.B., Eccles, D., Paul, J., Wu, A.H., Gayther, S.A., Hogdall, E., Heitz, F., Kaye, S.B., Karlan, B.Y., Anton-Culver, H., Gronwald, J., Hogdall, C.K., Lambrechts, D., Fasching, P.A., Menon, U., Schildkraut, J., Pearce, C.L., Levine, D.A., Kjaer, S.K., Cramer, D., Flanagan, J.M., Phelan, C.M., Brown, R., Massuger, L.F.A.G., Song, H., Doherty, J.A., Krakstad, C., Liang, D., Odunsi, K., Berchuck, A., Jensen, A., Lubinski, J., Nevanlinna, H., Bean, Y.T., Lurie, G., Ziogas, A., Walsh, C., Despierre, E., Brinton, L., Hein, A., Rudolph, A., Dansonka-Mieszkowska, A., Olson, S.H., Harter, P., Tyrer, J., Vitonis, A.F., Brooks-Wilson, A., Aben, K.K.H., Pike, M.C., Ramus, S.J., Wik, E., Cybulski, C., Lin, J., Sucheston, L., Edwards, R., McGuire, V., Lester, J., Bois, A. du, Lundvall, L., et al., Charbonneau, B., Block, M.S., Bamlet, W.R., Vierkant, R.A., Kalli, K.R., Fogarty, Z., Rider, D.N., Sellers, T.A., Tworoger, S.S., Poole, E., Risch, H.A., Salvesen, H.B., Kiemeney, B., Baglietto, L., Giles, G.G., Severi, G., Trabert, B., Wentzensen, N., Chenevix-Trench, G., Whittemore, A.S., Sieh, W., Chang-Claude, J., Bandera, E.V., Orlow, I., Terry, K., Goodman, M.T., Thompson, P.J., Cook, L.S., Rossing, M.A., Ness, R.B., Narod, S.A., Kupryjanczyk, J., Lu, K., Butzow, R., Dork, T., Pejovic, T., Campbell, I., Le, N.D., Bunker, C.H., Bogdanova, N., Runnebaum, I.B., Eccles, D., Paul, J., Wu, A.H., Gayther, S.A., Hogdall, E., Heitz, F., Kaye, S.B., Karlan, B.Y., Anton-Culver, H., Gronwald, J., Hogdall, C.K., Lambrechts, D., Fasching, P.A., Menon, U., Schildkraut, J., Pearce, C.L., Levine, D.A., Kjaer, S.K., Cramer, D., Flanagan, J.M., Phelan, C.M., Brown, R., Massuger, L.F.A.G., Song, H., Doherty, J.A., Krakstad, C., Liang, D., Odunsi, K., Berchuck, A., Jensen, A., Lubinski, J., Nevanlinna, H., Bean, Y.T., Lurie, G., Ziogas, A., Walsh, C., Despierre, E., Brinton, L., Hein, A., Rudolph, A., Dansonka-Mieszkowska, A., Olson, S.H., Harter, P., Tyrer, J., Vitonis, A.F., Brooks-Wilson, A., Aben, K.K.H., Pike, M.C., Ramus, S.J., Wik, E., Cybulski, C., Lin, J., Sucheston, L., Edwards, R., McGuire, V., Lester, J., Bois, A. du, Lundvall, L., and et al.

Abstract

Contains fulltext : 136742.pdf (publisher's version ) (Closed access), A missense single-nucleotide polymorphism (SNP) in the immune modulatory gene IL1A has been associated with ovarian cancer risk (rs17561). Although the exact mechanism through which this SNP alters risk of ovarian cancer is not clearly understood, rs17561 has also been associated with risk of endometriosis, an epidemiologic risk factor for ovarian cancer. Interleukin-1alpha (IL1A) is both regulated by and able to activate NF-kappaB, a transcription factor family that induces transcription of many proinflammatory genes and may be an important mediator in carcinogenesis. We therefore tagged SNPs in more than 200 genes in the NF-kappaB pathway for a total of 2,282 SNPs (including rs17561) for genotype analysis of 15,604 cases of ovarian cancer in patients of European descent, including 6,179 of high-grade serous (HGS), 2,100 endometrioid, 1,591 mucinous, 1,034 clear cell, and 1,016 low-grade serous, including 23,235 control cases spanning 40 studies in the Ovarian Cancer Association Consortium. In this large population, we confirmed the association between rs17561 and clear cell ovarian cancer [OR, 0.84; 95% confidence interval (CI), 0.76-0.93; P = 0.00075], which remained intact even after excluding participants in the prior study (OR, 0.85; 95% CI, 0.75-0.95; P = 0.006). Considering a multiple-testing-corrected significance threshold of P < 2.5 x 10(-5), only one other variant, the TNFSF10 SNP rs6785617, was associated significantly with a risk of ovarian cancer (low malignant potential tumors OR, 0.85; 95% CI, 0.79-0.91; P = 0.00002). Our results extend the evidence that borderline tumors may have a distinct genetic etiology. Further investigation of how these SNPs might modify ovarian cancer associations with other inflammation-related risk factors is warranted.

Published
2014

18. Alcohol consumption and pancreatic cancer: a pooled analysis in the International Pancreatic Cancer Case–Control Consortium (PanC4)

Author

Lucenteforte, E., primary, La Vecchia, C., additional, Silverman, D., additional, Petersen, G.M., additional, Bracci, P.M., additional, Ji, B.T., additional, Bosetti, C., additional, Li, D., additional, Gallinger, S., additional, Miller, A.B., additional, Bueno-de-Mesquita, H.B., additional, Talamini, R., additional, Polesel, J., additional, Ghadirian, P., additional, Baghurst, P.A., additional, Zatonski, W., additional, Fontham, E., additional, Bamlet, W.R., additional, Holly, E.A., additional, Gao, Y.T., additional, Negri, E., additional, Hassan, M., additional, Cotterchio, M., additional, Su, J., additional, Maisonneuve, P., additional, Boffetta, P., additional, and Duell, E.J., additional

Published
2012
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19. Reply to Are cohort data on smokeless tobacco use and pancreatic cancer confounded by alcohol use?

Author

Bertuccio, P., primary, La Vecchia, C., additional, Silverman, D.T., additional, Petersen, G.M., additional, Bracci, P.M., additional, Negri, E., additional, Li, D., additional, Risch, H.A., additional, Olson, S.H., additional, Gallinger, S., additional, Miller, A.B., additional, Bueno-de-Mesquita, H.B., additional, Talamini, R., additional, Polesel, J., additional, Ghadirian, P., additional, Baghurst, P.A., additional, Zatonski, W., additional, Fontham, E., additional, Bamlet, W.R., additional, Holly, E.A., additional, Lucenteforte, E., additional, Hassan, M., additional, Yu, H., additional, Kurtz, R.C., additional, Cotterchio, M., additional, Su, J., additional, Maisonneuve, P., additional, Duell, E.J., additional, Bosetti, C., additional, and Boffetta, P., additional

Published
2011
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20. SUBCUTANEOUS IGF-1 IS NOT BENEFICIAL IN 2-YEAR ALS TRIAL

Author

Howe, C. L., primary, Bergstrom, R. A., additional, Horazdovsky, B. F., additional, Sorenson, E.J., additional, Windbank, A.J., additional, Mandrekar, J.N., additional, Bamlet, W.R., additional, Appel, S.H., additional, Armon, C., additional, Barkhaus, P.E., additional, Bosch, P., additional, Boylan, K., additional, David, W.S., additional, Feldman, E., additional, Glass, J., additional, Gutmann, L., additional, Katz, J., additional, King, W., additional, Luciano, C.A., additional, McCluskey, L.F., additional, Nash, S., additional, Newman, D.S., additional, Pascuzzi, R.M., additional, Pioro, E., additional, Sams, L.J., additional, Scelsa, S., additional, Simpson, E.P., additional, Subramony, S.H., additional, Tiryaki, E., additional, and Thornton, C.A., additional

Published
2009
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21. Alcohol consumption and pancreatic cancer: a pooled analysis in the International Pancreatic Cancer Case–Control Consortium (PanC4)

Author

Manal M. Hassan, Anthony B. Miller, E. A. Holly, Paolo Boffetta, Parviz Ghadirian, William R. Bamlet, Jerry Polesel, Ersilia Lucenteforte, C. La Vecchia, Michelle Cotterchio, Elizabeth T. H. Fontham, Steve Gallinger, Eric J. Duell, J. Su, Donghui Li, Bu Tian Ji, Debra T. Silverman, Paige M. Bracci, Witold Zatonski, R. Talamini, Eva Negri, Yu-Tang Gao, Patrick Maisonneuve, Cristina Bosetti, H. B. Bueno-de-Mesquita, Gloria M. Petersen, Peter A. Baghurst, Lucenteforte, E., La Vecchia, C., Silverman, D., Petersen, G.M., Bracci, P.M., Ji, B.T., Bosetti, C., Li, D., Gallinger, S., Miller, A.B., Bueno-de-Mesquita, H.B., Talamini, R., Polesel, J., Ghadirian, P., Baghurst, P.A., Zatonski, W., Fontham, E., Bamlet, W.R., Holly, E.A., Gao, Y.T., Negri, E., Hassan, M., Cotterchio, M., Su, J., Maisonneuve, P., Boffetta, P., Duell, E.J., International Prevention Research Institute (IPRI), The Tisch Cancer Institute, and Icahn School of Medicine at Mount Sinai [New York] (MSSM)

Subjects
Adult, Male, Oncology, medicine.medical_specialty, Pathology, alcohol drinking, case–control, studies, ethanol, pancreatic cancer, pooled analysis, risk factors, Alcohol, chemistry.chemical_compound, Internal medicine, Pancreatic cancer, Odds Ratio, medicine, Adult Aged Alcohol Drinking/*adverse effects Case-Control Studies Confounding Factors (Epidemiology) Female Humans Logistic Models Male Middle Aged Odds Ratio Pancreatic Neoplasms/*epidemiology/etiology Pancreatitis/complications Risk Factors Smoking/adverse effects, Humans, risk of pancreatic cancer, Aged, business.industry, Smoking, Confounding Factors, Epidemiologic, Original Articles, Hematology, Middle Aged, medicine.disease, Pancreatic Neoplasms, Logistic Models, Pooled analysis, Pancreatitis, chemistry, Case-Control Studies, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, Female, business, Alcohol consumption, heavy alcohol consumptio
Abstract

Lucenteforte, E La Vecchia, C Silverman, D Petersen, G M Bracci, P M Ji, B T Bosetti, C Li, D Gallinger, S Miller, A B Bueno-de-Mesquita, H B Talamini, R Polesel, J Ghadirian, P Baghurst, P A Zatonski, W Fontham, E Bamlet, W R Holly, E A Gao, Y T Negri, E Hassan, M Cotterchio, M Su, J Maisonneuve, P Boffetta, P Duell, E J eng CA098889/CA/NCI NIH HHS/ CA108370/CA/NCI NIH HHS/ CA109767/CA/NCI NIH HHS/ CA59706/CA/NCI NIH HHS/ CA89726/CA/NCI NIH HHS/ N01-CP-05225/CP/NCI NIH HHS/ N01-CP-05227/CP/NCI NIH HHS/ N01-CP-31022/CP/NCI NIH HHS/ N01-CP-51089/CP/NCI NIH HHS/ N01-CP-51090/CP/NCI NIH HHS/ N01-CP-51092/CP/NCI NIH HHS/ N01-PC-35136/PC/NCI NIH HHS/ Meta-Analysis Research Support, N.I.H., Extramural Research Support, N.I.H., Intramural Research Support, Non-U.S. Gov't England 2011/05/04 06:00 Ann Oncol. 2012 Feb;23(2):374-82. doi: 10.1093/annonc/mdr120. Epub 2011 May 2.; International audience; BACKGROUND: Heavy alcohol drinking has been related to pancreatic cancer, but the issue is still unsolved. METHODS: To evaluate the role of alcohol consumption in relation to pancreatic cancer, we conducted a pooled analysis of 10 case-control studies (5585 cases and 11,827 controls) participating in the International Pancreatic Cancer Case-Control Consortium. We computed pooled odds ratios (ORs) by estimating study-specific ORs adjusted for selected covariates and pooling them using random effects models. RESULTS: Compared with abstainers and occasional drinkers (< 1 drink per day), we observed no association for light-to-moderate alcohol consumption (/= 9 drinks per day). Results did not change substantially when we evaluated associations by tobacco smoking status, or when we excluded participants who reported a history of pancreatitis, or participants whose data were based upon proxy responses. Further, no notable differences in pooled risk estimates emerged across strata of sex, age, race, study type, and study area. CONCLUSION: This collaborative-pooled analysis provides additional evidence for a positive association between heavy alcohol consumption and the risk of pancreatic cancer.

Published
2012

22. Diabetes, antidiabetic medications, and pancreatic cancer risk: an analysis from the International Pancreatic Cancer Case-Control Consortium

Author

C. La Vecchia, Robert C. Kurtz, Michelle Cotterchio, Anna E. Prizment, Ghislaine Scelo, Sean P. Cleary, Gloria M. Petersen, Joshua E. Muscat, Sara H. Olson, E. Fabianova, Paige M. Bracci, Manal M. Hassan, P. Ghadirian, William R. Bamlet, Anthony B. Miller, Steve Gallinger, Pagona Lagiou, Witold Zatonski, Donghui Li, H. Bas Bueno-de-Mesquita, Vladimir Janout, Eva Negri, Valentina Rosato, Peter A. Baghurst, Eric J. Duell, Patrick Maisonneuve, Cristina Bosetti, Diego Serraino, Rachel E. Neale, E. A. Holly, Ivana Holcatova, Dimitrios Trichopoulos, Elizabeth T. H. Fontham, Debra T. Silverman, Kristin E. Anderson, Paolo Boffetta, Lenka Foretova, Jerry Polesel, Ersilia Lucenteforte, Bosetti, C., Rosato, V., Li, D., Silverman, D., Petersen, G.M., Bracci, P.M., Neale, R.E., Muscat, J., Anderson, K., Gallinger, S., Olson, S.H., Miller, A.B., Bas Bueno-de-Mesquita, H., Scelo, G., Janout, V., Holcatova, I., Lagiou, P., Serraino, D., Lucenteforte, E., Fabianova, E., Ghadirian, P., Baghurst, P.A., Zatonski, W., Foretova, L., Fontham, E., Bamlet, W.R., Holly, E.A., Negri, E., Hassan, M., Prizment, A., Cotterchio, M., Cleary, S., Kurtz, R.C., Maisonneuve, P., Trichopoulos, D., Polesel, J., Duell, E.J., Boffetta, P., and La Vecchia, C.

Subjects
Adult, Male, medicine.medical_specialty, insulin, pancreatic cancer, oral antidiabetics, pancreatic cance r, Risk Factors, Diabetes mellitus, Internal medicine, Pancreatic cancer, medicine, Humans, Hypoglycemic Agents, Aged, Aged, 80 and over, 2. Zero hunger, diabetes, business.industry, Smoking, Absolute risk reduction, Cancer, Type 2 Diabetes Mellitus, case–control study, Hematology, Odds ratio, Original Articles, Middle Aged, medicine.disease, Confidence interval, pooled analysis, 3. Good health, Pancreatic Neoplasms, Logistic Models, Endocrinology, Diabetes Mellitus, Type 2, Oncology, diabete, Case-Control Studies, oral antidiabetic, Female, business, Body mass index
Abstract

BACKGROUND: Type 2 diabetes mellitus has been associated with an excess risk of pancreatic cancer, but the magnitude of the risk and the time-risk relationship are unclear, and there is limited information on the role of antidiabetic medications. PATIENTS AND METHODS: We analyzed individual-level data from 15 case-control studies within the Pancreatic Cancer Case-Control Consortium, including 8305 cases and 13 987 controls. Pooled odds ratios (ORs) were estimated from multiple logistic regression models, adjusted for relevant covariates. RESULTS: Overall, 1155 (15%) cases and 1087 (8%) controls reported a diagnosis of diabetes 2 or more years before cancer diagnosis (or interview, for controls), corresponding to an OR of 1.90 (95% confidence interval, CI, 1.72-2.09). Consistent risk estimates were observed across strata of selected covariates, including body mass index and tobacco smoking. Pancreatic cancer risk decreased with duration of diabetes, but a significant excess risk was still evident 20 or more years after diabetes diagnosis (OR 1.30, 95% CI 1.03-1.63). Among diabetics, long duration of oral antidiabetic use was associated with a decreased pancreatic cancer risk (OR 0.31, 95% CI 0.14-0.69, for =15 years). Conversely, insulin use was associated with a pancreatic cancer risk in the short term (OR 5.60, 95% CI 3.75-8.35, for

Published
2014

23. Cigarette smoking and pancreatic cancer : an analysis from the International Pancreatic Cancer Case-Control Consortium (PanC4)

Author

Yu-Tang Gao, Parviz Ghadirian, E. A. Holly, Michelle Cotterchio, C. La Vecchia, Gloria M. Petersen, Steven Gallinger, Donghui Li, Patrick Maisonneuve, Cristina Bosetti, Elizabeth T. H. Fontham, R. Talamini, H. B. Bueno-de-Mesquita, Sara H. Olson, Paola Bertuccio, Paige M. Bracci, Jerry Polesel, Bu Tian Ji, Ersilia Lucenteforte, Debra T. Silverman, William R. Bamlet, J. Su, Witold Zatonski, Paolo Boffetta, Eva Negri, Peter A. Baghurst, Robert C. Kurtz, Manal M. Hassan, Anthony B. Miller, Herbert Yu, Harvey A. Risch, Eric J. Duell, International Prevention Research Institute (IPRI), The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai [New York] (MSSM), Bosetti, C., Lucenteforte, E., Silverman, D.T., Petersen, G., Bracci, P.M., Ji, B.T., Negri, E., Li, D., Risch, H.A., Olson, S.H., Gallinger, S., Miller, A.B., Bueno-de-Mesquita, H.B., Talamini, R., Polesel, J., Ghadirian, P., Baghurst, P.A., Zatonski, W., Fontham, E., Bamlet, W.R., Holly, E.A., Bertuccio, P., Gao, Y.T., Hassan, M., Yu, H., Kurtz, R.C., Cotterchio, M., Su, J., Maisonneuve, P., Duell, E.J., Boffetta, P., and La Vecchia, C.

Subjects
medicine.medical_specialty, Multivariate analysis, analysi, pancreatic cancer, cigarette smoking, cancer, Sensitivity and Specificity, PANC4, Cigarette smoking, Internal medicine, Pancreatic cancer, Odds Ratio, medicine, case–control study, pooled analysis, Humans, and pancreatic, Case-Control Studies Humans Logistic Models Multivariate Analysis Odds Ratio Pancreatic Neoplasms/*etiology Sensitivity and Specificity Smoking/*adverse effects, Cigarette, Cancer, Pancreatic, business.industry, Smoking, Case-control study, Original Articles, Hematology, Odds ratio, medicine.disease, Former Smoker, Confidence interval, Surgery, Pancreatic Neoplasms, Case-Control, Logistic Models, Oncology, International, Case-Control Studies, Meta-analysis, Multivariate Analysis, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, Corrigendum, business, Consortium
Abstract

Bosetti, C Lucenteforte, E Silverman, D T Petersen, G Bracci, P M Ji, B T Negri, E Li, D Risch, H A Olson, S H Gallinger, S Miller, A B Bueno-de-Mesquita, H B Talamini, R Polesel, J Ghadirian, P Baghurst, P A Zatonski, W Fontham, E Bamlet, W R Holly, E A Bertuccio, P Gao, Y T Hassan, M Yu, H Kurtz, R C Cotterchio, M Su, J Maisonneuve, P Duell, E J Boffetta, P La Vecchia, C eng 5R01-CA098870/CA/NCI NIH HHS/ CA098889/CA/NCI NIH HHS/ CA108370/CA/NCI NIH HHS/ CA109767/CA/NCI NIH HHS/ CA59706/CA/NCI NIH HHS/ CA89726/CA/NCI NIH HHS/ N01-CP-05225/CP/NCI NIH HHS/ N01-CP-05227/CP/NCI NIH HHS/ N01-CP-31022/CP/NCI NIH HHS/ N01-CP-51089/CP/NCI NIH HHS/ N01-CP-51090/CP/NCI NIH HHS/ N01-CP-51092/CP/NCI NIH HHS/ N01-PC-35136/PC/NCI NIH HHS/ P50 CA102701/CA/NCI NIH HHS/ R01 CA97075/CA/NCI NIH HHS/ Canadian Institutes of Health Research/Canada Meta-Analysis Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't England 2011/11/23 06:00 Ann Oncol. 2012 Jul;23(7):1880-8. doi: 10.1093/annonc/mdr541. Epub 2011 Nov 21.; International audience; 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

Published
2012

24. Cigar and pipe smoking, smokeless tobacco use and pancreatic cancer: An analysis from the International Pancreatic Cancer Case-Control Consortium (PanC4)

Author

Witold Zatonski, Eva Negri, Elizabeth T. H. Fontham, Debra T. Silverman, Donghui Li, Eric J. Duell, Sara H. Olson, Michelle Cotterchio, H. B. Bueno-de-Mesquita, Steve Gallinger, Paige M. Bracci, Herbert Yu, Paolo Boffetta, E. A. Holly, Harvey A. Risch, Paola Bertuccio, William R. Bamlet, J. Su, C. La Vecchia, Jerry Polesel, Ersilia Lucenteforte, Gloria M. Petersen, Robert C. Kurtz, Peter A. Baghurst, Patrick Maisonneuve, Cristina Bosetti, Parviz Ghadirian, Manal M. Hassan, Anthony B. Miller, R. Talamini, Bertuccio, P., La Vecchia, C., Silverman, D.T., Petersen, G.M., Bracci, P.M., Negri, E., Li, D., Risch, H.A., Olson, S.H., Gallinger, S., Miller, A.B., Bueno-de-Mesquita, H.B., Talamini, R., Polesel, J., Ghadirian, P., Baghurst, P.A., Zatonski, W., Fontham, E.T., Bamlet, W.R., Holly, E.A., Lucenteforte, E., Hassan, M., Yu, H., Kurtz, R.C., Cotterchio, M., Su, J., Maisonneuve, P., Duell, E.J., Bosetti, C., and Boffetta, P.

Subjects
Oncology, Adult, Male, Risk, medicine.medical_specialty, Cigar Smoking, Pancreatic disease, Tobacco, Smokeless, pancreatic cancer, tobacco, smoking, cigar, pancreatic cancer, pooled analysis, smokeless tobacco, tobacco, pipe, Pancreatic cancer, Internal medicine, Epidemiology, medicine, Humans, cancer, education, Aged, Aged, 80 and over, Smoking pipe, education.field_of_study, business.industry, Cigar, technology, industry, and agriculture, Cancer, Hematology, Tobacco Use Disorder, Original Articles, smokeless tobacco, Middle Aged, medicine.disease, Surgery, Pancreatic Neoplasms, stomatognathic diseases, pipe, Smokeless tobacco, Case-Control Studies, pancreatic, Female, Biostatistics, pooled analysis, business
Abstract

Background: Cigarette smoking is the best-characterized risk factor for pancreatic cancer. However, data are limited for other tobacco smoking products and smokeless tobacco. Materials and methods: We conducted a pooled analysis of cigar and pipe smoking and smokeless tobacco use and risk of pancreatic cancer using data from 11 case-control studies (6056 cases and 11 338 controls) within the International Pancreatic Cancer Case-Control Consortium (PanC4). Pooled odds ratios (OR) and the corresponding 95% confidence intervals (CI) were estimated by unconditional multiple logistic regression models adjusted for study center and selected covariates. Results: Compared with never tobacco users, the OR for cigar-only smokers was 1.6 (95% CI: 1.2-2.3), i.e. comparable to that of cigarette-only smokers (OR 1.5; 95% CI 1.4-1.6). The OR was 1.1 (95% CI 0.69-1.6) for pipeonly smokers. There was some evidence of increasing risk with increasing amount of cigar smoked per day (OR 1.82 for = 10 grams of tobacco), although not with duration. The OR for ever smokeless tobacco users as compared with never tobacco users was 0.98 (95% CI 0.75-1.3). Conclusion: This collaborative analysis provides evidence that cigar smoking is associated with an excess risk of pancreatic cancer, while no significant association emerged for pipe smoking and smokeless tobacco use. © The Author 2011. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved.

Published
2011

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