87 results on '"Campbell P.T."'
Number of results to display per page
Search Results
2. Outcomes in Patients with Acute Cellular Rejection Grade 1R: Is the Debate Over?
- Author
-
Lampert, B., primary, Williams, C., additional, Montfort, J. Hernandez, additional, Obrien, R. Kursel, additional, Aggarwal-Gupta, C., additional, Ravichandran, A., additional, Rao, R., additional, Campbell, P.T., additional, Yaranov, D., additional, Carey, S., additional, Olymbios, M., additional, Armer-Cabral, M., additional, Zhang, Z., additional, and Hall, S., additional
- Published
- 2024
- Full Text
- View/download PDF
3. Beyond the Basics of Athletic Hip Evaluation
- Author
-
Ashley M. Campbell, P.T., D.P.T., S.C.S and Michael L. Voight, P.T., D.H.Sc., O.C.S., S.C.S., A.T.C., F.A.P.T.A.
- Subjects
Sports medicine ,RC1200-1245 - Abstract
Abstract: There is a growing trend in the world of orthopedics and sports medicine revolving around the nonarthritic hip. The incidence of hip arthroscopy has exponentially grown in the past decade and despite the importance of the recognition of these hip pathologies as contributors to pain and dysfunction, there is an ever-increasing rate of “failed” procedures emerging in the literature. The etiology of femoroacetabular impingement (FAI) syndrome and associated pathologies of the hip are now better understood. With this understanding there appears a tendency to point a finger at the hip joint without consideration for the involvement of the surrounding joints or extraarticular structures. Because of the nature of the morphological condition of FAI and the high incidence of a gradual progression of pain and impairments over time, as opposed to an acute injury, there is a need for a more robust assessment of the hip. The purpose of this commentary is to discuss the importance of a combined traditional orthopedic exam, imaging, and movement assessment in diagnosis and treatment recommendations in those with nonarthritic hip pain. It is our belief that this combined model can assist in identifying movement dysfunction that may lead to poor surgical outcomes and developing improved nonoperative or preoperative care pathways. Level of evidence: Level V.
- Published
- 2022
- Full Text
- View/download PDF
4. (789) - Outcomes in Patients with Acute Cellular Rejection Grade 1R: Is the Debate Over?
- Author
-
Lampert, B., Montfort, J. Hernandez, Obrien, R. Kursel, Aggarwal-Gupta, C., Ravichandran, A., Rao, R., Campbell, P.T., Yaranov, D., Carey, S., Olymbios, M., Armer-Cabral, M., Zhang, Z., and Hall, S.
- Published
- 2024
- Full Text
- View/download PDF
5. Beyond the Basics of Athletic Hip Evaluation
- Author
-
Ashley M. Campbell, P.T., D.P.T., S.C.S and Michael L. Voight, P.T., D.H.Sc., O.C.S., S.C.S., A.T.C., F.A.P.T.A.
- Subjects
musculoskeletal diseases ,Sports medicine ,Rehabilitation ,Public Health, Environmental and Occupational Health ,Physical Therapy, Sports Therapy and Rehabilitation ,Orthopedics and Sports Medicine ,RC1200-1245 - Abstract
There is a growing trend in the world of orthopedics and sports medicine revolving around the nonarthritic hip. The incidence of hip arthroscopy has exponentially grown in the past decade and despite the importance of the recognition of these hip pathologies as contributors to pain and dysfunction, there is an ever-increasing rate of “failed” procedures emerging in the literature. The etiology of femoroacetabular impingement (FAI) syndrome and associated pathologies of the hip are now better understood. With this understanding there appears a tendency to point a finger at the hip joint without consideration for the involvement of the surrounding joints or extraarticular structures. Because of the nature of the morphological condition of FAI and the high incidence of a gradual progression of pain and impairments over time, as opposed to an acute injury, there is a need for a more robust assessment of the hip. The purpose of this commentary is to discuss the importance of a combined traditional orthopedic exam, imaging, and movement assessment in diagnosis and treatment recommendations in those with nonarthritic hip pain. It is our belief that this combined model can assist in identifying movement dysfunction that may lead to poor surgical outcomes and developing improved nonoperative or preoperative care pathways. Level of evidence: Level V.
- Published
- 2021
6. Response to Li and Hopper.
- Author
-
Thomas M., Sakoda L.C., Hoffmeister M., Rosenthal E.A., Lee J.K., van Duijnhoven F.J.B., Platz E.A., Wu A.H., Dampier C.H., de la Chapelle A., Wolk A., Joshi A.D., Burnett-Hartman A., Gsur A., Lindblom A., Castells A., Win A.K., Namjou B., Van Guelpen B., Tangen C.M., He Q., Li C.I., Schafmayer C., Joshu C.E., Ulrich C.M., Bishop D.T., Buchanan D.D., Schaid D., Drew D.A., Muller D.C., Duggan D., Crosslin D.R., Albanes D., Giovannucci E.L., Larson E., Qu F., Mentch F., Giles G.G., Hakonarson H., Hampel H., Stanaway I.B., Figueiredo J.C., Huyghe J.R., Minnier J., Chang-Claude J., Hampe J., Harley J.B., Visvanathan K., Curtis K.R., Offit K., Li L., Le Marchand L., Vodickova L., Gunter M.J., Jenkins M.A., Slattery M.L., Lemire M., Woods M.O., Song M., Murphy N., Lindor N.M., Dikilitas O., Pharoah P.D.P., Campbell P.T., Newcomb P.A., Milne R.L., MacInnis R.J., Castellvi-Bel S., Ogino S., Berndt S.I., Bezieau S., Thibodeau S.N., Gallinger S.J., Zaidi S.H., Harrison T.A., Keku T.O., Hudson T.J., Vymetalkova V., Moreno V., Martin V., Arndt V., Wei W.-Q., Chung W., Su Y.-R., Hayes R.B., White E., Vodicka P., Casey G., Gruber S.B., Schoen R.E., Chan A.T., Potter J.D., Brenner H., Jarvik G.P., Corley D.A., Peters U., Hsu L., Thomas M., Sakoda L.C., Hoffmeister M., Rosenthal E.A., Lee J.K., van Duijnhoven F.J.B., Platz E.A., Wu A.H., Dampier C.H., de la Chapelle A., Wolk A., Joshi A.D., Burnett-Hartman A., Gsur A., Lindblom A., Castells A., Win A.K., Namjou B., Van Guelpen B., Tangen C.M., He Q., Li C.I., Schafmayer C., Joshu C.E., Ulrich C.M., Bishop D.T., Buchanan D.D., Schaid D., Drew D.A., Muller D.C., Duggan D., Crosslin D.R., Albanes D., Giovannucci E.L., Larson E., Qu F., Mentch F., Giles G.G., Hakonarson H., Hampel H., Stanaway I.B., Figueiredo J.C., Huyghe J.R., Minnier J., Chang-Claude J., Hampe J., Harley J.B., Visvanathan K., Curtis K.R., Offit K., Li L., Le Marchand L., Vodickova L., Gunter M.J., Jenkins M.A., Slattery M.L., Lemire M., Woods M.O., Song M., Murphy N., Lindor N.M., Dikilitas O., Pharoah P.D.P., Campbell P.T., Newcomb P.A., Milne R.L., MacInnis R.J., Castellvi-Bel S., Ogino S., Berndt S.I., Bezieau S., Thibodeau S.N., Gallinger S.J., Zaidi S.H., Harrison T.A., Keku T.O., Hudson T.J., Vymetalkova V., Moreno V., Martin V., Arndt V., Wei W.-Q., Chung W., Su Y.-R., Hayes R.B., White E., Vodicka P., Casey G., Gruber S.B., Schoen R.E., Chan A.T., Potter J.D., Brenner H., Jarvik G.P., Corley D.A., Peters U., and Hsu L.
- Published
- 2021
7. 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
8. Circulating adipokine concentrations and risk of five obesity-related cancers: A Mendelian randomization study.
- Author
-
Dimou N.L., Papadimitriou N., Mariosa D., Johansson M., Brennan P., Peters U., Chanock S.J., Purdue M., Bishop D.T., Gago-Dominquez M., Giles G.G., Moreno V., Platz E.A., Tangen C.M., Wolk A., Zheng W., Wu X., Campbell P.T., Giovannucci E., Lin Y., Gunter M.J., Murphy N., Dimou N.L., Papadimitriou N., Mariosa D., Johansson M., Brennan P., Peters U., Chanock S.J., Purdue M., Bishop D.T., Gago-Dominquez M., Giles G.G., Moreno V., Platz E.A., Tangen C.M., Wolk A., Zheng W., Wu X., Campbell P.T., Giovannucci E., Lin Y., Gunter M.J., and Murphy N.
- Abstract
Obesity is considered a chronic inflammatory state characterized by continued secretion of adipokines and cytokines. Experimental and epidemiological evidence indicates that circulating adipokines may be associated with the development of obesity-related cancers, but it is unclear if these associations are causal or confounded. We examined potential causal associations of specific adipokines (adiponectin, leptin, soluble leptin receptor [sOB-R] and plasminogen activator inhibitor-1 [PAI-1]) with five obesity-related cancers (colorectal, pancreatic, renal cell carcinoma [RCC], ovarian and endometrial) using Mendelian randomization (MR) methods. We used summary-level data from large genetic consortia for 114 530 cancer cases and 245 284 controls. We constructed genetic instruments using 18 genetic variants for adiponectin, 2 for leptin and 4 for both sOB-R and PAI-1 (P value for inclusion<5 x 10-8). Causal estimates were obtained using two-sample MR methods. In the inverse-variance weighted models, we found an inverse association between adiponectin and risk of colorectal cancer (odds ratio per 1 mug/mL increment in adiponectin concentration: 0.90 [95% confidence interval = 0.84-0.97]; P =.01); but, evidence of horizontal pleiotropy was detected and the association was not present when this was taken into consideration. No association was found for adiponectin and risks of pancreatic cancer, RCC, ovarian cancer and endometrial cancer. Leptin, sOB-R and PAI-1 were also similarly unrelated to risk of obesity-related cancers. Despite the large sample size, our MR analyses do not support causal effects of circulating adiponectin, leptin, sOB-R and PAI-1 concentrations on the development of five obesity-related cancers.Copyright © 2020 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of Union for International Cancer Control.
- Published
- 2021
9. Hepcidin-regulating iron metabolism genes and pancreatic ductal adenocarcinoma: a pathway analysis of genome-wide association studies.
- Author
-
Julian-Serrano S., Yuan F., Wheeler W., Benyamin B., Machiela M.J., Arslan A.A., Beane-Freeman L.E., Bracci P.M., Duell E.J., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Marchand L.L., Neale R.E., Shu X.-O., Van Den Eeden S.K., Visvanathan K., Zheng W., Albanes D., Andreotti G., Ardanaz E., Babic A., Berndt S.I., Brais L.K., Brennan P., Bueno-de-Mesquita B., Buring J.E., Chanock S.J., Childs E.J., Chung C.C., Fabianova E., Foretova L., Fuchs C.S., Gaziano J.M., Gentiluomo M., Giovannucci E.L., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holcatova I., Holly E.A., Hung R.I., Janout V., Kurtz R.C., Lee I.-M., Malats N., McKean D., Milne R.L., Newton C.C., Oberg A.L., Perdomo S., Peters U., Porta M., Rothman N., Schulze M.B., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., Weiderpass E., Wenstzensen N., White E., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Zhong J., Kraft P., Li D., Campbell P.T., Petersen G.M., Wolpin B.M., Risch H.A., Amundadottir L.T., Klein A.P., Yu K., Stolzenberg-Solomon R.Z., Julian-Serrano S., Yuan F., Wheeler W., Benyamin B., Machiela M.J., Arslan A.A., Beane-Freeman L.E., Bracci P.M., Duell E.J., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Marchand L.L., Neale R.E., Shu X.-O., Van Den Eeden S.K., Visvanathan K., Zheng W., Albanes D., Andreotti G., Ardanaz E., Babic A., Berndt S.I., Brais L.K., Brennan P., Bueno-de-Mesquita B., Buring J.E., Chanock S.J., Childs E.J., Chung C.C., Fabianova E., Foretova L., Fuchs C.S., Gaziano J.M., Gentiluomo M., Giovannucci E.L., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holcatova I., Holly E.A., Hung R.I., Janout V., Kurtz R.C., Lee I.-M., Malats N., McKean D., Milne R.L., Newton C.C., Oberg A.L., Perdomo S., Peters U., Porta M., Rothman N., Schulze M.B., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., Weiderpass E., Wenstzensen N., White E., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Zhong J., Kraft P., Li D., Campbell P.T., Petersen G.M., Wolpin B.M., Risch H.A., Amundadottir L.T., Klein A.P., Yu K., and Stolzenberg-Solomon R.Z.
- Abstract
BACKGROUND: Epidemiological studies have suggested positive associations for iron and red meat intake with risk of pancreatic ductal adenocarcinoma (PDAC). Inherited pathogenic variants in genes involved in the hepcidin-regulating iron metabolism pathway are known to cause iron overload and hemochromatosis. OBJECTIVE(S): The objective of this study was to determine whether common genetic variation in the hepcidin-regulating iron metabolism pathway is associated with PDAC. METHOD(S): We conducted a pathway analysis of the hepcidin-regulating genes using single nucleotide polymorphism (SNP) summary statistics generated from 4 genome-wide association studies in 2 large consortium studies using the summary data-based adaptive rank truncated product method. Our population consisted of 9253 PDAC cases and 12,525 controls of European descent. Our analysis included 11 hepcidin-regulating genes [bone morphogenetic protein 2 (BMP2), bone morphogenetic protein 6 (BMP6), ferritin heavy chain 1 (FTH1), ferritin light chain (FTL), hepcidin (HAMP), homeostatic iron regulator (HFE), hemojuvelin (HJV), nuclear factor erythroid 2-related factor 2 (NRF2), ferroportin 1 (SLC40A1), transferrin receptor 1 (TFR1), and transferrin receptor 2 (TFR2)] and their surrounding genomic regions (+/-20 kb) for a total of 412 SNPs. RESULT(S): The hepcidin-regulating gene pathway was significantly associated with PDAC (P = 0.002), with the HJV, TFR2, TFR1, BMP6, and HAMP genes contributing the most to the association. CONCLUSION(S): Our results support that genetic susceptibility related to the hepcidin-regulating gene pathway is associated with PDAC risk and suggest a potential role of iron metabolism in pancreatic carcinogenesis. Further studies are needed to evaluate effect modification by intake of iron-rich foods on this association.Copyright Published by Oxford University Press on behalf of the American Society for Nutrition 2021.
- Published
- 2021
10. Genetically predicted circulating c-reactive protein concentration and colorectal cancer survival: A mendelian randomization consortium study.
- Author
-
Hua X., Dai J.Y., Lindstrom S., Harrison T.A., Lin Y., Alberts S.R., Alwers E., Berndt S.I., Brenner H., Buchanan D.D., Campbell P.T., Casey G., Chang-Claude J., Gallinger S., Giles G.G., Goldberg R.M., Gunter M.J., Hoffmeister M., Jenkins M.A., Joshi A.D., Ma W., Milne R.L., Murphy N., Pai R.K., Sakoda L.C., Schoen R.E., Shi Q., Slattery M.L., Song M., White E., Le Marchand L., Chan A.T., Peters U., Newcomb P.A., Hua X., Dai J.Y., Lindstrom S., Harrison T.A., Lin Y., Alberts S.R., Alwers E., Berndt S.I., Brenner H., Buchanan D.D., Campbell P.T., Casey G., Chang-Claude J., Gallinger S., Giles G.G., Goldberg R.M., Gunter M.J., Hoffmeister M., Jenkins M.A., Joshi A.D., Ma W., Milne R.L., Murphy N., Pai R.K., Sakoda L.C., Schoen R.E., Shi Q., Slattery M.L., Song M., White E., Le Marchand L., Chan A.T., Peters U., and Newcomb P.A.
- Abstract
Background: A positive association between circulating Creactive protein (CRP) and colorectal cancer survival was reported in observational studies, which are susceptible to unmeasured confounding and reverse causality.Weused a Mendelian randomization approach to evaluate the association between genetically predicted CRP concentrations and colorectal cancer-specific survival. Method(s): We used individual-level data for 16,918 eligible colorectal cancer cases of European ancestry from 15 studies within the International Survival Analysis of Colorectal Cancer Consortium. Wecalculated a genetic-risk score based on 52 CRP-associated genetic variants identified from genome-wide association studies. Because of the non-collapsibility of hazard ratios from Cox proportional hazards models, we used the additive hazards model to calculate hazard differences (HD) and 95% confidence intervals (CI) for the association between genetically predicted CRP concentrations and colorectal cancer-specific survival, overall and by stage at diagnosis and tumor location. Analyses were adjusted for age at diagnosis, sex, body mass index, genotyping platform, study, and principal components. Result(s): Of the 5,395 (32%) deaths accrued over up to 10 years of follow-up, 3,808 (23%) were due to colorectal cancer. Genetically predicted CRP concentration was not associated with colorectal cancer-specific survival (HD, 1.15; 95% CI, 2.76 to 0.47 per 100,000 person-years; P = 0.16). Similarly, no associations were observed in subgroup analyses by stage at diagnosis or tumor location. Conclusion(s): Despite adequate power to detect moderate associations, our results did not support a causal effect of circulating CRP concentrations on colorectal cancer-specific survival.Copyright © 2021 American Association for Cancer Research Inc.. All rights reserved.
- Published
- 2021
11. 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
12. Association of body mass index with colorectal cancer risk by genome-wide variants.
- Author
-
Giles G.G., Lin Y., Bien S.A., Figueiredo J.C., Harrison T.A., Guinter M.A., Berndt S.I., Brenner H., Chan A.T., Chang-Claude J., Gallinger S.J., Gapstur S.M., Campbell P.T., Giovannucci E., Gruber S.B., Gunter M., Ogino S., Potter J.D., Rennert G., Rennert H.S., Robinson J., Sakoda L.C., Slattery M.L., Song Y., White E., Woods M.O., Casey G., Hsu L., Peters U., Hoffmeister M., Jacobs E.J., Jenkins M.A., Le Marchand L., Li L., McLaughlin J.R., Murphy N., Milne R.L., Newcomb P.A., Newton C., Giles G.G., Lin Y., Bien S.A., Figueiredo J.C., Harrison T.A., Guinter M.A., Berndt S.I., Brenner H., Chan A.T., Chang-Claude J., Gallinger S.J., Gapstur S.M., Campbell P.T., Giovannucci E., Gruber S.B., Gunter M., Ogino S., Potter J.D., Rennert G., Rennert H.S., Robinson J., Sakoda L.C., Slattery M.L., Song Y., White E., Woods M.O., Casey G., Hsu L., Peters U., Hoffmeister M., Jacobs E.J., Jenkins M.A., Le Marchand L., Li L., McLaughlin J.R., Murphy N., Milne R.L., Newcomb P.A., and Newton C.
- Abstract
Background: Body mass index (BMI) is a complex phenotype that may interact with genetic variants to influence colorectal cancer risk. Method(s): We tested multiplicative statistical interactions between BMI (per 5 kg/m2) and approximately 2.7 million single nucleotide polymorphisms with colorectal cancer risk among 14 059 colorectal cancer case (53.2% women) and 14 416 control (53.8% women) participants. All analyses were stratified by sex a priori. Statistical methods included 2-step (ie, Cocktail method) and single-step (ie, case-control logistic regression and a joint 2-degree of freedomtest) procedures. All statistical tests were two-sided. Result(s): Each 5 kg/m2 increase in BMI was associated with higher risks of colorectal cancer, less so for women (odds ratio [OR] = 1.14, 95% confidence intervals [CI] = 1.11 to 1.18; P = 9.75 x 10-17) than for men (OR = 1.26, 95% CI = 1.20 to 1.32; P = 2.13 x 10-24). The 2-step Cocktail method identified an interaction for women, but not men, between BMI and a SMAD7 intronic variant at 18q21.1 (rs4939827; Pobserved = .0009; Pthreshold = .005). A joint 2-degree of freedom test was consistent with this finding for women (joint P = 2.43 x 10-10). Each 5 kg/m2 increase in BMI was more strongly associated with colorectal cancer risk for women with the rs4939827-CC genotype (OR = 1.24, 95% CI = 1.16 to 1.32; P = 2.60 x 10-10) than for women with the CT (OR = 1.14, 95% CI = 1.09 to 1.19; P = 1.04 x 10-8) or TT (OR = 1.07, 95% CI = 1.01 to 1.14; P = .02) genotypes. Conclusion(s): These results provide novel insights on a potential mechanism through which a SMAD7 variant, previously identified as a susceptibility locus for colorectal cancer, and BMI may influence colorectal cancer risk for women.Copyright © The Author(s) 2020.
- Published
- 2021
13. Genetically predicted circulating concentrations of micronutrients and risk of colorectal cancer among individuals of European descent: a Mendelian randomization study.
- Author
-
Hampe J., Zuber V., Cross A.J., Perez-Cornago A., Hunter D.J., van Duijnhoven F.J.B., Albanes D., Arndt V., Berndt S.I., Bezieau S., Bishop D.T., Boehm J., Brenner H., Burnett-Hartman A., Campbell P.T., Casey G., Castellvi-Bel S., Chan A.T., Chang-Claude J., de la Chapelle A., Figueiredo J.C., Gallinger S.J., Giles G.G., Goodman P.J., Gsur A., Markozannes G., Hampel H., Hoffmeister M., Jenkins M.A., Keku T.O., Kweon S.-S., Larsson S.C., Le Marchand L., Li C.I., Li L., Lindblom A., Martin V., Milne R.L., Moreno V., Nan H., Nassir R., Newcomb P.A., Offit K., Pharoah P.D.P., Platz E.A., Potter J.D., Qi L., Rennert G., Sakoda L.C., Schafmayer C., Slattery M.L., Snetselaar L., Schenk J., Thibodeau S.N., Ulrich C.M., Van Guelpen B., Harlid S., Visvanathan K., Vodickova L., Wang H., White E., Wolk A., Woods M.O., Wu A.H., Zheng W., Bueno-de-Mesquita B., Boutron-Ruault M.-C., Hughes D.J., Jakszyn P., Kuhn T., Palli D., Riboli E., Giovannucci E.L., Banbury B.L., Gruber S.B., Peters U., Gunter M.J., Tsilidis K.K., Papadimitriou N., Dimou N., Gill D., Lewis S.J., Martin R.M., Murphy N., Burrows K., Lopez D.S., Key T.J., Travis R.C., Hampe J., Zuber V., Cross A.J., Perez-Cornago A., Hunter D.J., van Duijnhoven F.J.B., Albanes D., Arndt V., Berndt S.I., Bezieau S., Bishop D.T., Boehm J., Brenner H., Burnett-Hartman A., Campbell P.T., Casey G., Castellvi-Bel S., Chan A.T., Chang-Claude J., de la Chapelle A., Figueiredo J.C., Gallinger S.J., Giles G.G., Goodman P.J., Gsur A., Markozannes G., Hampel H., Hoffmeister M., Jenkins M.A., Keku T.O., Kweon S.-S., Larsson S.C., Le Marchand L., Li C.I., Li L., Lindblom A., Martin V., Milne R.L., Moreno V., Nan H., Nassir R., Newcomb P.A., Offit K., Pharoah P.D.P., Platz E.A., Potter J.D., Qi L., Rennert G., Sakoda L.C., Schafmayer C., Slattery M.L., Snetselaar L., Schenk J., Thibodeau S.N., Ulrich C.M., Van Guelpen B., Harlid S., Visvanathan K., Vodickova L., Wang H., White E., Wolk A., Woods M.O., Wu A.H., Zheng W., Bueno-de-Mesquita B., Boutron-Ruault M.-C., Hughes D.J., Jakszyn P., Kuhn T., Palli D., Riboli E., Giovannucci E.L., Banbury B.L., Gruber S.B., Peters U., Gunter M.J., Tsilidis K.K., Papadimitriou N., Dimou N., Gill D., Lewis S.J., Martin R.M., Murphy N., Burrows K., Lopez D.S., Key T.J., and Travis R.C.
- Abstract
BACKGROUND: The literature on associations of circulating concentrations of minerals and vitamins with risk of colorectal cancer is limited and inconsistent. Evidence from randomized controlled trials (RCTs) to support the efficacy of dietary modification or nutrient supplementation for colorectal cancer prevention is also limited. OBJECTIVE(S): To complement observational and RCT findings, we investigated associations of genetically predicted concentrations of 11 micronutrients (beta-carotene, calcium, copper, folate, iron, magnesium, phosphorus, selenium, vitamin B-6, vitamin B-12, and zinc) with colorectal cancer risk using Mendelian randomization (MR). METHOD(S): Two-sample MR was conducted using 58,221 individuals with colorectal cancer and 67,694 controls from the Genetics and Epidemiology of Colorectal Cancer Consortium, Colorectal Cancer Transdisciplinary Study, and Colon Cancer Family Registry. Inverse variance-weighted MR analyses were performed with sensitivity analyses to assess the impact of potential violations of MR assumptions. RESULT(S): Nominally significant associations were noted for genetically predicted iron concentration and higher risk of colon cancer [ORs per SD (ORSD): 1.08; 95% CI: 1.00, 1.17; P value=0.05] and similarly for proximal colon cancer, and for vitamin B-12 concentration and higher risk of colorectal cancer (ORSD: 1.12; 95% CI: 1.03, 1.21; P value=0.01) and similarly for colon cancer. A nominally significant association was also noted for genetically predicted selenium concentration and lower risk of colon cancer (ORSD: 0.98; 95% CI: 0.96, 1.00; P value=0.05) and similarly for distal colon cancer. These associations were robust to sensitivity analyses. Nominally significant inverse associations were observed for zinc and risk of colorectal and distal colon cancers, but sensitivity analyses could not be performed. None of these findings survived correction for multiple testing. Genetically predicted concentrations of beta-caroten
- Published
- 2021
14. Salicylic acid and risk of colorectal cancer: A two-sample mendelian randomization study.
- Author
-
Nounu A., Richmond R.C., Stewart I.D., Surendran P., Wareham N.J., Butterworth A., Weinstein S.J., Albanes D., Baron J.A., Hopper J.L., Figueiredo J.C., Newcomb P.A., Lindor N.M., Casey G., Platz E.A., Marchand L.L., Ulrich C.M., Li C.I., van Dujinhoven F.J.B., Gsur A., Campbell P.T., Moreno V., Vodicka P., Vodickova L., Amitay E., Alwers E., Chang-Claude J., Sakoda L.C., Slattery M.L., Schoen R.E., Gunter M.J., Castellvi-Bel S., Kim H.-R., Kweon S.-S., Chan A.T., Li L., Zheng W., Bishop D.T., Buchanan D.D., Giles G.G., Gruber S.B., Rennert G., Stadler Z.K., Harrison T.A., Lin Y., Keku T.O., Woods M.O., Schafmayer C., Van Guelpen B., Gallinger S., Hampel H., Berndt S.I., Pharoah P.D.P., Lindblom A., Wolk A., Wu A.H., White E., Peters U., Drew D.A., Scherer D., Bermejo J.L., Brenner H., Hoffmeister M., Williams A.C., Relton C.L., Nounu A., Richmond R.C., Stewart I.D., Surendran P., Wareham N.J., Butterworth A., Weinstein S.J., Albanes D., Baron J.A., Hopper J.L., Figueiredo J.C., Newcomb P.A., Lindor N.M., Casey G., Platz E.A., Marchand L.L., Ulrich C.M., Li C.I., van Dujinhoven F.J.B., Gsur A., Campbell P.T., Moreno V., Vodicka P., Vodickova L., Amitay E., Alwers E., Chang-Claude J., Sakoda L.C., Slattery M.L., Schoen R.E., Gunter M.J., Castellvi-Bel S., Kim H.-R., Kweon S.-S., Chan A.T., Li L., Zheng W., Bishop D.T., Buchanan D.D., Giles G.G., Gruber S.B., Rennert G., Stadler Z.K., Harrison T.A., Lin Y., Keku T.O., Woods M.O., Schafmayer C., Van Guelpen B., Gallinger S., Hampel H., Berndt S.I., Pharoah P.D.P., Lindblom A., Wolk A., Wu A.H., White E., Peters U., Drew D.A., Scherer D., Bermejo J.L., Brenner H., Hoffmeister M., Williams A.C., and Relton C.L.
- Abstract
Salicylic acid (SA) has observationally been shown to decrease colorectal cancer (CRC) risk. Aspirin (acetylsalicylic acid, that rapidly deacetylates to SA) is an effective primary and secondary chemopreventive agent. Through a Mendelian randomization (MR) approach, we aimed to address whether levels of SA affected CRC risk, stratifying by aspirin use. A two-sample MR analysis was performed using GWAS summary statistics of SA (INTERVAL and EPIC-Norfolk, N = 14,149) and CRC (CCFR, CORECT, GECCO and UK Biobank, 55,168 cases and 65,160 controls). The DACHS study (4410 cases and 3441 controls) was used for replication and stratification of aspirin use. SNPs proxying SA were selected via three methods: (1) functional SNPs that influence the activity of aspirin-metabolising enzymes; (2) pathway SNPs present in enzymes' coding regions; and (3) genome-wide significant SNPs. We found no association between functional SNPs and SA levels. The pathway and genome-wide SNPs showed no association between SA and CRC risk (OR:1.03, 95% CI: 0.84-1.27 and OR: 1.08, 95% CI:0.86-1.34, respectively). Results remained unchanged upon aspirin use stratification. We found little evidence to suggest that an SD increase in genetically predicted SA protects against CRC risk in the general population and upon stratification by aspirin use.Copyright © 2021 by the authors. Li-censee MDPI, Basel, Switzerland.
- Published
- 2021
15. Genetically predicted circulating concentrations of micronutrients and risk of colorectal cancer among individuals of European descent: A Mendelian randomization study.
- Author
-
Tsilidis K.K., Papadimitriou N., Dimou N., Gill D., Lewis S.J., Martin R.M., Murphy N., Markozannes G., Zuber V., Cross A.J., Burrows K., Lopez D.S., Key T.J., Travis R.C., Perez-Cornago A., Hunter D.J., Van Duijnhoven F.J.B., Albanes D., Arndt V., Berndt S.I., Bezieau S., Bishop D.T., Boehm J., Brenner H., Burnett-Hartman A., Campbell P.T., Casey G., Castellvi-Bel S., Chan A.T., Chang-Claude J., De La Chapelle A., Figueiredo J.C., Gallinger S.J., Giles G.G., Goodman P.J., Gsur A., Hampe J., Hampel H., Hoffmeister M., Jenkins M.A., Keku T.O., Kweon S.-S., Larsson S.C., Le Marchand L., Li C.I., Li L., Lindblom A., Martin V., Milne R.L., Moreno V., Nan H., Nassir R., Newcomb P.A., Offit K., Pharoah P.D.P., Platz E.A., Potter J.D., Qi L., Rennert G., Sakoda L.C., Schafmayer C., Slattery M.L., Snetselaar L., Schenk J., Thibodeau S.N., Ulrich C.M., Van Guelpen B., Harlid S., Visvanathan K., Vodickova L., Wang H., White E., Wolk A., Woods M.O., Wu A.H., Zheng W., Bueno-De-Mesquita B., Boutron-Ruault M.-C., Hughes D.J., Jakszyn P., Kuhn T., Palli D., Riboli E., Giovannucci E.L., Banbury B.L., Gruber S.B., Peters U., Gunter M.J., Tsilidis K.K., Papadimitriou N., Dimou N., Gill D., Lewis S.J., Martin R.M., Murphy N., Markozannes G., Zuber V., Cross A.J., Burrows K., Lopez D.S., Key T.J., Travis R.C., Perez-Cornago A., Hunter D.J., Van Duijnhoven F.J.B., Albanes D., Arndt V., Berndt S.I., Bezieau S., Bishop D.T., Boehm J., Brenner H., Burnett-Hartman A., Campbell P.T., Casey G., Castellvi-Bel S., Chan A.T., Chang-Claude J., De La Chapelle A., Figueiredo J.C., Gallinger S.J., Giles G.G., Goodman P.J., Gsur A., Hampe J., Hampel H., Hoffmeister M., Jenkins M.A., Keku T.O., Kweon S.-S., Larsson S.C., Le Marchand L., Li C.I., Li L., Lindblom A., Martin V., Milne R.L., Moreno V., Nan H., Nassir R., Newcomb P.A., Offit K., Pharoah P.D.P., Platz E.A., Potter J.D., Qi L., Rennert G., Sakoda L.C., Schafmayer C., Slattery M.L., Snetselaar L., Schenk J., Thibodeau S.N., Ulrich C.M., Van Guelpen B., Harlid S., Visvanathan K., Vodickova L., Wang H., White E., Wolk A., Woods M.O., Wu A.H., Zheng W., Bueno-De-Mesquita B., Boutron-Ruault M.-C., Hughes D.J., Jakszyn P., Kuhn T., Palli D., Riboli E., Giovannucci E.L., Banbury B.L., Gruber S.B., Peters U., and Gunter M.J.
- Abstract
Background: The literature on associations of circulating concentrations of minerals and vitamins with risk of colorectal cancer is limited and inconsistent. Evidence from randomized controlled trials (RCTs) to support the efficacy of dietary modification or nutrient supplementation for colorectal cancer prevention is also limited. Objective(s): To complement observational and RCT findings, we investigated associations of genetically predicted concentrations of 11 micronutrients (beta-carotene, calcium, copper, folate, iron, magnesium, phosphorus, selenium, vitamin B-6, vitamin B-12, and zinc) with colorectal cancer risk using Mendelian randomization (MR). Method(s): Two-sample MR was conducted using 58,221 individuals with colorectal cancer and 67,694 controls from the Genetics and Epidemiology of Colorectal Cancer Consortium, Colorectal Cancer Transdisciplinary Study, and Colon Cancer Family Registry. Inverse variance-weighted MR analyses were performed with sensitivity analyses to assess the impact of potential violations of MR assumptions. Result(s): Nominally significant associations were noted for genetically predicted iron concentration and higher risk of colon cancer [ORs per SD (ORSD): 1.08 95% CI: 1.00, 1.17 P value = 0.05] and similarly for proximal colon cancer, and for vitamin B-12 concentration and higher risk of colorectal cancer (ORSD: 1.12 95% CI: 1.03, 1.21 P value = 0.01) and similarly for colon cancer. A nominally significant association was also noted for genetically predicted selenium concentration and lower risk of colon cancer (ORSD: 0.98 95% CI: 0.96, 1.00 P value = 0.05) and similarly for distal colon cancer. These associations were robust to sensitivity analyses. Nominally significant inverse associations were observed for zinc and risk of colorectal and distal colon cancers, but sensitivity analyses could not be performed. None of these findings survived correction for multiple testing. Genetically predicted concentrations of beta-caroten
- Published
- 2021
16. Postmenopausal hormone therapy and colorectal cancer risk by molecularly defined subtypes and tumor location.
- Author
-
Labadie J.D., Harrison T.A., Banbury B., Amtay E.L., Bernd S., Brenner H., Buchanan D.D., Campbell P.T., Cao Y., Chan A.T., Chang-Claude J., Englishc D., Figueiredo J.C., Gallingerc S.J., Gilesc G.G., Gunter M.J., Hoffmeisterc M., Hsu L., Jenkins M.A., Lin Y., Milnec R.L., Moreno V., Murphyc N., Ogino S., Phipps A.I., Sakoda L.C., Slattery M.L., Southey M.C., Sun W., Thibodeau S.N., Van Guelpen B., Zaidi S.H., Peters U., Newcomb P.A., Labadie J.D., Harrison T.A., Banbury B., Amtay E.L., Bernd S., Brenner H., Buchanan D.D., Campbell P.T., Cao Y., Chan A.T., Chang-Claude J., Englishc D., Figueiredo J.C., Gallingerc S.J., Gilesc G.G., Gunter M.J., Hoffmeisterc M., Hsu L., Jenkins M.A., Lin Y., Milnec R.L., Moreno V., Murphyc N., Ogino S., Phipps A.I., Sakoda L.C., Slattery M.L., Southey M.C., Sun W., Thibodeau S.N., Van Guelpen B., Zaidi S.H., Peters U., and Newcomb P.A.
- Abstract
Background: Postmenopausal hormone therapy (HT) is associated with a decreased colorectal cancer (CRC) risk. As CRC is a heterogeneous disease, we evaluated whether the association of HT and CRC differs across etiologically relevant, molecularly defined tumor subtypes and tumor location. Method(s): We pooled data on tumor subtypes (microsatellite instability status, CpG island methylator phenotype status, BRAF and KRAS mutations, pathway: Adenoma-carcinoma, alternate, serrated), tumor location (proximal colon, distal colon, rectum), and HT use among 8220 postmenopausal women (3898 CRC cases and 4322 controls) from 8 observational studies. We used multinomial logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CIs) for the association of ever vs never HT use with each tumor subtype compared with controls. Models were adjusted for study, age, body mass index, smoking status, and CRC family history. All statistical tests were 2- sided. Result(s): Among postmenopausal women, ever HT use was associated with a 38% reduction in overall CRC risk (OR =0.62, 95% CI = 0.56 to 0.69). This association was similar according to microsatellite instability, CpG island methylator phenotype and BRAF or KRAS status. However, the association was attenuated for tumors arising through the serrated pathway (OR = 0.81, 95% CI = 0.66 to 1.01) compared with the adenoma-carcinoma pathway (OR = 0.63, 95% CI = 0.55 to 0.73; Phet =.04) and alternate pathway (OR = 0.61, 95% CI = 0.51 to 0.72). Additionally, proximal colon tumors had a weaker association (OR = 0.71, 95% CI = 0.62 to 0.80) compared with rectal (OR = 0.54, 95% CI = 0.46 to 0.63) and distal colon (OR = 0.57, 95% CI = 0.49 to 0.66; Phet =.01) tumors. Conclusion(s): We observed a strong inverse association between HT use and overall CRC risk, which may predominantly reflect a benefit of HT use for tumors arising through the adenoma-carcinoma and alternate pathways as well as distal colon and rectal tumors.Copy
- Published
- 2021
17. A combined proteomics and mendelian randomization approach to investigate the effects of aspirin-targeted proteins on colorectal cancer.
- Author
-
Pharoah P.D.P., Nounu A., Greenhough A., Heesom K.J., Richmond R.C., Zheng J., Weinstein S.J., Albanes D., Gallinger S., Hampel H., Berndt S.I., Lindblom A., Wolk A., Wu A.H., White E., Peters U., Drew D.A., Scherer D., Bermejo J.L., Williams A.C., Relton C.L., Baron J.A., Hopper J.L., Figueiredo J.C., Newcomb P.A., Lindor N.M., Casey G., Platz E.A., Le Marchand L., Ulrich C.M., Li C.I., van Duijnhoven F.J.B., Gsur A., Campbell P.T., Moreno V., Vodicka P., Vodickova L., Brenner H., Chang-Claude J., Hoffmeister M., Sakoda L.C., Slattery M.L., Schoen R.E., Gunter M.J., Castellvi-Bel S., Kim H.R., Kweon S.-S., Chan A.T., Li L., Zheng W., Bishop D.T., Buchanan D.D., Giles G.G., Gruber S.B., Rennert G., Stadler Z.K., Harrison T.A., Lin Y., Keku T.O., Woods M.O., Schafmayer C., van Guelpen B., Pharoah P.D.P., Nounu A., Greenhough A., Heesom K.J., Richmond R.C., Zheng J., Weinstein S.J., Albanes D., Gallinger S., Hampel H., Berndt S.I., Lindblom A., Wolk A., Wu A.H., White E., Peters U., Drew D.A., Scherer D., Bermejo J.L., Williams A.C., Relton C.L., Baron J.A., Hopper J.L., Figueiredo J.C., Newcomb P.A., Lindor N.M., Casey G., Platz E.A., Le Marchand L., Ulrich C.M., Li C.I., van Duijnhoven F.J.B., Gsur A., Campbell P.T., Moreno V., Vodicka P., Vodickova L., Brenner H., Chang-Claude J., Hoffmeister M., Sakoda L.C., Slattery M.L., Schoen R.E., Gunter M.J., Castellvi-Bel S., Kim H.R., Kweon S.-S., Chan A.T., Li L., Zheng W., Bishop D.T., Buchanan D.D., Giles G.G., Gruber S.B., Rennert G., Stadler Z.K., Harrison T.A., Lin Y., Keku T.O., Woods M.O., Schafmayer C., and van Guelpen B.
- Abstract
Background: Evidence for aspirin's chemopreventative properties on colorectal cancer (CRC) is substantial, but its mechanism of action is not well-understood. We combined a proteomic approach with Mendelian randomization (MR) to identify possible new aspirin targets that decrease CRC risk. Method(s): Human colorectal adenoma cells (RG/C2) were treated with aspirin (24 hours) and a stable isotope labeling with amino acids in cell culture (SILAC) based proteomics approach identified altered protein expression. Protein quantitative trait loci (pQTLs) from INTERVAL (N 1/4 3,301) and expression QTLs (eQTLs) from the eQTLGen Consortium (N 1/4 31,684) were used as genetic proxies for protein and mRNA expression levels. Two-sample MR of mRNA/protein expression on CRC risk was performed using eQTL/pQTL data combined with CRC genetic summary data from the Colon Cancer Family Registry (CCFR), Colorectal Transdisciplinary (CORECT), Genetics and Epidemiology of Colorectal Cancer (GECCO) consortia and UK Biobank (55,168 cases and 65,160 controls). Result(s): Altered expression was detected for 125/5886 proteins. Of these, aspirin decreased MCM6, RRM2, and ARFIP2 expression, and MR analysis showed that a standard deviation increase in mRNA/protein expression was associated with increased CRC risk (OR: 1.08, 95% CI, 1.03-1.13; OR: 3.33, 95% CI, 2.46-4.50; and OR: 1.15, 95% CI, 1.02-1.29, respectively). Conclusion(s): MCM6 and RRM2 are involved in DNA repair whereby reduced expression may lead to increased DNA aberrations and ultimately cancer cell death, whereas ARFIP2 is involved in actin cytoskeletal regulation, indicating a possible role in aspirin's reduction of metastasis. Impact: Our approach has shown how laboratory experiments and population-based approaches can combine to identify aspirin-targeted proteins possibly affecting CRC risk.Copyright ©2020 American Association for Cancer Research.
- Published
- 2021
18. Mismatch repair polymorphisms and risk of colon cancer, tumour microsatellite instability and interactions with lifestyle factors
- Author
-
Campbell, P.T., Curtin, K., Ulrich, C.M., Samowitz, W.S., Bigler, J., Velicer, C.M., Caan, B., Potter, J.D., and Slattery, M.L.
- Subjects
Colon cancer -- Genetic aspects ,Colon cancer -- Risk factors ,Colon cancer -- Research ,Gene mutations -- Research ,Life style -- Health aspects ,Life style -- Research ,Health - Published
- 2009
19. Circulating bilirubin levels and risk of colorectal cancer: serological and Mendelian randomization analyses
- Author
-
Seyed Khoei, N., Jenab, M., Murphy, N., Banbury, B.L., Carreras-Torres, R., Viallon, V., Kühn, T., Bueno-de-Mesquita, B., Aleksandrova, K., Cross, A.J., Weiderpass, E., Stepien, M., Bulmer, A., Tjønneland, A., Boutron-Ruault, M.C., Severi, G., Carbonnel, F., Katzke, V., Boeing, H., Bergmann, M.M., Trichopoulou, A., Karakatsani, A., Martimianaki, G., Palli, D., Tagliabue, G., Panico, S., Tumino, R., Sacerdote, C., Skeie, G., Merino, S., Bonet, C., Rodríguez-Barranco, M., Gil, L., Chirlaque, M.D., Ardanaz, E., Myte, R., Hultdin, J., Perez-Cornago, A., Aune, D., Tsilidis, K.K., Albanes, D., Baron, J.A., Berndt, S.I., Bézieau, S., Brenner, H., Campbell, P.T., Casey, G., Chang-Claude, J., Chanock, S.J., Cotterchio, M., Gallinger, S., Gruber, S.B., Haile, R.W., Hampe, J., Hoffmeister, M., Hopper, J.L., Hsu, L., Huyghe, J.R., Jenkins, M.A., Joshi, A.D., Kampman, E., Larsson, S.C., Le Marchand, L., Li, C.I., Li, L., Lindblom, A., Lindor, N.M., Martín, V., Moreno, V., Newcomb, P.A., Offit, K., Ogino, S., Parfrey, P.S., Pharoah, P.D.P., Rennert, G., Sakoda, L.C., Schafmayer, C., Schmit, S.L., Schoen, R.E., Slattery, M.L., Thibodeau, S.N., Ulrich, C.M., van Duijnhoven, F.J.B., Weigl, K., Weinstein, S.J., White, E., Wolk, A., Woods, M.O., Wu, A.H., Zhang, X., Ferrari, P., Anton, G., Peters, A., Peters, U., Gunter, M.J., Wagner, K.H., and Freisling, H.
- Subjects
Bilirubin ,Cancer ,Colorectal Cancer ,Anti-oxidants ,Mendelian Randomization Analysis - Abstract
Background Bilirubin, a byproduct of hemoglobin breakdown and purported anti-oxidant, is thought to be cancer preventive. We conducted complementary serological and Mendelian randomization (MR) analyses to investigate whether alterations in circulating levels of bilirubin are associated with risk of colorectal cancer (CRC). We decided a priori to perform analyses separately in men and women based on suggestive evidence that associations may differ by sex. Methods In a case-control study nested in the European Prospective Investigation into Cancer and Nutrition (EPIC), pre-diagnostic unconjugated bilirubin (UCB, the main component of total bilirubin) concentrations were measured by high-performance liquid chromatography in plasma samples of 1386 CRC cases and their individually matched controls. Additionally, 115 single-nucleotide polymorphisms (SNPs) robustly associated (P < 5 x 10(-8)) with circulating total bilirubin were instrumented in a 2-sample MR to test for a potential causal effect of bilirubin on CRC risk in 52,775 CRC cases and 45,940 matched controls in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), the Colon Cancer Family Registry (CCFR), and the Colorectal Transdisciplinary (CORECT) study. Results The associations between circulating UCB levels and CRC risk differed by sex (P-heterogeneity = 0.008). Among men, higher levels of UCB were positively associated with CRC risk (odds ratio [OR] = 1.19, 95% confidence interval [CI] = 1.04-1.36; per 1-SD increment of log-UCB). In women, an inverse association was observed (OR = 0.86 (0.76-0.97)). In the MR analysis of the mainUGT1A1SNP (rs6431625), genetically predicted higher levels of total bilirubin were associated with a 7% increase in CRC risk in men (OR = 1.07 (1.02-1.12);P = 0.006; per 1-SD increment of total bilirubin), while there was no association in women (OR = 1.01 (0.96-1.06);P = 0.73). Raised bilirubin levels, predicted by instrumental variables excluding rs6431625, were suggestive of an inverse association with CRC in men, but not in women. These differences by sex did not reach formal statistical significance (P-heterogeneity >= 0.2). Conclusions Additional insight into the relationship between circulating bilirubin and CRC is needed in order to conclude on a potential causal role of bilirubin in CRC development.
- Published
- 2020
20. Circulating bilirubin levels and risk of colorectal cancer: Serological and Mendelian randomization analyses
- Author
-
Seyed Khoei, N. Jenab, M. Murphy, N. Banbury, B.L. Carreras-Torres, R. Viallon, V. Kühn, T. Bueno-De-Mesquita, B. Aleksandrova, K. Cross, A.J. Weiderpass, E. Stepien, M. Bulmer, A. Tjønneland, A. Boutron-Ruault, M.-C. Severi, G. Carbonnel, F. Katzke, V. Boeing, H. Bergmann, M.M. Trichopoulou, A. Karakatsani, A. Martimianaki, G. Palli, D. Tagliabue, G. Panico, S. Tumino, R. Sacerdote, C. Skeie, G. Merino, S. Bonet, C. Rodríguez-Barranco, M. Gil, L. Chirlaque, M.-D. Ardanaz, E. Myte, R. Hultdin, J. Perez-Cornago, A. Aune, D. Tsilidis, K.K. Albanes, D. Baron, J.A. Berndt, S.I. Bézieau, S. Brenner, H. Campbell, P.T. Casey, G. Chan, A.T. Chang-Claude, J. Chanock, S.J. Cotterchio, M. Gallinger, S. Gruber, S.B. Haile, R.W. Hampe, J. Hoffmeister, M. Hopper, J.L. Hsu, L. Huyghe, J.R. Jenkins, M.A. Joshi, A.D. Kampman, E. Larsson, S.C. Le Marchand, L. Li, C.I. Li, L. Lindblom, A. Lindor, N.M. Martín, V. Moreno, V. Newcomb, P.A. Offit, K. Ogino, S. Parfrey, P.S. Pharoah, P.D.P. Rennert, G. Sakoda, L.C. Schafmayer, C. Schmit, S.L. Schoen, R.E. Slattery, M.L. Thibodeau, S.N. Ulrich, C.M. Van Duijnhoven, F.J.B. Weigl, K. Weinstein, S.J. White, E. Wolk, A. Woods, M.O. Wu, A.H. Zhang, X. Ferrari, P. Anton, G. Peters, A. Peters, U. Gunter, M.J. Wagner, K.-H. Freisling, H.
- Abstract
Background: Bilirubin, a byproduct of hemoglobin breakdown and purported anti-oxidant, is thought to be cancer preventive. We conducted complementary serological and Mendelian randomization (MR) analyses to investigate whether alterations in circulating levels of bilirubin are associated with risk of colorectal cancer (CRC). We decided a priori to perform analyses separately in men and women based on suggestive evidence that associations may differ by sex. Methods: In a case-control study nested in the European Prospective Investigation into Cancer and Nutrition (EPIC), pre-diagnostic unconjugated bilirubin (UCB, the main component of total bilirubin) concentrations were measured by high-performance liquid chromatography in plasma samples of 1386 CRC cases and their individually matched controls. Additionally, 115 single-nucleotide polymorphisms (SNPs) robustly associated (P < 5 × 10-8) with circulating total bilirubin were instrumented in a 2-sample MR to test for a potential causal effect of bilirubin on CRC risk in 52,775 CRC cases and 45,940 matched controls in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), the Colon Cancer Family Registry (CCFR), and the Colorectal Transdisciplinary (CORECT) study. Results: The associations between circulating UCB levels and CRC risk differed by sex (P heterogeneity = 0.008). Among men, higher levels of UCB were positively associated with CRC risk (odds ratio [OR] = 1.19, 95% confidence interval [CI] = 1.04-1.36; per 1-SD increment of log-UCB). In women, an inverse association was observed (OR = 0.86 (0.76-0.97)). In the MR analysis of the main UGT1A1 SNP (rs6431625), genetically predicted higher levels of total bilirubin were associated with a 7% increase in CRC risk in men (OR = 1.07 (1.02-1.12); P = 0.006; per 1-SD increment of total bilirubin), while there was no association in women (OR = 1.01 (0.96-1.06); P = 0.73). Raised bilirubin levels, predicted by instrumental variables excluding rs6431625, were suggestive of an inverse association with CRC in men, but not in women. These differences by sex did not reach formal statistical significance (P heterogeneity ≥ 0.2). Conclusions: Additional insight into the relationship between circulating bilirubin and CRC is needed in order to conclude on a potential causal role of bilirubin in CRC development. © 2020 The Author(s).
- Published
- 2020
21. Assessment of polygenic architecture and risk prediction based on common variants across fourteen cancers.
- Author
-
Houlston R., Choudhury P.P., Easton D.F., Milne R.L., Simard J., Hall P., Michailidou K., Dennis J., Schmidt M.K., Chang-Claude J., Gharahkhani P., Whiteman D., O'Mara T.A., Spurdle A.B., Thompson D.J., Tomlinson I., De Vivo I., Campbell P.T., Hoffmeister M., Jenkins M., Peters U., Hsu L., Gruber S.B., Casey G., Schmit S.L., Landi M.T., Law M.H., Iles M.M., Demenais F., Kumar R., MacGregor S., Bishop D.T., Ward S.V., Bondy M.L., Wiencke J.K., Melin B., Barnholtz-Sloan J., Kinnersley B., Wrensch M.R., Hung R.J., Caporaso N.E., Berndt S.I., Birmann B.M., Camp N.J., Kraft P., Rothman N., Slager S.L., Berchuck A., Pharoah P.D.P., Sellers T.A., Gayther S.A., Pearce C.L., Goode E.L., Schildkraut J.M., Moysich K.B., Amos C.I., Brennan P., McKay J., Amundadottir L.T., Jacobs E.J., Klein A.P., Petersen G.M., Risch H.A., Stolzenberg-Solomon R.Z., Wolpin B.M., Li D., Eeles R.A., Haiman C.A., Kote-Jarai Z., Schumacher F.R., Al Olama A.A., Purdue M.P., Scelo G., Dalgaard M.D., Greene M.H., Grotmol T., Kanetsky P.A., McGlynn K.A., Nathanson K.L., Turnbull C., Wiklund F., Chanock S.J., Chatterjee N., Garcia-Closas M., Zhang Y.D., Hurson A.N., Zhang H., Houlston R., Choudhury P.P., Easton D.F., Milne R.L., Simard J., Hall P., Michailidou K., Dennis J., Schmidt M.K., Chang-Claude J., Gharahkhani P., Whiteman D., O'Mara T.A., Spurdle A.B., Thompson D.J., Tomlinson I., De Vivo I., Campbell P.T., Hoffmeister M., Jenkins M., Peters U., Hsu L., Gruber S.B., Casey G., Schmit S.L., Landi M.T., Law M.H., Iles M.M., Demenais F., Kumar R., MacGregor S., Bishop D.T., Ward S.V., Bondy M.L., Wiencke J.K., Melin B., Barnholtz-Sloan J., Kinnersley B., Wrensch M.R., Hung R.J., Caporaso N.E., Berndt S.I., Birmann B.M., Camp N.J., Kraft P., Rothman N., Slager S.L., Berchuck A., Pharoah P.D.P., Sellers T.A., Gayther S.A., Pearce C.L., Goode E.L., Schildkraut J.M., Moysich K.B., Amos C.I., Brennan P., McKay J., Amundadottir L.T., Jacobs E.J., Klein A.P., Petersen G.M., Risch H.A., Stolzenberg-Solomon R.Z., Wolpin B.M., Li D., Eeles R.A., Haiman C.A., Kote-Jarai Z., Schumacher F.R., Al Olama A.A., Purdue M.P., Scelo G., Dalgaard M.D., Greene M.H., Grotmol T., Kanetsky P.A., McGlynn K.A., Nathanson K.L., Turnbull C., Wiklund F., Chanock S.J., Chatterjee N., Garcia-Closas M., Zhang Y.D., Hurson A.N., and Zhang H.
- Abstract
Genome-wide association studies (GWAS) have led to the identification of hundreds of susceptibility loci across cancers, but the impact of further studies remains uncertain. Here we analyse summary-level data from GWAS of European ancestry across fourteen cancer sites to estimate the number of common susceptibility variants (polygenicity) and underlying effect-size distribution. All cancers show a high degree of polygenicity, involving at a minimum of thousands of loci. We project that sample sizes required to explain 80% of GWAS heritability vary from 60,000 cases for testicular to over 1,000,000 cases for lung cancer. The maximum relative risk achievable for subjects at the 99th risk percentile of underlying polygenic risk scores (PRS), compared to average risk, ranges from 12 for testicular to 2.5 for ovarian cancer. We show that PRS have potential for risk stratification for cancers of breast, colon and prostate, but less so for others because of modest heritability and lower incidence.Copyright © 2020, This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply.
- Published
- 2020
22. Association Between Molecular Subtypes of Colorectal Tumors and Patient Survival, Based on Pooled Analysis of 7 International Studies.
- Author
-
Slattery M.L., Song M., Peters U., Hoffmeister M., Zaidi S.H., Phipps A.I., Ogino S., Alwers E., Harrison T., Banbury B., Brenner H., Campbell P.T., Chang-Claude J., Buchanan D., Chan A.T., Farris A.B., Figueiredo J.C., Gallinger S., Giles G.G., Jenkins M., Milne R.L., Newcomb P.A., Slattery M.L., Song M., Peters U., Hoffmeister M., Zaidi S.H., Phipps A.I., Ogino S., Alwers E., Harrison T., Banbury B., Brenner H., Campbell P.T., Chang-Claude J., Buchanan D., Chan A.T., Farris A.B., Figueiredo J.C., Gallinger S., Giles G.G., Jenkins M., Milne R.L., and Newcomb P.A.
- Abstract
Background and Aims: The heterogeneity among colorectal tumors is probably due to differences in developmental pathways and might associate with patient survival times. We studied the relationship among markers of different subtypes of colorectal tumors and patient survival. Method(s): We pooled data from 7 observational studies, comprising 5010 patients with colorectal cancer. All the studies collected information on microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and mutations in KRAS and BRAF in tumors. Tumors with complete marker data were classified as type 1 (MSI-high, CIMP-positive, with pathogenic mutations in BRAF but not KRAS), type 2 (not MSI-high, CIMP-positive, with pathogenic mutations in BRAF but not KRAS), type 3 (not MSI-high or CIMP, with pathogenic mutations in KRAS but not BRAF), type 4 (not MSI-high or CIMP, no pathogenic mutations in BRAF or KRAS), or type 5 (MSI-high, no CIMP, no pathogenic mutations in BRAF or KRAS). We used Cox regression to estimate hazard ratios (HR) and 95% confidence intervals (CIs) for associations of these subtypes and tumor markers with disease-specific survival (DSS) and overall survival times, adjusting for age, sex, stage at diagnosis, and study population. Result(s): Patients with type 2 colorectal tumors had significantly shorter time of DSS than patients with type 4 tumors (HRDSS 1.66; 95% CI 1.33-2.07), regardless of sex, age, or stage at diagnosis. Patients without MSI-high tumors had significantly shorter time of DSS compared with patients with MSI-high tumors (HRDSS 0.42; 95% CI 0.27-0.64), regardless of other tumor markers or stage, or patient sex or age. Conclusion(s): In a pooled analysis of data from 7 observational studies of patients with colorectal cancer, we found that tumor subtypes, defined by combinations of 4 common tumor markers, were associated with differences in survival time. Colorectal tumor subtypes might therefore be used in determining patients' prognoses.Copyri
- Published
- 2020
23. Genome-wide Modeling of Polygenic Risk Score in Colorectal Cancer Risk.
- Author
-
Huyghe J.R., Thomas M., Sakoda L.C., Hoffmeister M., Rosenthal E.A., Lee J.K., van Duijnhoven F.J.B., Platz E.A., Wu A.H., Dampier C.H., de la Chapelle A., Wolk A., Joshi A.D., Burnett-Hartman A., Gsur A., Lindblom A., Castells A., Win A.K., Namjou B., Van Guelpen B., Tangen C.M., He Q., Li C.I., Schafmayer C., Joshu C.E., Ulrich C.M., Bishop D.T., Buchanan D.D., Schaid D., Drew D.A., Muller D.C., Duggan D., Crosslin D.R., Albanes D., Giovannucci E.L., Larson E., Qu F., Mentch F., Giles G.G., Hakonarson H., Hampel H., Stanaway I.B., Figueiredo J.C., Minnier J., Chang-Claude J., Hampe J., Harley J.B., Visvanathan K., Curtis K.R., Offit K., Li L., Le Marchand L., Vodickova L., Gunter M.J., Jenkins M.A., Slattery M.L., Lemire M., Woods M.O., Song M., Murphy N., Lindor N.M., Dikilitas O., Pharoah P.D.P., Campbell P.T., Newcomb P.A., Milne R.L., MacInnis R.J., Castellvi-Bel S., Ogino S., Berndt S.I., Bezieau S., Thibodeau S.N., Gallinger S.J., Zaidi S.H., Harrison T.A., Keku T.O., Hudson T.J., Vymetalkova V., Moreno V., Martin V., Arndt V., Wei W.-Q., Chung W., Su Y.-R., Hayes R.B., White E., Vodicka P., Casey G., Gruber S.B., Schoen R.E., Chan A.T., Potter J.D., Brenner H., Jarvik G.P., Corley D.A., Peters U., Hsu L., Huyghe J.R., Thomas M., Sakoda L.C., Hoffmeister M., Rosenthal E.A., Lee J.K., van Duijnhoven F.J.B., Platz E.A., Wu A.H., Dampier C.H., de la Chapelle A., Wolk A., Joshi A.D., Burnett-Hartman A., Gsur A., Lindblom A., Castells A., Win A.K., Namjou B., Van Guelpen B., Tangen C.M., He Q., Li C.I., Schafmayer C., Joshu C.E., Ulrich C.M., Bishop D.T., Buchanan D.D., Schaid D., Drew D.A., Muller D.C., Duggan D., Crosslin D.R., Albanes D., Giovannucci E.L., Larson E., Qu F., Mentch F., Giles G.G., Hakonarson H., Hampel H., Stanaway I.B., Figueiredo J.C., Minnier J., Chang-Claude J., Hampe J., Harley J.B., Visvanathan K., Curtis K.R., Offit K., Li L., Le Marchand L., Vodickova L., Gunter M.J., Jenkins M.A., Slattery M.L., Lemire M., Woods M.O., Song M., Murphy N., Lindor N.M., Dikilitas O., Pharoah P.D.P., Campbell P.T., Newcomb P.A., Milne R.L., MacInnis R.J., Castellvi-Bel S., Ogino S., Berndt S.I., Bezieau S., Thibodeau S.N., Gallinger S.J., Zaidi S.H., Harrison T.A., Keku T.O., Hudson T.J., Vymetalkova V., Moreno V., Martin V., Arndt V., Wei W.-Q., Chung W., Su Y.-R., Hayes R.B., White E., Vodicka P., Casey G., Gruber S.B., Schoen R.E., Chan A.T., Potter J.D., Brenner H., Jarvik G.P., Corley D.A., Peters U., and Hsu L.
- Abstract
Accurate colorectal cancer (CRC) risk prediction models are critical for identifying individuals at low and high risk of developing CRC, as they can then be offered targeted screening and interventions to address their risks of developing disease (if they are in a high-risk group) and avoid unnecessary screening and interventions (if they are in a low-risk group). As it is likely that thousands of genetic variants contribute to CRC risk, it is clinically important to investigate whether these genetic variants can be used jointly for CRC risk prediction. In this paper, we derived and compared different approaches to generating predictive polygenic risk scores (PRS) from genome-wide association studies (GWASs) including 55,105 CRC-affected case subjects and 65,079 control subjects of European ancestry. We built the PRS in three ways, using (1) 140 previously identified and validated CRC loci; (2) SNP selection based on linkage disequilibrium (LD) clumping followed by machine-learning approaches; and (3) LDpred, a Bayesian approach for genome-wide risk prediction. We tested the PRS in an independent cohort of 101,987 individuals with 1,699 CRC-affected case subjects. The discriminatory accuracy, calculated by the age- and sex-adjusted area under the receiver operating characteristics curve (AUC), was highest for the LDpred-derived PRS (AUC = 0.654) including nearly 1.2 M genetic variants (the proportion of causal genetic variants for CRC assumed to be 0.003), whereas the PRS of the 140 known variants identified from GWASs had the lowest AUC (AUC = 0.629). Based on the LDpred-derived PRS, we are able to identify 30% of individuals without a family history as having risk for CRC similar to those with a family history of CRC, whereas the PRS based on known GWAS variants identified only top 10% as having a similar relative risk. About 90% of these individuals have no family history and would have been considered average risk under current screening guidelines, but might be
- Published
- 2020
24. Associations between reproductive factors and biliary tract cancers in women from the Biliary Tract Cancers Pooling Project.
- Author
-
Shadyab A.H., Weiderpass E., Wolk A., Yang H.-I., Zheng W., McGlynn K.A., Campbell P.T., Koshiol J., Jackson S.S., Adami H.-O., Andreotti G., Beane-Freeman L.E., de Gonzalez A.B., Buring J.E., Fraser G.E., Freedman N.D., Gapstur S.M., Gierach G., Giles G.G., Grodstein F., Hartge P., Jenab M., Kirsh V., Knutsen S.F., Lan Q., Larsson S.C., Lee I.-M., Lee M.-H., Liao L.M., Milne R.L., Monroe K.R., Neuhouser M.L., O'Brien K.M., Petrick J.L., Purdue M.P., Rohan T.E., Sandin S., Sandler D.P., Sawada N., Simon T.G., Sinha R., Stolzenberg-Solomon R., Tsugane S., Shadyab A.H., Weiderpass E., Wolk A., Yang H.-I., Zheng W., McGlynn K.A., Campbell P.T., Koshiol J., Jackson S.S., Adami H.-O., Andreotti G., Beane-Freeman L.E., de Gonzalez A.B., Buring J.E., Fraser G.E., Freedman N.D., Gapstur S.M., Gierach G., Giles G.G., Grodstein F., Hartge P., Jenab M., Kirsh V., Knutsen S.F., Lan Q., Larsson S.C., Lee I.-M., Lee M.-H., Liao L.M., Milne R.L., Monroe K.R., Neuhouser M.L., O'Brien K.M., Petrick J.L., Purdue M.P., Rohan T.E., Sandin S., Sandler D.P., Sawada N., Simon T.G., Sinha R., Stolzenberg-Solomon R., and Tsugane S.
- Abstract
Background & Aims: Gallbladder cancer (GBC) is known to have a female predominance while other biliary tract cancers (BTCs) have a male predominance. However, the role of female reproductive factors in BTC etiology remains unclear. Method(s): We pooled data from 19 studies of >1.5 million women participating in the Biliary Tract Cancers Pooling Project to examine the associations of parity, age at menarche, reproductive years, and age at menopause with BTC. Associations for age at menarche and reproductive years with BTC were analyzed separately for Asian and non-Asian women. Hazard ratios (HRs) and 95% CIs were estimated using Cox proportional hazards models, stratified by study. Result(s): During 21,681,798 person-years of follow-up, 875 cases of GBC, 379 of intrahepatic bile duct cancer (IHBDC), 450 of extrahepatic bile duct cancer (EHBDC), and 261 of ampulla of Vater cancer (AVC) occurred. High parity was associated with risk of GBC (HR >=5 vs. 0 births 1.72; 95% CI 1.25-2.38). Age at menarche (HR per year increase 1.15; 95% CI 1.06-1.24) was associated with GBC risk in Asian women while reproductive years were associated with GBC risk (HR per 5 years 1.13; 95% CI 1.04-1.22) in non-Asian women. Later age at menarche was associated with IHBDC (HR 1.19; 95% CI 1.09-1.31) and EHBDC (HR 1.11; 95% CI 1.01-1.22) in Asian women only. Conclusion(s): We observed an increased risk of GBC with increasing parity. Among Asian women, older age at menarche was associated with increased risk for GBC, IHBDC, and EHBDC, while increasing reproductive years was associated with GBC in non-Asian women. These results suggest that sex hormones have distinct effects on cancers across the biliary tract that vary by geography. Lay summary: Our findings show that the risk of gallbladder cancer is increased among women who have given birth (especially women with 5 or more children). In women from Asian countries, later age at menarche increases the risk of gallbladder cancer, intrahepatic b
- Published
- 2020
25. Circulating Levels of Insulin-like Growth Factor 1 and Insulin-like Growth Factor Binding Protein 3 Associate With Risk of Colorectal Cancer Based on Serologic and Mendelian Randomization Analyses.
- Author
-
English D., Van Guelpen B., Visvanathan K., Vodicka P., Vodickova L., Vymetalkova V., Wang H., White E., Wolk A., Woods M.O., Wu A.H., Zheng W., Peters U., Gunter M.J., Murphy N., Carreras-Torres R., Song M., Chan A.T., Martin R.M., Papadimitriou N., Dimou N., Tsilidis K.K., Banbury B., Bradbury K.E., Besevic J., Rinaldi S., Riboli E., Cross A.J., Travis R.C., Agnoli C., Albanes D., Berndt S.I., Bezieau S., Bishop D.T., Brenner H., Buchanan D.D., Onland-Moret N.C., Burnett-Hartman A., Campbell P.T., Casey G., Castellvi-Bel S., Chang-Claude J., Chirlaque M.-D., de la Chapelle A., Figueiredo J.C., Gallinger S.J., Giles G.G., Gruber S.B., Gsur A., Hampe J., Hampel H., Harrison T.A., Hoffmeister M., Hsu L., Huang W.-Y., Huyghe J.R., Jenkins M.A., Keku T.O., Kuhn T., Kweon S.-S., Le Marchand L., Li C.I., Li L., Lindblom A., Martin V., Milne R.L., Moreno V., Newcomb P.A., Offit K., Ogino S., Ose J., Perduca V., Phipps A.I., Platz E.A., Potter J.D., Qu C., Rennert G., Sakoda L.C., Schafmayer C., Schoen R.E., Slattery M.L., Tangen C.M., Ulrich C.M., van Duijnhoven F.J.B., English D., Van Guelpen B., Visvanathan K., Vodicka P., Vodickova L., Vymetalkova V., Wang H., White E., Wolk A., Woods M.O., Wu A.H., Zheng W., Peters U., Gunter M.J., Murphy N., Carreras-Torres R., Song M., Chan A.T., Martin R.M., Papadimitriou N., Dimou N., Tsilidis K.K., Banbury B., Bradbury K.E., Besevic J., Rinaldi S., Riboli E., Cross A.J., Travis R.C., Agnoli C., Albanes D., Berndt S.I., Bezieau S., Bishop D.T., Brenner H., Buchanan D.D., Onland-Moret N.C., Burnett-Hartman A., Campbell P.T., Casey G., Castellvi-Bel S., Chang-Claude J., Chirlaque M.-D., de la Chapelle A., Figueiredo J.C., Gallinger S.J., Giles G.G., Gruber S.B., Gsur A., Hampe J., Hampel H., Harrison T.A., Hoffmeister M., Hsu L., Huang W.-Y., Huyghe J.R., Jenkins M.A., Keku T.O., Kuhn T., Kweon S.-S., Le Marchand L., Li C.I., Li L., Lindblom A., Martin V., Milne R.L., Moreno V., Newcomb P.A., Offit K., Ogino S., Ose J., Perduca V., Phipps A.I., Platz E.A., Potter J.D., Qu C., Rennert G., Sakoda L.C., Schafmayer C., Schoen R.E., Slattery M.L., Tangen C.M., Ulrich C.M., and van Duijnhoven F.J.B.
- Abstract
Background & Aims: Human studies examining associations between circulating levels of insulin-like growth factor 1 (IGF1) and insulin-like growth factor binding protein 3 (IGFBP3) and colorectal cancer risk have reported inconsistent results. We conducted complementary serologic and Mendelian randomization (MR) analyses to determine whether alterations in circulating levels of IGF1 or IGFBP3 are associated with colorectal cancer development. Method(s): Serum levels of IGF1 were measured in blood samples collected from 397,380 participants from the UK Biobank, from 2006 through 2010. Incident cancer cases and cancer cases recorded first in death certificates were identified through linkage to national cancer and death registries. Complete follow-up was available through March 31, 2016. For the MR analyses, we identified genetic variants associated with circulating levels of IGF1 and IGFBP3. The association of these genetic variants with colorectal cancer was examined with 2-sample MR methods using genome-wide association study consortia data (52,865 cases with colorectal cancer and 46,287 individuals without [controls]) Results: After a median follow-up period of 7.1 years, 2665 cases of colorectal cancer were recorded. In a multivariable-adjusted model, circulating level of IGF1 associated with colorectal cancer risk (hazard ratio per 1 standard deviation increment of IGF1, 1.11; 95% confidence interval [CI] 1.05-1.17). Similar associations were found by sex, follow-up time, and tumor subsite. In the MR analyses, a 1 standard deviation increment in IGF1 level, predicted based on genetic factors, was associated with a higher risk of colorectal cancer risk (odds ratio 1.08; 95% CI 1.03-1.12; P = 3.3 x 10-4). Level of IGFBP3, predicted based on genetic factors, was associated with colorectal cancer risk (odds ratio per 1 standard deviation increment, 1.12; 95% CI 1.06-1.18; P = 4.2 x 10-5). Colorectal cancer risk was associated with only 1 variant in the IGFBP3 gene re
- Published
- 2020
26. Adiposity, metabolites, and colorectal cancer risk: Mendelian randomization study.
- Author
-
Hsu L., Berndt S.I., Bezieau S., Bishop D.T., Brenner H., Buchanan D.D., Burnett-Hartman A., Casey G., Castellvi-Bel S., Chan A.T., Chang-Claude J., Cross A.J., de la Chapelle A., Figueiredo J.C., Gallinger S.J., Gapstur S.M., Giles G.G., Gruber S.B., Gsur A., Hampe J., Hampel H., Harrison T.A., Hoffmeister M., Huang W.-Y., Huyghe J.R., Jenkins M.A., Joshu C.E., Keku T.O., Kuhn T., Kweon S.-S., Le Marchand L., Li C.I., Li L., Lindblom A., Martin V., May A.M., Milne R.L., Moreno V., Newcomb P.A., Offit K., Ogino S., Phipps A.I., Platz E.A., Potter J.D., Qu C., Quiros J.R., Rennert G., Riboli E., Sakoda L.C., Schafmayer C., Schoen R.E., Slattery M.L., Tangen C.M., Tsilidis K.K., Ulrich C.M., van Duijnhoven F.J.B., van Guelpen B., Visvanathan K., Vodicka P., Vodickova L., Wang H., White E., Wolk A., Woods M.O., Wu A.H., Campbell P.T., Zheng W., Peters U., Vincent E.E., Gunter M.J., Bull C.J., Bell J.A., Murphy N., Sanderson E., Davey Smith G., Timpson N.J., Banbury B.L., Albanes D., Hsu L., Berndt S.I., Bezieau S., Bishop D.T., Brenner H., Buchanan D.D., Burnett-Hartman A., Casey G., Castellvi-Bel S., Chan A.T., Chang-Claude J., Cross A.J., de la Chapelle A., Figueiredo J.C., Gallinger S.J., Gapstur S.M., Giles G.G., Gruber S.B., Gsur A., Hampe J., Hampel H., Harrison T.A., Hoffmeister M., Huang W.-Y., Huyghe J.R., Jenkins M.A., Joshu C.E., Keku T.O., Kuhn T., Kweon S.-S., Le Marchand L., Li C.I., Li L., Lindblom A., Martin V., May A.M., Milne R.L., Moreno V., Newcomb P.A., Offit K., Ogino S., Phipps A.I., Platz E.A., Potter J.D., Qu C., Quiros J.R., Rennert G., Riboli E., Sakoda L.C., Schafmayer C., Schoen R.E., Slattery M.L., Tangen C.M., Tsilidis K.K., Ulrich C.M., van Duijnhoven F.J.B., van Guelpen B., Visvanathan K., Vodicka P., Vodickova L., Wang H., White E., Wolk A., Woods M.O., Wu A.H., Campbell P.T., Zheng W., Peters U., Vincent E.E., Gunter M.J., Bull C.J., Bell J.A., Murphy N., Sanderson E., Davey Smith G., Timpson N.J., Banbury B.L., and Albanes D.
- Abstract
Background: Higher adiposity increases the risk of colorectal cancer (CRC), but whether this relationship varies by anatomical sub-site or by sex is unclear. Further, the metabolic alterations mediating the effects of adiposity on CRC are not fully understood. Method(s): We examined sex- and site-specific associations of adiposity with CRC risk and whether adiposity-associated metabolites explain the associations of adiposity with CRC. Genetic variants from genome-wide association studies of body mass index (BMI) and waist-to-hip ratio (WHR, unadjusted for BMI; N = 806,810), and 123 metabolites from targeted nuclear magnetic resonance metabolomics (N = 24,925), were used as instruments. Sex-combined and sex-specific Mendelian randomization (MR) was conducted for BMI and WHR with CRC risk (58,221 cases and 67,694 controls in the Genetics and Epidemiology of Colorectal Cancer Consortium, Colorectal Cancer Transdisciplinary Study, and Colon Cancer Family Registry). Sex-combined MR was conducted for BMI and WHR with metabolites, for metabolites with CRC, and for BMI and WHR with CRC adjusted for metabolite classes in multivariable models. Result(s): In sex-specific MR analyses, higher BMI (per 4.2 kg/m2) was associated with 1.23 (95% confidence interval (CI) = 1.08, 1.38) times higher CRC odds among men (inverse-variance-weighted (IVW) model); among women, higher BMI (per 5.2 kg/m2) was associated with 1.09 (95% CI = 0.97, 1.22) times higher CRC odds. WHR (per 0.07 higher) was more strongly associated with CRC risk among women (IVW OR = 1.25, 95% CI = 1.08, 1.43) than men (IVW OR = 1.05, 95% CI = 0.81, 1.36). BMI or WHR was associated with 104/123 metabolites at false discovery rate-corrected P <= 0.05; several metabolites were associated with CRC, but not in directions that were consistent with the mediation of positive adiposity-CRC relations. In multivariable MR analyses, associations of BMI and WHR with CRC were not attenuated following adjustment for representative
- Published
- 2020
27. Shared heritability and functional enrichment across six solid cancers (vol 10, 431, 2019)
- Author
-
Jiang, X., Finucane, H.K., Schumacher, F.R., Schmit, S.L., Tyrer, J.P., Han, Y., Michailidou, K., Lesseur, C., Kuchenbaecker, K.B., Dennis, J., Conti, D.V., Casey, G., Gaudet, M.M., Huyghe, J.R., Albanes, D., Aldrich, M.C., Andrew, A.S., Andrulis, I.L., Anton-Culver, H., Antoniou, A.C., Antonenkova, N.N., Arnold, S.M., Aronson, K.J., Arun, B.K., Bandera, E.V., Barkardottir, R.B., Barnes, D.R., Batra, J., Beckmann, M.W., Benitez, J., Benlloch, S., Berchuck, A., Berndt, S.I., Bickeboller, H., Bien, S.A., Blomqvist, C., Boccia, S., Bogdanova, N.V., Bojesen, S.E., Bolla, M.K., Brauch, H., Brenner, H., Brenton, J.D., Brook, M.N., Brunet, J., Brunnstrom, H., Buchanan, D.D., Burwinkel, B., Butzow, R., Cadoni, G., Caldes, T., Caligo, M.A., Campbell, I., Campbell, P.T., Cancel-Tassin, G., Cannon-Albright, L., Campa, D., Caporaso, N., Carvalho, A.L., Chan, A.T., Chang-Claude, J., Chanock, S.J., Chen, C., Christiani, D.C., Claes, K.B.M., Claessens, F., Clements, J., Collee, J.M., Correa, M.C., Couch, F.J., Cox, A., Cunningham, J.M., Cybulski, C., Czene, K., Daly, M.B., deFazio, A., Devilee, P., Diez, O., Gago-Dominguez, M., Donovan, J.L., Dork, T., Duell, E.J., Dunning, A.M., Dwek, M., Eccles, D.M., Edlund, C.K., Edwards, D.R.V., Ellberg, C., Evans, D.G., Fasching, P.A., Ferris, R.L., Liloglou, T., Figueiredo, J.C., Fletcher, O., Fortner, R.T., Fostira, F., Franceschi, S., Friedman, E., Gallinger, S.J., Ganz, P.A., Garber, J., Garcia-Saenz, J.A., Gayther, S.A., Giles, G.G., Godwin, A.K., Goldberg, M.S., Goldgar, D.E., Goode, E.L., Goodman, M.T., Goodman, G., Grankvist, K., Greene, M.H., Gronberg, H., Gronwald, J., Guenel, P., Hakansson, N., Hall, P., Hamann, U., Hamdy, F.C., Hamilton, R.J., Hampe, J., Haugen, A., Heitz, F., Herrero, R., Hillemanns, P., Hoffmeister, M., Hogdall, E., Hong, Y.C., Hopper, J.L., Houlston, R., Hulick, P.J., Hunter, D.J., Huntsman, D.G., Idos, G., Imyanitov, E.N., Ingles, S.A., Isaacs, C., Jakubowska, A., James, P., Jenkins, M.A., Johansson, M., John, E.M., Joshi, A.D., Kaneva, R., Karlan, B.Y., Kelemen, L.E., Kuhl, T., Khaw, K.T., Khusnutdinova, E., Kibel, A.S., Kiemeney, L.A., Kim, J., Kjaer, S.K., Knight, J.A., Kogevinas, M., Kote-Jarai, Z., Koutros, S., Kristensen, V.N., Kupryjanczyk, J., Lacko, M., Lam, S., Lambrechts, D., Landi, M.T., Lazarus, P., N.D. le, Lee, E., Lejbkowicz, F., Lenz, H.J., Leslie, G., Lessel, D., Lester, J., Levine, D.A., Li, L., Li, C.I., Lindblom, A., Lindor, N.M., Liu, G., Loupakis, F., Lubinski, J., Maehle, L., Maier, C., Mannermaa, A., Marchand, L., Margolin, S., May, T., McGuffog, L., Meindl, A., Middha, P., Miller, A., Milne, R.L., MacInnis, R.J., Modugno, F., Montagna, M., Moreno, V., Moysich, K.B., Mucci, L., Muir, K., Mulligan, A.M., Nathanson, K.L., Neal, D.E., Ness, A.R., Neuhausen, S.L., Nevanlinna, H., Newcomb, P.A., Newcomb, L.F., Nielsen, F.C., Nikitina-Zake, L., Nordestgaard, B.G., Nussbaum, R.L., Offit, K., Olah, E., Olama, A.A. al, Olopade, O.I., Olshan, A.F., Olsson, H., Osorio, A., Pandha, H., Park, J.Y., Pashayan, N., Parsons, M.T., Pejovic, T., Penney, K.L., Peters, W.H.M., Phelan, C.M., Phipps, A.I., Plaseska-Karanfilska, D., Pring, M., Prokofyeva, D., Radice, P., Stefansson, K., Ramus, S.J., Raskin, L., Rennert, G., Rennert, H.S., Rensburg, E.J., Riggan, M.J., Risch, H.A., Risch, A., Roobol, M.J., Rosenstein, B.S., Rossing, M.A., Ruyck, K., Saloustros, E., Sandler, D.P., Sawyer, E.J., Schabath, M.B., Schleutker, J., Schmidt, M.K., Setiawan, V.W., Shen, H.B., Siegel, E.M., Sieh, W., Singer, C.F., Slattery, M.L., Sorensen, K.D., Southey, M.C., Spurdle, A.B., Stanford, J.L., Stevens, V.L., Stintzing, S., Stone, J., Sundfeldt, K., Sutphen, R., Swerdlow, A.J., Tajara, E.H., Tangen, C.M., Tardon, A., Taylor, J.A., Teare, M.D., Teixeira, M.R., Terry, M.B., Terry, K.L., Thibodeau, S.N., Thomassen, M., Bjorge, L., Tischkowitz, M., Toland, A.E., Torres, D., Townsend, P.A., Travis, R.C., Tung, N., and Tworoger
- Published
- 2019
28. Genetic variant predictors of gene expression provide new insight into risk of colorectal cancer
- Author
-
Bien, S.A. Su, Y.-R. Conti, D.V. Harrison, T.A. Qu, C. Guo, X. Lu, Y. Albanes, D. Auer, P.L. Banbury, B.L. Berndt, S.I. Bézieau, S. Brenner, H. Buchanan, D.D. Caan, B.J. Campbell, P.T. Carlson, C.S. Chan, A.T. Chang-Claude, J. Chen, S. Connolly, C.M. Easton, D.F. Feskens, E.J.M. Gallinger, S. Giles, G.G. Gunter, M.J. Hampe, J. Huyghe, J.R. Hoffmeister, M. Hudson, T.J. Jacobs, E.J. Jenkins, M.A. Kampman, E. Kang, H.M. Kühn, T. Küry, S. Lejbkowicz, F. Le Marchand, L. Milne, R.L. Li, L. Li, C.I. Lindblom, A. Lindor, N.M. Martín, V. McNeil, C.E. Melas, M. Moreno, V. Newcomb, P.A. Offit, K. Pharaoh, P.D.P. Potter, J.D. Qu, C. Riboli, E. Rennert, G. Sala, N. Schafmayer, C. Scacheri, P.C. Schmit, S.L. Severi, G. Slattery, M.L. Smith, J.D. Trichopoulou, A. Tumino, R. Ulrich, C.M. van Duijnhoven, F.J.B. Van Guelpen, B. Weinstein, S.J. White, E. Wolk, A. Woods, M.O. Wu, A.H. Abecasis, G.R. Casey, G. Nickerson, D.A. Gruber, S.B. Hsu, L. Zheng, W. Peters, U.
- Abstract
Genome-wide association studies have reported 56 independently associated colorectal cancer (CRC) risk variants, most of which are non-coding and believed to exert their effects by modulating gene expression. The computational method PrediXcan uses cis-regulatory variant predictors to impute expression and perform gene-level association tests in GWAS without directly measured transcriptomes. In this study, we used reference datasets from colon (n = 169) and whole blood (n = 922) transcriptomes to test CRC association with genetically determined expression levels in a genome-wide analysis of 12,186 cases and 14,718 controls. Three novel associations were discovered from colon transverse models at FDR ≤ 0.2 and further evaluated in an independent replication including 32,825 cases and 39,933 controls. After adjusting for multiple comparisons, we found statistically significant associations using colon transcriptome models with TRIM4 (discovery P = 2.2 × 10− 4, replication P = 0.01), and PYGL (discovery P = 2.3 × 10− 4, replication P = 6.7 × 10− 4). Interestingly, both genes encode proteins that influence redox homeostasis and are related to cellular metabolic reprogramming in tumors, implicating a novel CRC pathway linked to cell growth and proliferation. Defining CRC risk regions as one megabase up- and downstream of one of the 56 independent risk variants, we defined 44 non-overlapping CRC-risk regions. Among these risk regions, we identified genes associated with CRC (P < 0.05) in 34/44 CRC-risk regions. Importantly, CRC association was found for two genes in the previously reported 2q25 locus, CXCR1 and CXCR2, which are potential cancer therapeutic targets. These findings provide strong candidate genes to prioritize for subsequent laboratory follow-up of GWAS loci. This study is the first to implement PrediXcan in a large colorectal cancer study and findings highlight the utility of integrating transcriptome data in GWAS for discovery of, and biological insight into, risk loci. © 2019, The Author(s).
- Published
- 2019
29. Discovery of common and rare genetic risk variants for colorectal cancer
- Author
-
Huyghe, J.R. Bien, S.A. Harrison, T.A. Kang, H.M. Chen, S. Schmit, S.L. Conti, D.V. Qu, C. Jeon, J. Edlund, C.K. Greenside, P. Wainberg, M. Schumacher, F.R. Smith, J.D. Levine, D.M. Nelson, S.C. Sinnott-Armstrong, N.A. Albanes, D. Alonso, M.H. Anderson, K. Arnau-Collell, C. Arndt, V. Bamia, C. Banbury, B.L. Baron, J.A. Berndt, S.I. Bézieau, S. Bishop, D.T. Boehm, J. Boeing, H. Brenner, H. Brezina, S. Buch, S. Buchanan, D.D. Burnett-Hartman, A. Butterbach, K. Caan, B.J. Campbell, P.T. Carlson, C.S. Castellví-Bel, S. Chan, A.T. Chang-Claude, J. Chanock, S.J. Chirlaque, M.-D. Cho, S.H. Connolly, C.M. Cross, A.J. Cuk, K. Curtis, K.R. de la Chapelle, A. Doheny, K.F. Duggan, D. Easton, D.F. Elias, S.G. Elliott, F. English, D.R. Feskens, E.J.M. Figueiredo, J.C. Fischer, R. FitzGerald, L.M. Forman, D. Gala, M. Gallinger, S. Gauderman, W.J. Giles, G.G. Gillanders, E. Gong, J. Goodman, P.J. Grady, W.M. Grove, J.S. Gsur, A. Gunter, M.J. Haile, R.W. Hampe, J. Hampel, H. Harlid, S. Hayes, R.B. Hofer, P. Hoffmeister, M. Hopper, J.L. Hsu, W.-L. Huang, W.-Y. Hudson, T.J. Hunter, D.J. Ibañez-Sanz, G. Idos, G.E. Ingersoll, R. Jackson, R.D. Jacobs, E.J. Jenkins, M.A. Joshi, A.D. Joshu, C.E. Keku, T.O. Key, T.J. Kim, H.R. Kobayashi, E. Kolonel, L.N. Kooperberg, C. Kühn, T. Küry, S. Kweon, S.-S. Larsson, S.C. Laurie, C.A. Le Marchand, L. Leal, S.M. Lee, S.C. Lejbkowicz, F. Lemire, M. Li, C.I. Li, L. Lieb, W. Lin, Y. Lindblom, A. Lindor, N.M. Ling, H. Louie, T.L. Männistö, S. Markowitz, S.D. Martín, V. Masala, G. McNeil, C.E. Melas, M. Milne, R.L. Moreno, L. Murphy, N. Myte, R. Naccarati, A. Newcomb, P.A. Offit, K. Ogino, S. Onland-Moret, N.C. Pardini, B. Parfrey, P.S. Pearlman, R. Perduca, V. Pharoah, P.D.P. Pinchev, M. Platz, E.A. Prentice, R.L. Pugh, E. Raskin, L. Rennert, G. Rennert, H.S. Riboli, E. Rodríguez-Barranco, M. Romm, J. Sakoda, L.C. Schafmayer, C. Schoen, R.E. Seminara, D. Shah, M. Shelford, T. Shin, M.-H. Shulman, K. Sieri, S. Slattery, M.L. Southey, M.C. Stadler, Z.K. Stegmaier, C. Su, Y.-R. Tangen, C.M. Thibodeau, S.N. Thomas, D.C. Thomas, S.S. Toland, A.E. Trichopoulou, A. Ulrich, C.M. Van Den Berg, D.J. van Duijnhoven, F.J.B. Van Guelpen, B. van Kranen, H. Vijai, J. Visvanathan, K. Vodicka, P. Vodickova, L. Vymetalkova, V. Weigl, K. Weinstein, S.J. White, E. Win, A.K. Wolf, C.R. Wolk, A. Woods, M.O. Wu, A.H. Zaidi, S.H. Zanke, B.W. Zhang, Q. Zheng, W. Scacheri, P.C. Potter, J.D. Bassik, M.C. Kundaje, A. Casey, G. Moreno, V. Abecasis, G.R. Nickerson, D.A. Gruber, S.B. Hsu, L. Peters, U.
- Abstract
To further dissect the genetic architecture of colorectal cancer (CRC), we performed whole-genome sequencing of 1,439 cases and 720 controls, imputed discovered sequence variants and Haplotype Reference Consortium panel variants into genome-wide association study data, and tested for association in 34,869 cases and 29,051 controls. Findings were followed up in an additional 23,262 cases and 38,296 controls. We discovered a strongly protective 0.3% frequency variant signal at CHD1. In a combined meta-analysis of 125,478 individuals, we identified 40 new independent signals at P < 5 × 10 −8 , bringing the number of known independent signals for CRC to ~100. New signals implicate lower-frequency variants, Krüppel-like factors, Hedgehog signaling, Hippo-YAP signaling, long noncoding RNAs and somatic drivers, and support a role for immune function. Heritability analyses suggest that CRC risk is highly polygenic, and larger, more comprehensive studies enabling rare variant analysis will improve understanding of biology underlying this risk and influence personalized screening strategies and drug development. © 2018, This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply.
- Published
- 2019
30. Correction to: Genetic variant predictors of gene expression provide new insight into risk of colorectal cancer (Human Genetics, (2019), 138, 4, (307-326), 10.1007/s00439-019-01989-8)
- Author
-
Bien, S.A. Su, Y.-R. Conti, D.V. Harrison, T.A. Qu, C. Guo, X. Lu, Y. Albanes, D. Auer, P.L. Banbury, B.L. Berndt, S.I. Bézieau, S. Brenner, H. Buchanan, D.D. Caan, B.J. Campbell, P.T. Carlson, C.S. Chan, A.T. Chang-Claude, J. Chen, S. Connolly, C.M. Easton, D.F. Feskens, E.J.M. Gallinger, S. Giles, G.G. Gunter, M.J. Hampe, J. Huyghe, J.R. Hoffmeister, M. Hudson, T.J. Jacobs, E.J. Jenkins, M.A. Kampman, E. Kang, H.M. Kühn, T. Küry, S. Lejbkowicz, F. Le Marchand, L. Milne, R.L. Li, L. Li, C.I. Lindblom, A. Lindor, N.M. Martín, V. McNeil, C.E. Melas, M. Moreno, V. Newcomb, P.A. Offit, K. Pharaoh, P.D.P. Potter, J.D. Qu, C. Riboli, E. Rennert, G. Sala, N. Schafmayer, C. Scacheri, P.C. Schmit, S.L. Severi, G. Slattery, M.L. Smith, J.D. Trichopoulou, A. Tumino, R. Ulrich, C.M. van Duijnhoven, F.J.B. Van Guelpen, B. Weinstein, S.J. White, E. Wolk, A. Woods, M.O. Wu, A.H. Abeçasis, G.R. Casey, G. Nickerson, D.A. Gruber, S.B. Hsu, L. Zheng, W. Peters, U.
- Abstract
Every author has erroneously been assigned to the affiliation “62”. The affiliation 62 belongs to the author Graham Casey. © 2019, Springer-Verlag GmbH Germany, part of Springer Nature.
- Published
- 2019
31. Shared heritability and functional enrichment across six solid cancers.
- Author
-
Fletcher O., Tardon A., Taylor J.A., Teare M.D., Teixeira M.R., Terry M.B., Terry K.L., Thibodeau S.N., Thomassen M., Bjorge L., Tischkowitz M., Toland A.E., Torres D., Townsend P.A., Travis R.C., Tung N., Tworoger S.S., Ulrich C.M., Usmani N., Vachon C.M., Van Nieuwenhuysen E., Vega A., Aguado-Barrera M.E., Wang Q., Webb P.M., Weinberg C.R., Weinstein S., Weissler M.C., Weitzel J.N., West C.M.L., White E., Whittemore A.S., Wichmann H.-E., Wiklund F., Winqvist R., Wolk A., Woll P., Woods M., Wu A.H., Wu X., Yannoukakos D., Zheng W., Zienolddiny S., Ziogas A., Zorn K.K., Lane J.M., Saxena R., Thomas D., Hung R.J., Diergaarde B., McKay J., Peters U., Hsu L., Garcia-Closas M., Eeles R.A., Chenevix-Trench G., Brennan P.J., Haiman C.A., Simard J., Easton D.F., Gruber S.B., Pharoah P.D.P., Price A.L., Pasaniuc B., Amos C.I., Kraft P., Lindstrom S., Chen C., Anton-Culver H., Antoniou A.C., Antonenkova N.N., Arnold S.M., Jiang X., Finucane H.K., Schumacher F.R., Schmit S.L., Tyrer J.P., Han Y., Michailidou K., Lesseur C., Kuchenbaecker K.B., Dennis J., Conti D.V., Casey G., Gaudet M.M., Huyghe J.R., Albanes D., Aldrich M.C., Andrew A.S., Andrulis I.L., Aronson K.J., Arun B.K., Bandera E.V., Barkardottir R.B., Barnes D.R., Batra J., Beckmann M.W., Benitez J., Benlloch S., Berchuck A., Berndt S.I., Bickeboller H., Bien S.A., Blomqvist C., Boccia S., Bogdanova N.V., Bojesen S.E., Bolla M.K., Brauch H., Brenner H., Brenton J.D., Brook M.N., Brunet J., Brunnstrom H., Buchanan D.D., Burwinkel B., Butzow R., Cadoni G., Caldes T., Caligo M.A., Campbell I., Campbell P.T., Cancel-Tassin G., Cannon-Albright L., Campa D., Caporaso N., Carvalho A.L., Chan A.T., Chang-Claude J., Chanock S.J., Christiani D.C., Claes K.B.M., Claessens F., Clements J., Collee J.M., Correa M.C., Couch F.J., Cox A., Cunningham J.M., Cybulski C., Czene K., Daly M.B., deFazio A., Devilee P., Diez O., Gago-Dominguez M., Donovan J.L., Dork T., Duell E.J., Dunning A.M., Dwek M., Eccles D.M., Edlund C.K., Edwards D.R.V., Ellberg C., Evans D.G., Fasching P.A., Ferris R.L., Liloglou T., Figueiredo J.C., Fortner R.T., Fostira F., Franceschi S., Friedman E., Gallinger S.J., Ganz P.A., Garber J., Garcia-Saenz J.A., Gayther S.A., Giles G.G., Godwin A.K., Goldberg M.S., Goldgar D.E., Goode E.L., Goodman M.T., Goodman G., Grankvist K., Greene M.H., Gronberg H., Gronwald J., Guenel P., Hakansson N., Hall P., Hamann U., Hamdy F.C., Hamilton R.J., Hampe J., Haugen A., Heitz F., Herrero R., Hillemanns P., Hoffmeister M., Hogdall E., Hong Y.-C., Hopper J.L., Houlston R., Hulick P.J., Hunter D.J., Huntsman D.G., Idos G., Imyanitov E.N., Ingles S.A., Isaacs C., Jakubowska A., James P., Jenkins M.A., Johansson M., John E.M., Joshi A.D., Kaneva R., Karlan B.Y., Kelemen L.E., Kuhl T., Khaw K.-T., Khusnutdinova E., Kibel A.S., Kiemeney L.A., Kim J., Kjaer S.K., Knight J.A., Kogevinas M., Kote-Jarai Z., Koutros S., Kristensen V.N., Kupryjanczyk J., Lacko M., Lam S., Lambrechts D., Landi M.T., Lazarus P., Le N.D., Lee E., Lejbkowicz F., Lenz H.-J., Leslie G., Lessel D., Lester J., Levine D.A., Li L., Li C.I., Lindblom A., Lindor N.M., Liu G., Loupakis F., Lubinski J., Maehle L., Maier C., Mannermaa A., Marchand L.L., Margolin S., May T., McGuffog L., Meindl A., Middha P., Miller A., Milne R.L., MacInnis R.J., Modugno F., Montagna M., Moreno V., Moysich K.B., Mucci L., Muir K., Mulligan A.M., Nathanson K.L., Neal D.E., Ness A.R., Neuhausen S.L., Nevanlinna H., Newcomb P.A., Newcomb L.F., Nielsen F.C., Nikitina-Zake L., Nordestgaard B.G., Nussbaum R.L., Offit K., Olah E., Olama A.A.A., Olopade O.I., Olshan A.F., Olsson H., Osorio A., Pandha H., Park J.Y., Pashayan N., Parsons M.T., Pejovic T., Penney K.L., Peters W.H.M., Phelan C.M., Phipps A.I., Plaseska-Karanfilska D., Pring M., Prokofyeva D., Radice P., Stefansson K., Ramus S.J., Raskin L., Rennert G., Rennert H.S., van Rensburg E.J., Riggan M.J., Risch H.A., Risch A., Roobol M.J., Rosenstein B.S., Rossing M.A., De Ruyck K., Saloustros E., Sandler D.P., Sawyer E.J., Schabath M.B., Schleutker J., Schmidt M.K., Setiawan V.W., Shen H., Siegel E.M., Sieh W., Singer C.F., Slattery M.L., Sorensen K.D., Southey M.C., Spurdle A.B., Stanford J.L., Stevens V.L., Stintzing S., Stone J., Sundfeldt K., Sutphen R., Swerdlow A.J., Tajara E.H., Tangen C.M., Fletcher O., Tardon A., Taylor J.A., Teare M.D., Teixeira M.R., Terry M.B., Terry K.L., Thibodeau S.N., Thomassen M., Bjorge L., Tischkowitz M., Toland A.E., Torres D., Townsend P.A., Travis R.C., Tung N., Tworoger S.S., Ulrich C.M., Usmani N., Vachon C.M., Van Nieuwenhuysen E., Vega A., Aguado-Barrera M.E., Wang Q., Webb P.M., Weinberg C.R., Weinstein S., Weissler M.C., Weitzel J.N., West C.M.L., White E., Whittemore A.S., Wichmann H.-E., Wiklund F., Winqvist R., Wolk A., Woll P., Woods M., Wu A.H., Wu X., Yannoukakos D., Zheng W., Zienolddiny S., Ziogas A., Zorn K.K., Lane J.M., Saxena R., Thomas D., Hung R.J., Diergaarde B., McKay J., Peters U., Hsu L., Garcia-Closas M., Eeles R.A., Chenevix-Trench G., Brennan P.J., Haiman C.A., Simard J., Easton D.F., Gruber S.B., Pharoah P.D.P., Price A.L., Pasaniuc B., Amos C.I., Kraft P., Lindstrom S., Chen C., Anton-Culver H., Antoniou A.C., Antonenkova N.N., Arnold S.M., Jiang X., Finucane H.K., Schumacher F.R., Schmit S.L., Tyrer J.P., Han Y., Michailidou K., Lesseur C., Kuchenbaecker K.B., Dennis J., Conti D.V., Casey G., Gaudet M.M., Huyghe J.R., Albanes D., Aldrich M.C., Andrew A.S., Andrulis I.L., Aronson K.J., Arun B.K., Bandera E.V., Barkardottir R.B., Barnes D.R., Batra J., Beckmann M.W., Benitez J., Benlloch S., Berchuck A., Berndt S.I., Bickeboller H., Bien S.A., Blomqvist C., Boccia S., Bogdanova N.V., Bojesen S.E., Bolla M.K., Brauch H., Brenner H., Brenton J.D., Brook M.N., Brunet J., Brunnstrom H., Buchanan D.D., Burwinkel B., Butzow R., Cadoni G., Caldes T., Caligo M.A., Campbell I., Campbell P.T., Cancel-Tassin G., Cannon-Albright L., Campa D., Caporaso N., Carvalho A.L., Chan A.T., Chang-Claude J., Chanock S.J., Christiani D.C., Claes K.B.M., Claessens F., Clements J., Collee J.M., Correa M.C., Couch F.J., Cox A., Cunningham J.M., Cybulski C., Czene K., Daly M.B., deFazio A., Devilee P., Diez O., Gago-Dominguez M., Donovan J.L., Dork T., Duell E.J., Dunning A.M., Dwek M., Eccles D.M., Edlund C.K., Edwards D.R.V., Ellberg C., Evans D.G., Fasching P.A., Ferris R.L., Liloglou T., Figueiredo J.C., Fortner R.T., Fostira F., Franceschi S., Friedman E., Gallinger S.J., Ganz P.A., Garber J., Garcia-Saenz J.A., Gayther S.A., Giles G.G., Godwin A.K., Goldberg M.S., Goldgar D.E., Goode E.L., Goodman M.T., Goodman G., Grankvist K., Greene M.H., Gronberg H., Gronwald J., Guenel P., Hakansson N., Hall P., Hamann U., Hamdy F.C., Hamilton R.J., Hampe J., Haugen A., Heitz F., Herrero R., Hillemanns P., Hoffmeister M., Hogdall E., Hong Y.-C., Hopper J.L., Houlston R., Hulick P.J., Hunter D.J., Huntsman D.G., Idos G., Imyanitov E.N., Ingles S.A., Isaacs C., Jakubowska A., James P., Jenkins M.A., Johansson M., John E.M., Joshi A.D., Kaneva R., Karlan B.Y., Kelemen L.E., Kuhl T., Khaw K.-T., Khusnutdinova E., Kibel A.S., Kiemeney L.A., Kim J., Kjaer S.K., Knight J.A., Kogevinas M., Kote-Jarai Z., Koutros S., Kristensen V.N., Kupryjanczyk J., Lacko M., Lam S., Lambrechts D., Landi M.T., Lazarus P., Le N.D., Lee E., Lejbkowicz F., Lenz H.-J., Leslie G., Lessel D., Lester J., Levine D.A., Li L., Li C.I., Lindblom A., Lindor N.M., Liu G., Loupakis F., Lubinski J., Maehle L., Maier C., Mannermaa A., Marchand L.L., Margolin S., May T., McGuffog L., Meindl A., Middha P., Miller A., Milne R.L., MacInnis R.J., Modugno F., Montagna M., Moreno V., Moysich K.B., Mucci L., Muir K., Mulligan A.M., Nathanson K.L., Neal D.E., Ness A.R., Neuhausen S.L., Nevanlinna H., Newcomb P.A., Newcomb L.F., Nielsen F.C., Nikitina-Zake L., Nordestgaard B.G., Nussbaum R.L., Offit K., Olah E., Olama A.A.A., Olopade O.I., Olshan A.F., Olsson H., Osorio A., Pandha H., Park J.Y., Pashayan N., Parsons M.T., Pejovic T., Penney K.L., Peters W.H.M., Phelan C.M., Phipps A.I., Plaseska-Karanfilska D., Pring M., Prokofyeva D., Radice P., Stefansson K., Ramus S.J., Raskin L., Rennert G., Rennert H.S., van Rensburg E.J., Riggan M.J., Risch H.A., Risch A., Roobol M.J., Rosenstein B.S., Rossing M.A., De Ruyck K., Saloustros E., Sandler D.P., Sawyer E.J., Schabath M.B., Schleutker J., Schmidt M.K., Setiawan V.W., Shen H., Siegel E.M., Sieh W., Singer C.F., Slattery M.L., Sorensen K.D., Southey M.C., Spurdle A.B., Stanford J.L., Stevens V.L., Stintzing S., Stone J., Sundfeldt K., Sutphen R., Swerdlow A.J., Tajara E.H., and Tangen C.M.
- Abstract
Quantifying the genetic correlation between cancers can provide important insights into the mechanisms driving cancer etiology. Using genome-wide association study summary statistics across six cancer types based on a total of 296,215 cases and 301,319 controls of European ancestry, here we estimate the pair-wise genetic correlations between breast, colorectal, head/neck, lung, ovary and prostate cancer, and between cancers and 38 other diseases. We observed statistically significant genetic correlations between lung and head/neck cancer (rg = 0.57, p = 4.6 x 10-8), breast and ovarian cancer (rg = 0.24, p = 7 x 10-5), breast and lung cancer (rg = 0.18, p =1.5 x 10-6) and breast and colorectal cancer (rg = 0.15, p = 1.1 x 10-4). We also found that multiple cancers are genetically correlated with non-cancer traits including smoking, psychiatric diseases and metabolic characteristics. Functional enrichment analysis revealed a significant excess contribution of conserved and regulatory regions to cancer heritability. Our comprehensive analysis of cross-cancer heritability suggests that solid tumors arising across tissues share in part a common germline genetic basis.Copyright © 2019, The Author(s).
- Published
- 2019
32. Publisher Correction: Shared heritability and functional enrichment across six solid cancers (Nature Communications, (2019), 10, 1, (431), 10.1038/s41467-018-08054-4).
- Author
-
Tangen C.M., Wu X., Yannoukakos D., Zheng W., Zienolddiny S., Ziogas A., Zorn K.K., Lane J.M., Saxena R., Thomas D., Hung R.J., Diergaarde B., McKay J., Peters U., Hsu L., Garcia-Closas M., Eeles R.A., Chenevix-Trench G., Brennan P.J., Haiman C.A., Simard J., Easton D.F., Gruber S.B., Pharoah P.D.P., Price A.L., Pasaniuc B., Amos C.I., Kraft P., Lindstrom S., Chen C., Jiang X., Finucane H.K., Schumacher F.R., Schmit S.L., Tyrer J.P., Han Y., Michailidou K., Lesseur C., Kuchenbaecker K.B., Dennis J., Conti D.V., Casey G., Gaudet M.M., Huyghe J.R., Albanes D., Aldrich M.C., Andrew A.S., Andrulis I.L., Anton-Culver H., Antoniou A.C., Antonenkova N.N., Arnold S.M., Aronson K.J., Arun B.K., Bandera E.V., Barkardottir R.B., Barnes D.R., Batra J., Beckmann M.W., Benitez J., Benlloch S., Berchuck A., Berndt S.I., Bickeboller H., Bien S.A., Blomqvist C., Boccia S., Bogdanova N.V., Bojesen S.E., Bolla M.K., Brauch H., Brenner H., Brenton J.D., Brook M.N., Brunet J., Brunnstrom H., Buchanan D.D., Burwinkel B., Butzow R., Cadoni G., Caldes T., Caligo M.A., Campbell I., Campbell P.T., Cancel-Tassin G., Cannon-Albright L., Campa D., Caporaso N., Carvalho A.L., Chan A.T., Chang-Claude J., Chanock S.J., Christiani D.C., Claes K.B.M., Claessens F., Clements J., Collee J.M., Correa M.C., Couch F.J., Cox A., Cunningham J.M., Cybulski C., Czene K., Daly M.B., deFazio A., Devilee P., Diez O., Gago-Dominguez M., Donovan J.L., Dork T., Duell E.J., Dunning A.M., Dwek M., Eccles D.M., Edlund C.K., Edwards D.R.V., Ellberg C., Evans D.G., Fasching P.A., Ferris R.L., Liloglou T., Figueiredo J.C., Fletcher O., Fortner R.T., Fostira F., Franceschi S., Friedman E., Gallinger S.J., Ganz P.A., Garber J., Garcia-Saenz J.A., Gayther S.A., Giles G.G., Godwin A.K., Goldberg M.S., Goldgar D.E., Goode E.L., Goodman M.T., Goodman G., Grankvist K., Greene M.H., Gronberg H., Gronwald J., Guenel P., Hakansson N., Hall P., Hamann U., Hamdy F.C., Hamilton R.J., Hampe J., Haugen A., Heitz F., Herrero R., Hillemanns P., Hoffmeister M., Hogdall E., Hong Y.-C., Hopper J.L., Houlston R., Hulick P.J., Hunter D.J., Huntsman D.G., Idos G., Imyanitov E.N., Ingles S.A., Isaacs C., Jakubowska A., James P., Jenkins M.A., Johansson M., John E.M., Joshi A.D., Kaneva R., Karlan B.Y., Kelemen L.E., Kuhl T., Khaw K.-T., Khusnutdinova E., Kibel A.S., Kiemeney L.A., Kim J., Kjaer S.K., Knight J.A., Kogevinas M., Kote-Jarai Z., Koutros S., Kristensen V.N., Kupryjanczyk J., Lacko M., Lam S., Lambrechts D., Landi M.T., Lazarus P., Le N.D., Lee E., Lejbkowicz F., Lenz H.-J., Leslie G., Lessel D., Lester J., Levine D.A., Li L., Li C.I., Lindblom A., Lindor N.M., Liu G., Loupakis F., Lubinski J., Maehle L., Maier C., Mannermaa A., Marchand L.L., Margolin S., May T., McGuffog L., Meindl A., Middha P., Miller A., Milne R.L., MacInnis R.J., Modugno F., Montagna M., Moreno V., Moysich K.B., Mucci L., Muir K., Mulligan A.M., Nathanson K.L., Neal D.E., Ness A.R., Neuhausen S.L., Nevanlinna H., Newcomb P.A., Newcomb L.F., Nielsen F.C., Nikitina-Zake L., Nordestgaard B.G., Nussbaum R.L., Offit K., Olah E., Olama A.A.A., Olopade O.I., Olshan A.F., Olsson H., Osorio A., Pandha H., Park J.Y., Pashayan N., Parsons M.T., Pejovic T., Penney K.L., Peters W.H.M., Phelan C.M., Phipps A.I., Plaseska-Karanfilska D., Pring M., Prokofyeva D., Radice P., Stefansson K., Ramus S.J., Raskin L., Rennert G., Rennert H.S., van Rensburg E.J., Riggan M.J., Risch H.A., Risch A., Roobol M.J., Rosenstein B.S., Rossing M.A., De Ruyck K., Saloustros E., Sandler D.P., Sawyer E.J., Schabath M.B., Schleutker J., Schmidt M.K., Setiawan V.W., Shen H., Siegel E.M., Sieh W., Singer C.F., Slattery M.L., Sorensen K.D., Southey M.C., Spurdle A.B., Stanford J.L., Stevens V.L., Stintzing S., Stone J., Sundfeldt K., Sutphen R., Swerdlow A.J., Tajara E.H., Tardon A., Taylor J.A., Teare M.D., Teixeira M.R., Terry M.B., Terry K.L., Thibodeau S.N., Thomassen M., Bjorge L., Tischkowitz M., Toland A.E., Torres D., Townsend P.A., Travis R.C., Tung N., Tworoger S.S., Ulrich C.M., Usmani N., Vachon C.M., Van Nieuwenhuysen E., Vega A., Aguado-Barrera M.E., Wang Q., Webb P.M., Weinberg C.R., Weinstein S., Weissler M.C., Weitzel J.N., West C.M.L., White E., Whittemore A.S., Wichmann H.-E., Wiklund F., Winqvist R., Wolk A., Woll P., Woods M., Wu A.H., Tangen C.M., Wu X., Yannoukakos D., Zheng W., Zienolddiny S., Ziogas A., Zorn K.K., Lane J.M., Saxena R., Thomas D., Hung R.J., Diergaarde B., McKay J., Peters U., Hsu L., Garcia-Closas M., Eeles R.A., Chenevix-Trench G., Brennan P.J., Haiman C.A., Simard J., Easton D.F., Gruber S.B., Pharoah P.D.P., Price A.L., Pasaniuc B., Amos C.I., Kraft P., Lindstrom S., Chen C., Jiang X., Finucane H.K., Schumacher F.R., Schmit S.L., Tyrer J.P., Han Y., Michailidou K., Lesseur C., Kuchenbaecker K.B., Dennis J., Conti D.V., Casey G., Gaudet M.M., Huyghe J.R., Albanes D., Aldrich M.C., Andrew A.S., Andrulis I.L., Anton-Culver H., Antoniou A.C., Antonenkova N.N., Arnold S.M., Aronson K.J., Arun B.K., Bandera E.V., Barkardottir R.B., Barnes D.R., Batra J., Beckmann M.W., Benitez J., Benlloch S., Berchuck A., Berndt S.I., Bickeboller H., Bien S.A., Blomqvist C., Boccia S., Bogdanova N.V., Bojesen S.E., Bolla M.K., Brauch H., Brenner H., Brenton J.D., Brook M.N., Brunet J., Brunnstrom H., Buchanan D.D., Burwinkel B., Butzow R., Cadoni G., Caldes T., Caligo M.A., Campbell I., Campbell P.T., Cancel-Tassin G., Cannon-Albright L., Campa D., Caporaso N., Carvalho A.L., Chan A.T., Chang-Claude J., Chanock S.J., Christiani D.C., Claes K.B.M., Claessens F., Clements J., Collee J.M., Correa M.C., Couch F.J., Cox A., Cunningham J.M., Cybulski C., Czene K., Daly M.B., deFazio A., Devilee P., Diez O., Gago-Dominguez M., Donovan J.L., Dork T., Duell E.J., Dunning A.M., Dwek M., Eccles D.M., Edlund C.K., Edwards D.R.V., Ellberg C., Evans D.G., Fasching P.A., Ferris R.L., Liloglou T., Figueiredo J.C., Fletcher O., Fortner R.T., Fostira F., Franceschi S., Friedman E., Gallinger S.J., Ganz P.A., Garber J., Garcia-Saenz J.A., Gayther S.A., Giles G.G., Godwin A.K., Goldberg M.S., Goldgar D.E., Goode E.L., Goodman M.T., Goodman G., Grankvist K., Greene M.H., Gronberg H., Gronwald J., Guenel P., Hakansson N., Hall P., Hamann U., Hamdy F.C., Hamilton R.J., Hampe J., Haugen A., Heitz F., Herrero R., Hillemanns P., Hoffmeister M., Hogdall E., Hong Y.-C., Hopper J.L., Houlston R., Hulick P.J., Hunter D.J., Huntsman D.G., Idos G., Imyanitov E.N., Ingles S.A., Isaacs C., Jakubowska A., James P., Jenkins M.A., Johansson M., John E.M., Joshi A.D., Kaneva R., Karlan B.Y., Kelemen L.E., Kuhl T., Khaw K.-T., Khusnutdinova E., Kibel A.S., Kiemeney L.A., Kim J., Kjaer S.K., Knight J.A., Kogevinas M., Kote-Jarai Z., Koutros S., Kristensen V.N., Kupryjanczyk J., Lacko M., Lam S., Lambrechts D., Landi M.T., Lazarus P., Le N.D., Lee E., Lejbkowicz F., Lenz H.-J., Leslie G., Lessel D., Lester J., Levine D.A., Li L., Li C.I., Lindblom A., Lindor N.M., Liu G., Loupakis F., Lubinski J., Maehle L., Maier C., Mannermaa A., Marchand L.L., Margolin S., May T., McGuffog L., Meindl A., Middha P., Miller A., Milne R.L., MacInnis R.J., Modugno F., Montagna M., Moreno V., Moysich K.B., Mucci L., Muir K., Mulligan A.M., Nathanson K.L., Neal D.E., Ness A.R., Neuhausen S.L., Nevanlinna H., Newcomb P.A., Newcomb L.F., Nielsen F.C., Nikitina-Zake L., Nordestgaard B.G., Nussbaum R.L., Offit K., Olah E., Olama A.A.A., Olopade O.I., Olshan A.F., Olsson H., Osorio A., Pandha H., Park J.Y., Pashayan N., Parsons M.T., Pejovic T., Penney K.L., Peters W.H.M., Phelan C.M., Phipps A.I., Plaseska-Karanfilska D., Pring M., Prokofyeva D., Radice P., Stefansson K., Ramus S.J., Raskin L., Rennert G., Rennert H.S., van Rensburg E.J., Riggan M.J., Risch H.A., Risch A., Roobol M.J., Rosenstein B.S., Rossing M.A., De Ruyck K., Saloustros E., Sandler D.P., Sawyer E.J., Schabath M.B., Schleutker J., Schmidt M.K., Setiawan V.W., Shen H., Siegel E.M., Sieh W., Singer C.F., Slattery M.L., Sorensen K.D., Southey M.C., Spurdle A.B., Stanford J.L., Stevens V.L., Stintzing S., Stone J., Sundfeldt K., Sutphen R., Swerdlow A.J., Tajara E.H., Tardon A., Taylor J.A., Teare M.D., Teixeira M.R., Terry M.B., Terry K.L., Thibodeau S.N., Thomassen M., Bjorge L., Tischkowitz M., Toland A.E., Torres D., Townsend P.A., Travis R.C., Tung N., Tworoger S.S., Ulrich C.M., Usmani N., Vachon C.M., Van Nieuwenhuysen E., Vega A., Aguado-Barrera M.E., Wang Q., Webb P.M., Weinberg C.R., Weinstein S., Weissler M.C., Weitzel J.N., West C.M.L., White E., Whittemore A.S., Wichmann H.-E., Wiklund F., Winqvist R., Wolk A., Woll P., Woods M., and Wu A.H.
- Abstract
An amendment to this paper has been published and can be accessed via a link at the top of the paper.Copyright © 2019, The Author(s).
- Published
- 2019
33. Erratum: Publisher Correction: Shared heritability and functional enrichment across six solid cancers (Nature communications (2019) 10 1 (431))
- Author
-
Jiang, X. (Xia), Finucane, H.K. (Hilary K.), Schumacher, F.R. (Fredrick R), Schmit, S.L. (Stephanie L.), Tyrer, J.P. (Jonathan P.), Han, Y. (Younghun), Michailidou, K. (Kyriaki), Lesseur, C. (Corina), Kuchenbaecker, K.B. (Karoline), Dennis, J. (Joe), Conti, G. (Giario), Casey, G. (Graham), Gaudet, M.M. (Mia M.), Huyghe, J.R. (Jeroen R.), Albanes, D. (Demetrius), Aldrich, M.C. (Melinda), Andrew, A.S. (Angeline S.), Andrulis, I.L. (Irene L.), Anton-Culver, H. (Hoda), Antoniou, A.C. (Antonis C.), Antonenkova, N.N. (Natalia N.), Arnold, S.M. (Susanne M.), Aronson, K.J. (Kristan J.), Arun, B.K. (Banu), Bandera, E.V. (Elisa), Barkardottir, R.B. (Rosa B.), Barnes, D. (Daniel), Batra, J. (Jyotsna), Beckmann, M.W. (Matthias), Benítez, J. (Javier), Benlloch, S. (Sara), Berchuck, A. (Andrew), Berndt, S.I. (Sonja), Bickeböller, H. (Heike), Bien, S.A. (Stephanie A.), Blomqvist, C. (Carl), Boccia, S. (Stefania), Bogdanova, N.V. (Natalia V.), Bojesen, S.E. (Stig), Bolla, M.K. (Manjeet K.), Brauch, H. (Hiltrud), Brenner, H. (Hermann), Brenton, J.D. (James D.), Brook, R.H., Brunet, J. (Joan), Brunnström, H. (Hans), Buchanan, D.D. (Daniel D.), Burwinkel, B. (Barbara), Butzow, R. (Ralf), Cadoni, G. (Gabriella), Caldes, T. (Trinidad), Caligo, M.A. (Maria A.), Campbell, I. (Ian), Campbell, P.T. (Peter T.), Cancel-Tassin, G. (Géraldine), Cannon-Albright, L.A. (Lisa), Campa, D. (Daniele), Caporaso, N.E. (Neil), Carvalho, A.L. (André L), Chan, A.T. (Andrew T.), Chang-Claude, J. (Jenny), Chanock, S.J. (Stephen), Chen, C. (Chu), Christiani, D.C. (David C.), Claes, K.B.M. (Kathleen B M), Claessens, F. (Frank), Clements, J. (Judith), Collée, J.M. (J Margriet), Correa, M.C. (Marcia Cruz), Couch, F.J. (Fergus), Cox, A. (Angela), Cunningham, J.M. (Julie), Cybulski, C. (Cezary), Czene, K. (Kamila), Daly, M.B. (Mary), DeFazio, A. (Anna), Devilee, P. (Peter), Diez, O. (Orland), Gago-Dominguez, M. (Manuela), Donovan, J.L. (Jenny L.), Dörk, T. (Thilo), Duell, E.J. (Eric), Dunning, A.M. (Alison M.), Dwek, M. (Miriam), Eccles, D. (Diana), Edlund, C.K. (Christopher), Edwards, D.R.V. (Digna R Velez), Ellberg, C. (Carolina), Evans, D.G. (D Gareth), Fasching, P.A. (Peter), Ferris, R.L. (Robert L.), Liloglou, T. (Triantafillos), Figueiredo, J.C. (Jane C.), Fletcher, O. (Olivia), Fortner, R.T. (Renée T), Fostira, F. (Florentia), Franceschi, S. (Silvia), Friedman, E. (Eitan), Gallinger, S. (Steve), Ganz, P.A. (Patricia), Garber, J. (Judy), García-Sáenz, J.A. (José A), Gayther, S.A. (Simon), Giles, G.G. (Graham G.), Godwin, A.K. (Andrew K.), Goldberg, M.S. (Mark), Goldgar, D.E. (David E.), Goode, E.L. (Ellen), Goodman, M.T. (Marc), Goodman, G. (Gary), Grankvist, K. (Kjell), Greene, M.H. (Mark H.), Grönberg, H. (Henrik), Gronwald, J. (Jacek), Guénel, P. (Pascal), Håkansson, N. (Niclas), Hall, P. (Per), Hamann, U. (Ute), Hamdy, F. (Freddie), Hamilton, R.J. (Robert J.), Hampe, J. (Jochen), Haugen, A. (Aage), Heitz, F. (Florian), Herrero, R. (Rolando), Hillemanns, P. (Peter), Hoffmeister, M. (Michael), Høgdall, E. (Estrid), Hong, Y.-C. (Yun-Chul), Hopper, J.L. (John), Houlston, R. (Richard), Hulick, P.J. (Peter J.), Hunter, D.J. (David), Huntsman, D.G. (David G.), Idos, G. (Gregory), Imyanitov, E.N. (Evgeny), Ingles, S.A. (Sue), Isaacs, C. (Claudine), Jakubowska, A. (Anna), James, M. (Margaret), Jenkins, M.A. (Mark A.), Johansson, M. (Mattias), Johansson, M. (Mikael), John, E.M. (Esther), Joshi, A.D. (Amit D.), Kaneva, R. (Radka), Karlan, B.Y. (Beth), Kelemen, L.E. (Linda E.), Kühl, T. (Tabea), Khaw, K.-T. (Kay-Tee), Khusnutdinova, E.K. (Elza), Kibel, A. (Adam), Kiemeney, L.A. (Lambertus A.), Kim, J. (Jongoh), Kjaer, M. (Michael), Knight, J.A. (Julia), Kogevinas, M. (Manolis), Kote-Jarai, Z., Koutros, S. (Stella), Kristensen, V. (Vessela), Kupryjanczyk, J. (Jolanta), Lacko, M. (Martin), Lam, S. (Stephan), Lambrechts, D. (Diether), Landi, M.T. (Maria Teresa), Lazarus, P. (Philip), Le, N.D. (Nhu D.), Lee, E. (Eunjung), Lejbkowicz, F. (Flavio), Lenz, H.-J. (Heinz-Josef), Leslie, G. (Goska), Lessel, D. (Davor), Lester, J. (Jenny), Levine, D.A. (Douglas), Li, L. (Li), Li, C.I. (Christopher I.), Lindblom, A. (Annika), Lindor, N.M. (Noralane), Liu, G. (Geoffrey), Loupakis, F. (Fotios), Lubinski, J. (Jan), Maehle, L., Maier, C. (Christiane), Mannermaa, A. (Arto), Le Marchand, L. (Loic), Margolin, S. (Sara), May, T. (Taymaa), McGuffog, L. (Lesley), Meindl, A. (Alfons), Middha, P. (Pooja), Miller, A. (Austin), Milne, R.L. (Roger), MacInnis, R.J. (Robert J.), Modugno, F. (Francesmary), Montagna, M. (Marco), Moreno, V. (Víctor), Moysich, K.B. (Kirsten), Mucci, L. (Lorelei), Muir, K. (Kenneth), Mulligan, A.-M. (Anna-Marie), Nathanson, K.L. (Katherine), Neal, D. (David), Ness, A.R. (Andrew R.), Neuhausen, S.L. (Susan L.), Nevanlinna, H. (Heli), Newcomb, P. (Polly), Newcomb, L.F. (Lisa F.), Nielsen, F. (Finn), Nikitina-Zake, L. (Liene), Nordestgaard, B.G. (Børge), Nussbaum, R. (Robert), Offit, K. (Kenneth), Olah, E. (Edith), Olama, A.A.A. (Ali Amin Al), Olopade, O.I. (Olofunmilayo), Olshan, A.F. (Andrew F.), Olsson, H. (Håkan), Osorio, A. (Ana), Pandha, H. (Hardev), Park, J.Y. (Jong Y.), Pashayan, N. (Nora), Parsons, M. (Marilyn), Pejovic, T. (Tanja), Penney, K.L. (Kathryn L.), Peters, W.H.M. (Wilbert), Phelan, C. (Catherine), Phipps, A.I. (Amanda I.), Plaseska-Karanfilska, D. (Dijana), Pring, M. (Miranda), Prokofyeva, D. (Darya), Radice, P. (Paolo), Stefansson, K. (Kari), Ramus, S.J. (Susan), Raskin, L. (Leon), Rennert, G. (Gad), Rennert, H.S. (Hedy S.), Rensburg, E.J. (Elizabeth) van, Riggan, M.J. (Marjorie J.), Risch, H.A. (Harvey A.), Risch, A. (Angela), Roobol, M.J. (Monique J.), Rosenstein, B.S. (Barry S.), Rossing, M.A. (Mary Anne), De Ruyck, K. (Kim), Saloustros, E. (Emmanouil), Sandler, D.P. (Dale P.), Sawyer, E.J. (Elinor J.), Schabath, M.B. (Matthew), Schleutker, J. (Johanna), Schmidt, M.K. (Marjanka), Setiawan, V.W. (V Wendy), Shen, H. (Hongbing), Siegel, E.M. (Erin M.), Sieh, W. (Weiva), Singer, C.F. (Christian), Slattery, M.L. (Martha L.), Sorensen, K.D. (Karina Dalsgaard), Southey, M.C. (Melissa), Spurdle, A.B. (Amanda), Stanford, J.L. (Janet L.), Stevens, V.L. (Victoria L.), Stintzing, S. (Sebastian), Stone, J. (Jennifer), Sundfeldt, K. (Karin), Sutphen, R. (Rebecca), Swerdlow, A.J. (Anthony ), Tajara, E.H. (Eloiza H.), Tangen, C.M. (Catherine M.), Tardón, A. (Adonina), Taylor, J.A. (Jack A.), Teare, M.D. (M Dawn), Teixeira, P.J., Terry, M.B. (Mary Beth), Terry, K.L. (Kathryn L.), Thibodeau, S.N. (Stephen), Thomassen, M. (Mads), Bjørge, L. (Line), Tischkowitz, M. (Marc), Toland, A.E. (Amanda), Torres, D. (Diana), Townsend, P.A. (Paul A.), Travis, S.P.L. (Simon), Tung, N. (Nadine), Tworoger, S. (Shelley), Ulrich, C. (Cornelia), Usmani, N. (Nawaid), Vachon, C. (Celine), Van Nieuwenhuysen, E. (Els), Vega, A. (Ana), Aguado-Barrera, M.E. (Miguel Elías), Wang, Q. (Qin), Webb, P. (Penny), Weinberg, C.R. (Clarice R.), Weinstein, S. (Stephanie), Weissler, M.C. (Mark C.), Weitzel, J.N. (Jeffrey), West, C.M.L. (Catharine M L), White, E. (Emily), Whittemore, A.S. (Alice), Wichmann, H.-E. (H-Erich), Wiklund, F. (Fredrik), Winqvist, R. (Robert), Wolk, K. (Kerstin), Woll, P.J. (Penella J), Woods, M.O. (Michael), Wu, A.H. (Anna H.), Wu, X. (Xifeng), Yannoukakos, D. (Drakoulis), Zheng, W. (Wei), Zienolddiny, S. (Shanbeh), Ziogas, A. (Argyrios), Zorn, K.K. (Kristin K.), Lane, J.M. (Jacqueline M.), Saxena, R. (Richa), Thomas, D.C. (Duncan), Hung, R.J. (Rayjean J.), Diergaarde, B. (Brenda), McKay, J. (James), Peters, U. (Ulrike), Hsu, L. (Li), García-Closas, M. (Montserrat), Eeles, R.A. (Rosalind A.), Chenevix-Trench, G. (Georgia), Brennan, P.J. (Paul J.), Haiman, C.A. (Christopher), Simard, J. (Jacques), Easton, D.F. (Douglas), Gruber, S.B. (Stephen), Pharoah, P.D.P. (Paul), Price, A.L. (Alkes L.), Pasaniuc, B. (Bogdan), Amos, C.I. (Christopher I.), Kraft, P. (Peter), Lindström, S. (Sara), Jiang, X. (Xia), Finucane, H.K. (Hilary K.), Schumacher, F.R. (Fredrick R), Schmit, S.L. (Stephanie L.), Tyrer, J.P. (Jonathan P.), Han, Y. (Younghun), Michailidou, K. (Kyriaki), Lesseur, C. (Corina), Kuchenbaecker, K.B. (Karoline), Dennis, J. (Joe), Conti, G. (Giario), Casey, G. (Graham), Gaudet, M.M. (Mia M.), Huyghe, J.R. (Jeroen R.), Albanes, D. (Demetrius), Aldrich, M.C. (Melinda), Andrew, A.S. (Angeline S.), Andrulis, I.L. (Irene L.), Anton-Culver, H. (Hoda), Antoniou, A.C. (Antonis C.), Antonenkova, N.N. (Natalia N.), Arnold, S.M. (Susanne M.), Aronson, K.J. (Kristan J.), Arun, B.K. (Banu), Bandera, E.V. (Elisa), Barkardottir, R.B. (Rosa B.), Barnes, D. (Daniel), Batra, J. (Jyotsna), Beckmann, M.W. (Matthias), Benítez, J. (Javier), Benlloch, S. (Sara), Berchuck, A. (Andrew), Berndt, S.I. (Sonja), Bickeböller, H. (Heike), Bien, S.A. (Stephanie A.), Blomqvist, C. (Carl), Boccia, S. (Stefania), Bogdanova, N.V. (Natalia V.), Bojesen, S.E. (Stig), Bolla, M.K. (Manjeet K.), Brauch, H. (Hiltrud), Brenner, H. (Hermann), Brenton, J.D. (James D.), Brook, R.H., Brunet, J. (Joan), Brunnström, H. (Hans), Buchanan, D.D. (Daniel D.), Burwinkel, B. (Barbara), Butzow, R. (Ralf), Cadoni, G. (Gabriella), Caldes, T. (Trinidad), Caligo, M.A. (Maria A.), Campbell, I. (Ian), Campbell, P.T. (Peter T.), Cancel-Tassin, G. (Géraldine), Cannon-Albright, L.A. (Lisa), Campa, D. (Daniele), Caporaso, N.E. (Neil), Carvalho, A.L. (André L), Chan, A.T. (Andrew T.), Chang-Claude, J. (Jenny), Chanock, S.J. (Stephen), Chen, C. (Chu), Christiani, D.C. (David C.), Claes, K.B.M. (Kathleen B M), Claessens, F. (Frank), Clements, J. (Judith), Collée, J.M. (J Margriet), Correa, M.C. (Marcia Cruz), Couch, F.J. (Fergus), Cox, A. (Angela), Cunningham, J.M. (Julie), Cybulski, C. (Cezary), Czene, K. (Kamila), Daly, M.B. (Mary), DeFazio, A. (Anna), Devilee, P. (Peter), Diez, O. (Orland), Gago-Dominguez, M. (Manuela), Donovan, J.L. (Jenny L.), Dörk, T. (Thilo), Duell, E.J. (Eric), Dunning, A.M. (Alison M.), Dwek, M. (Miriam), Eccles, D. (Diana), Edlund, C.K. (Christopher), Edwards, D.R.V. (Digna R Velez), Ellberg, C. (Carolina), Evans, D.G. (D Gareth), Fasching, P.A. (Peter), Ferris, R.L. (Robert L.), Liloglou, T. (Triantafillos), Figueiredo, J.C. (Jane C.), Fletcher, O. (Olivia), Fortner, R.T. (Renée T), Fostira, F. (Florentia), Franceschi, S. (Silvia), Friedman, E. (Eitan), Gallinger, S. (Steve), Ganz, P.A. (Patricia), Garber, J. (Judy), García-Sáenz, J.A. (José A), Gayther, S.A. (Simon), Giles, G.G. (Graham G.), Godwin, A.K. (Andrew K.), Goldberg, M.S. (Mark), Goldgar, D.E. (David E.), Goode, E.L. (Ellen), Goodman, M.T. (Marc), Goodman, G. (Gary), Grankvist, K. (Kjell), Greene, M.H. (Mark H.), Grönberg, H. (Henrik), Gronwald, J. (Jacek), Guénel, P. (Pascal), Håkansson, N. (Niclas), Hall, P. (Per), Hamann, U. (Ute), Hamdy, F. (Freddie), Hamilton, R.J. (Robert J.), Hampe, J. (Jochen), Haugen, A. (Aage), Heitz, F. (Florian), Herrero, R. (Rolando), Hillemanns, P. (Peter), Hoffmeister, M. (Michael), Høgdall, E. (Estrid), Hong, Y.-C. (Yun-Chul), Hopper, J.L. (John), Houlston, R. (Richard), Hulick, P.J. (Peter J.), Hunter, D.J. (David), Huntsman, D.G. (David G.), Idos, G. (Gregory), Imyanitov, E.N. (Evgeny), Ingles, S.A. (Sue), Isaacs, C. (Claudine), Jakubowska, A. (Anna), James, M. (Margaret), Jenkins, M.A. (Mark A.), Johansson, M. (Mattias), Johansson, M. (Mikael), John, E.M. (Esther), Joshi, A.D. (Amit D.), Kaneva, R. (Radka), Karlan, B.Y. (Beth), Kelemen, L.E. (Linda E.), Kühl, T. (Tabea), Khaw, K.-T. (Kay-Tee), Khusnutdinova, E.K. (Elza), Kibel, A. (Adam), Kiemeney, L.A. (Lambertus A.), Kim, J. (Jongoh), Kjaer, M. (Michael), Knight, J.A. (Julia), Kogevinas, M. (Manolis), Kote-Jarai, Z., Koutros, S. (Stella), Kristensen, V. (Vessela), Kupryjanczyk, J. (Jolanta), Lacko, M. (Martin), Lam, S. (Stephan), Lambrechts, D. (Diether), Landi, M.T. (Maria Teresa), Lazarus, P. (Philip), Le, N.D. (Nhu D.), Lee, E. (Eunjung), Lejbkowicz, F. (Flavio), Lenz, H.-J. (Heinz-Josef), Leslie, G. (Goska), Lessel, D. (Davor), Lester, J. (Jenny), Levine, D.A. (Douglas), Li, L. (Li), Li, C.I. (Christopher I.), Lindblom, A. (Annika), Lindor, N.M. (Noralane), Liu, G. (Geoffrey), Loupakis, F. (Fotios), Lubinski, J. (Jan), Maehle, L., Maier, C. (Christiane), Mannermaa, A. (Arto), Le Marchand, L. (Loic), Margolin, S. (Sara), May, T. (Taymaa), McGuffog, L. (Lesley), Meindl, A. (Alfons), Middha, P. (Pooja), Miller, A. (Austin), Milne, R.L. (Roger), MacInnis, R.J. (Robert J.), Modugno, F. (Francesmary), Montagna, M. (Marco), Moreno, V. (Víctor), Moysich, K.B. (Kirsten), Mucci, L. (Lorelei), Muir, K. (Kenneth), Mulligan, A.-M. (Anna-Marie), Nathanson, K.L. (Katherine), Neal, D. (David), Ness, A.R. (Andrew R.), Neuhausen, S.L. (Susan L.), Nevanlinna, H. (Heli), Newcomb, P. (Polly), Newcomb, L.F. (Lisa F.), Nielsen, F. (Finn), Nikitina-Zake, L. (Liene), Nordestgaard, B.G. (Børge), Nussbaum, R. (Robert), Offit, K. (Kenneth), Olah, E. (Edith), Olama, A.A.A. (Ali Amin Al), Olopade, O.I. (Olofunmilayo), Olshan, A.F. (Andrew F.), Olsson, H. (Håkan), Osorio, A. (Ana), Pandha, H. (Hardev), Park, J.Y. (Jong Y.), Pashayan, N. (Nora), Parsons, M. (Marilyn), Pejovic, T. (Tanja), Penney, K.L. (Kathryn L.), Peters, W.H.M. (Wilbert), Phelan, C. (Catherine), Phipps, A.I. (Amanda I.), Plaseska-Karanfilska, D. (Dijana), Pring, M. (Miranda), Prokofyeva, D. (Darya), Radice, P. (Paolo), Stefansson, K. (Kari), Ramus, S.J. (Susan), Raskin, L. (Leon), Rennert, G. (Gad), Rennert, H.S. (Hedy S.), Rensburg, E.J. (Elizabeth) van, Riggan, M.J. (Marjorie J.), Risch, H.A. (Harvey A.), Risch, A. (Angela), Roobol, M.J. (Monique J.), Rosenstein, B.S. (Barry S.), Rossing, M.A. (Mary Anne), De Ruyck, K. (Kim), Saloustros, E. (Emmanouil), Sandler, D.P. (Dale P.), Sawyer, E.J. (Elinor J.), Schabath, M.B. (Matthew), Schleutker, J. (Johanna), Schmidt, M.K. (Marjanka), Setiawan, V.W. (V Wendy), Shen, H. (Hongbing), Siegel, E.M. (Erin M.), Sieh, W. (Weiva), Singer, C.F. (Christian), Slattery, M.L. (Martha L.), Sorensen, K.D. (Karina Dalsgaard), Southey, M.C. (Melissa), Spurdle, A.B. (Amanda), Stanford, J.L. (Janet L.), Stevens, V.L. (Victoria L.), Stintzing, S. (Sebastian), Stone, J. (Jennifer), Sundfeldt, K. (Karin), Sutphen, R. (Rebecca), Swerdlow, A.J. (Anthony ), Tajara, E.H. (Eloiza H.), Tangen, C.M. (Catherine M.), Tardón, A. (Adonina), Taylor, J.A. (Jack A.), Teare, M.D. (M Dawn), Teixeira, P.J., Terry, M.B. (Mary Beth), Terry, K.L. (Kathryn L.), Thibodeau, S.N. (Stephen), Thomassen, M. (Mads), Bjørge, L. (Line), Tischkowitz, M. (Marc), Toland, A.E. (Amanda), Torres, D. (Diana), Townsend, P.A. (Paul A.), Travis, S.P.L. (Simon), Tung, N. (Nadine), Tworoger, S. (Shelley), Ulrich, C. (Cornelia), Usmani, N. (Nawaid), Vachon, C. (Celine), Van Nieuwenhuysen, E. (Els), Vega, A. (Ana), Aguado-Barrera, M.E. (Miguel Elías), Wang, Q. (Qin), Webb, P. (Penny), Weinberg, C.R. (Clarice R.), Weinstein, S. (Stephanie), Weissler, M.C. (Mark C.), Weitzel, J.N. (Jeffrey), West, C.M.L. (Catharine M L), White, E. (Emily), Whittemore, A.S. (Alice), Wichmann, H.-E. (H-Erich), Wiklund, F. (Fredrik), Winqvist, R. (Robert), Wolk, K. (Kerstin), Woll, P.J. (Penella J), Woods, M.O. (Michael), Wu, A.H. (Anna H.), Wu, X. (Xifeng), Yannoukakos, D. (Drakoulis), Zheng, W. (Wei), Zienolddiny, S. (Shanbeh), Ziogas, A. (Argyrios), Zorn, K.K. (Kristin K.), Lane, J.M. (Jacqueline M.), Saxena, R. (Richa), Thomas, D.C. (Duncan), Hung, R.J. (Rayjean J.), Diergaarde, B. (Brenda), McKay, J. (James), Peters, U. (Ulrike), Hsu, L. (Li), García-Closas, M. (Montserrat), Eeles, R.A. (Rosalind A.), Chenevix-Trench, G. (Georgia), Brennan, P.J. (Paul J.), Haiman, C.A. (Christopher), Simard, J. (Jacques), Easton, D.F. (Douglas), Gruber, S.B. (Stephen), Pharoah, P.D.P. (Paul), Price, A.L. (Alkes L.), Pasaniuc, B. (Bogdan), Amos, C.I. (Christopher I.), Kraft, P. (Peter), and Lindström, S. (Sara)
- Abstract
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
- Published
- 2019
- Full Text
- View/download PDF
34. High burden of infectious disease and antibiotic use in early life in Australian Aboriginal communities.
- Author
-
Campbell P.T., McVernon J., Lydeamore M.J., Andrews R.M., Cuningham W., Carapetis J., Kearns T., Clucas D., Dhurrkay R.G., Tong S.Y.C., Campbell P.T., McVernon J., Lydeamore M.J., Andrews R.M., Cuningham W., Carapetis J., Kearns T., Clucas D., Dhurrkay R.G., and Tong S.Y.C.
- Abstract
OBJECTIVE: To quantify the childhood infectious disease burden and antibiotic use in the Northern Territory's East Arnhem region through synthesis and analysis of historical data resources. METHOD(S): We combined primary health clinic data originally reported in three separate publications stemming from the East Arnhem Healthy Skin Project (Jan-01 to Sep-07). Common statistical techniques were used to explore the prevalence of infectious conditions and the seasonality of infections, and to measure rates of antibiotic use. RESULT(S): There was a high monthly prevalence of respiratory (mean: 32% [95% confidence interval (CI): 20%, 34%]) and skin (mean: 20% [95%CI: 19%, 22%]) infectious syndromes, with upper respiratory tract infections (mean: 29% [95%CI: 27%, 31%]) and skin sores (mean: 15% [95%CI: 14%, 17%]) the most common conditions. Antibiotics were frequently prescribed with 95% (95%CI: 91%, 97%) of children having received at least one antibiotic prescription by their first birthday, and 47% having received six antibiotic prescriptions; skin sores being a key driver. CONCLUSION(S): Early life infections drive high antibiotic prescribing rates in remote Aboriginal communities. Implications for public health: Eliminating skin disease could reduce antibiotic use by almost 20% in children under five years of age in this population.Copyright © 2019 The Authors.
- Published
- 2019
35. A biological model of scabies infection dynamics and treatment informs mass drug administration strategies to increase the likelihood of elimination
- Author
-
Lydeamore, M.J., primary, Campbell, P.T., additional, Regan, D.G., additional, Tong, S.Y.C., additional, Andrews, R.M., additional, Steer, A.C., additional, Romani, L., additional, Kaldor, J.M., additional, McVernon, J., additional, and McCaw, J.M., additional
- Published
- 2019
- Full Text
- View/download PDF
36. Mendelian randomization study of height and risk of colorectal cancer
- Author
-
Thrift, A.P., Gong, J., Peters, U., Chang-Claude, J., Rudolph, A., Slattery, M.L., Chan, A.T., Esko, T., Wood, A.R., Yang, J., Vedantam, S., Gustafsson, S., Pers, T.H., GIANT Consortium (Albrecht, E., Gieger, C., Grallert, H., Heid, I.M., Illig, T., Müller-Nurasyid, M., Peters, A., Thorand, B., Wichmann, H.-E.), Baron, J.A., Bézieau, S., Kuery, S., Ogino, S., Berndt, S.I., Casey, G., Haile, R.W., Du, M., Harrison, T.A., Thornquist, M., Duggan, D.J., Le Marchand, L., Lemire, M., Lindor, N.M., Seminara, D., Song, M., Thibodeau, S.N., Cotterchio, M., Win, A.K., Jenkins, M.A., Hopper, J.L., Ulrich, C.M., Potter, J.D., Newcomb, P.A., Schoen, R.E., Hoffmeister, M., Brenner, H., White, E.S., Hsu, L.A., and Campbell, P.T.
- Subjects
Male ,Gerontology ,medicine.medical_specialty ,Mendelian Randomization Causal Analysis ,Epidemiology ,Logistic regression ,Risk Factors ,Mendelian randomization ,Humans ,Medicine ,Sex Distribution ,Body Height ,Colorectal Cancer ,Aged ,Rectal Neoplasms ,business.industry ,Confounding ,Case-control study ,General Medicine ,Odds ratio ,Mendelian Randomization Analysis ,Middle Aged ,digestive system diseases ,Confidence interval ,Genetic epidemiology ,Case-Control Studies ,Colonic Neoplasms ,Female ,business ,Demography - Abstract
Background: For men and women, taller height is associated with increased risk of all cancers combined. For colorectal cancer (CRC), it is unclear whether the differential association of height by sex is real or is due to confounding or bias inherent in observational studies. We performed a Mendelian randomization study to examine the association between height and CRC risk. Methods: To minimize confounding and bias, we derived a weighted genetic risk score predicting height (using 696 genetic variants associated with height) in 10 226 CRC cases and 10 286 controls. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI) for associations between height, genetically predicted height and CRC. Results: Using conventional methods, increased height (per 10-cm increment) was associated with increased CRC risk (OR = 1.08, 95% CI = 1.02–1.15). In sex-specific analyses, height was associated with CRC risk for women (OR = 1.15, 95% CI = 1.05–1.26), but not men (OR = 0.98, 95% CI = 0.92–1.05). Consistent with these results, carrying greater numbers of (weighted) height-increasing alleles (per 1-unit increase) was associated with higher CRC risk for women and men combined (OR = 1.07, 95% CI = 1.01–1.14) and for women (OR = 1.09, 95% CI = 1.01–1.19). There was weaker evidence of an association for men (OR = 1.05, 95% CI = 0.96–1.15). Conclusion: We provide evidence for a causal association between height and CRC for women. The CRC-height association for men remains unclear and warrants further investigation in other large studies.
- Published
- 2015
37. Calculation of the age of the first infection for skin sores and scabies in five remote communities in northern Australia.
- Author
-
McVernon J., Campbell P.T., Cuningham W., Andrews R.M., Kearns T., Clucas D., Gundjirryirr Dhurrkay R., Carapetis J., Lydeamore M.J., Tong S.Y.C., McCaw J.M., McVernon J., Campbell P.T., Cuningham W., Andrews R.M., Kearns T., Clucas D., Gundjirryirr Dhurrkay R., Carapetis J., Lydeamore M.J., Tong S.Y.C., and McCaw J.M.
- Abstract
Prevalence of skin sores and scabies in remote Australian Aboriginal communities remains unacceptably high, with Group A Streptococcus (GAS) the dominant pathogen. We aim to better understand the drivers of GAS transmission using mathematical models. To estimate the force of infection, we quantified the age of first skin sores and scabies infection by pooling historical data from three studies conducted across five remote Aboriginal communities for children born between 2001 and 2005. We estimated the age of the first infection using the Kaplan-Meier estimator; parametric exponential mixture model; and Cox proportional hazards. For skin sores, the mean age of the first infection was approximately 10 months and the median was 7 months, with some heterogeneity in median observed by the community. For scabies, the mean age of the first infection was approximately 9 months and the median was 8 months, with significant heterogeneity by the community and an enhanced risk for children born between October and December. The young age of the first infection with skin sores and scabies reflects the high disease burden in these communities.Copyright © Cambridge University Press 2018.
- Published
- 2018
38. Clinical Profiles and Outcomes of Cardiac Transplant Recipients Using Allomap and Cylex Immuknow Assays
- Author
-
Krim, S.R., primary, Campbell, P.T., additional, Desai, S., additional, Mandras, S., additional, Bansal, A., additional, Patel, H., additional, Eiswirth, C., additional, and Ventura, H.O., additional
- Published
- 2015
- Full Text
- View/download PDF
39. B-Type Natriuretic Peptide Profiles in the Setting of Chronic Left Ventricular Assist Device Support
- Author
-
Krim, S.R., primary, Campbell, P.T., additional, Mehra, M.R., additional, and Ventura, H.O., additional
- Published
- 2014
- Full Text
- View/download PDF
40. Blood Pressure Profiles of Patients with Left Ventricular Assist Devices
- Author
-
Campbell, P.T., primary, Krim, S., additional, Desai, S., additional, Mandras, S., additional, Patel, H., additional, Mehra, M.R., additional, and Ventura, H., additional
- Published
- 2014
- Full Text
- View/download PDF
41. Regional Differences in Utilization and Outcomes of Left Ventricular Assist Devices: Insights from the INTERMACS Registry
- Author
-
Krim, S.R., primary, Vivo, R.P., additional, Campbell, P.T., additional, Naftel, D.C., additional, Estep, J.D., additional, Fonarow, G.C., additional, and Ventura, H.O., additional
- Published
- 2014
- Full Text
- View/download PDF
42. (809) - Clinical Profiles and Outcomes of Cardiac Transplant Recipients Using Allomap and Cylex Immuknow Assays
- Author
-
Krim, S.R., Campbell, P.T., Desai, S., Mandras, S., Bansal, A., Patel, H., Eiswirth, C., and Ventura, H.O.
- Published
- 2015
- Full Text
- View/download PDF
43. Body mass index and risk of colon and rectal cancer stratified by tumor location and sex
- Author
-
Campbell, P.T., primary, Manno, M., additional, McLaughlin, J.R., additional, Cotterchio, M., additional, Klar, N., additional, and Gallinger, S., additional
- Published
- 2004
- Full Text
- View/download PDF
44. Colorectal cancer risk among post-menopausal hormone users in a population-based familial case-control study
- Author
-
Campbell, P.T., primary, Cotterchio, M., additional, Klar, N., additional, Mclaughlin, J.R., additional, and Gallinger, S., additional
- Published
- 2003
- Full Text
- View/download PDF
45. (636) - B-Type Natriuretic Peptide Profiles in the Setting of Chronic Left Ventricular Assist Device Support
- Author
-
Krim, S.R., Campbell, P.T., Mehra, M.R., and Ventura, H.O.
- Published
- 2014
- Full Text
- View/download PDF
46. (583) - Blood Pressure Profiles of Patients with Left Ventricular Assist Devices
- Author
-
Campbell, P.T., Krim, S., Desai, S., Mandras, S., Patel, H., Mehra, M.R., and Ventura, H.
- Published
- 2014
- Full Text
- View/download PDF
47. (184) - Regional Differences in Utilization and Outcomes of Left Ventricular Assist Devices: Insights from the INTERMACS Registry
- Author
-
Krim, S.R., Vivo, R.P., Campbell, P.T., Naftel, D.C., Estep, J.D., Fonarow, G.C., and Ventura, H.O.
- Published
- 2014
- Full Text
- View/download PDF
48. A high statistics search for the ppφ−mass enhancement at 2.95 GeV
- Author
-
Armstrong, T.A., Baccari, B., Belletti, M., Booth, P.S.L., Campbell, P.T., Carroll, L.J., Costa, G., Donald, R.A., Edwards, D.N., Evangelista, C., Frame, D., French, B.R., Geer, S.H.P., Girtler, P., Ghidini, B., Hughes, I.S., Jackson, J.N., Königs, E., Lynch, J.G., Mandelli, L., Mättig, P., Miller, D.H., Minto, P.W., Mitaroff, W.A., Müller, K., Otter, G., Palano, A., Pensotti, S., Perini, L., Pinfold, J., Range, W.H., Richardson, J.A., Rudolph, G., Saleemi, F., Scott, L., Schlütter, H., Stewart, D.T., Tamborini, M., Thompson, A.S., Turnbull, R.M., Woodworth, P.L., and Zito, G.
- Abstract
An experiment has been undertaken at the CERN SPS, using the Omega spectrometer, aimed at confirming the enhancement observed in a ppφ−mass spectrum at 2.95 GeV [1]. With statistics of twelve times the original experiment no signal is seen. In the reaction φ−p→ppφ−p, the upper limit (four standard deviations) for the production of a resonance in the ppφ−system at 2.95 GeV, with a width ⩽ 30 MeV, is 50 nb.
- Published
- 1979
- Full Text
- View/download PDF
49. A partial-wave analysis of the (K+K−π−) system produced in π−p → K+K−π−p at 16 GeV/c
- Author
-
Armstrong, T.A., primary, Baccari, B., additional, Bonesini, M., additional, Booth, P.S.L., additional, Brun, R., additional, Campbell, P.T., additional, Carroll, L.J., additional, Costa, G., additional, Donald, R.A., additional, Edwards, D.N., additional, Frame, D., additional, French, B.R., additional, Geer, S.H.P., additional, Girtler, P., additional, Ghidini, B., additional, Hughes, I.S., additional, Jackson, J.N., additional, Lynch, J.G., additional, Mandelli, L., additional, Minto, P.W., additional, Mitaroff, W.A., additional, Müller, K., additional, Otter, G., additional, Palano, A., additional, Perini, L., additional, Pinfold, J., additional, Range, W.H., additional, Richardson, J.A., additional, Rudolph, G., additional, Saleemi, F., additional, Schlütter, H., additional, Schmitz, W., additional, Scott, L., additional, Stewart, D.T., additional, Tamborini, M., additional, Thompson, A.S., additional, and Turnbull, R.M., additional
- Published
- 1982
- Full Text
- View/download PDF
50. A study of the reaction π−p → φφn AT 16 GeV/c
- Author
-
Armstrong, T.A., primary, Baccari, B., additional, Booth, P.S.L., additional, Brun, R., additional, Campbell, P.T., additional, Carroll, L.J., additional, Costa, G., additional, Donald, R.A., additional, Edwards, D.N., additional, Evangelista, C., additional, Frame, D., additional, French, B.R., additional, Geer, S.H.P., additional, Ghidini, B., additional, Girtler, P., additional, Hughes, I.S., additional, Jackson, N.J., additional, Lynch, J.G., additional, Mandelli, L., additional, Mättig, P., additional, Minto, P.W., additional, Mitaroff, W.A., additional, Otter, G., additional, Palano, A., additional, Perini, L., additional, Pinfold, J., additional, Range, W.H., additional, Richardson, J.A., additional, Rudolph, G., additional, Saleemi, F., additional, Schlütter, H., additional, Schmitz, W., additional, Scott, L., additional, Stewart, D.T., additional, Tamborini, M., additional, Thompson, A.S., additional, Turnbull, R.M., additional, and Zito, G., additional
- Published
- 1982
- Full Text
- View/download PDF
Catalog
Books, media, physical & digital resources
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.