Pancreatic cancer risk is modulated by inflammatory potential of diet and ABO genotype: A consortia-based evaluation and replication study

Samuel O. Antwi; William R. Bamlet; Katrina S. Pedersen; Kari G. Chaffee; Harvey A. Risch; Nitin Shivappa; Susan E. Steck; Kristin E. Anderson; Paige M. Bracci; Jerry Polesel; Diego Serraino; Carlo La Vecchia; Cristina Bosetti; Donghui Li; Ann L. Oberg; Alan A. Arslan; Demetrius Albanes; Eric J. Duell; Inge Huybrechts; Laufey T. Amundadottir; Robert Hoover; Satu Mannisto; Stephen J. Chanock; Wei Zheng; Xiao Ou Shu; Magdalena Stepien; Federico Canzian; Bas Bueno-De-Mesquita; José Ramon Quirós; Anne Zeleniuch-Jacquotte; Fiona Bruinsma; Roger L. Milne; Graham G. Giles; James R. Hébert; Rachael Z. Stolzenberg-Solomon; Gloria M. Petersen

doi:10.1093/carcin/bgy072

Pancreatic cancer risk is modulated by inflammatory potential of diet and ABO genotype: A consortia-based evaluation and replication study

Samuel O. Antwi, William R. Bamlet, Katrina S. Pedersen, Kari G. Chaffee, Harvey A. Risch, Nitin Shivappa, Susan E. Steck, Kristin E. Anderson, Paige M. Bracci, Jerry Polesel, Diego Serraino, Carlo La Vecchia, Cristina Bosetti, Donghui Li, Ann L. Oberg, Alan A. Arslan, Demetrius Albanes, Eric J. Duell, Inge Huybrechts, Laufey T. AmundadottirRobert Hoover, Satu Mannisto, Stephen J. Chanock, Wei Zheng, Xiao Ou Shu, Magdalena Stepien, Federico Canzian, Bas Bueno-De-Mesquita, José Ramon Quirós, Anne Zeleniuch-Jacquotte, Fiona Bruinsma, Roger L. Milne, Graham G. Giles, James R. Hébert, Rachael Z. Stolzenberg-Solomon, Gloria M. Petersen

Research output: Contribution to journal › Article › peer-review

24 Scopus citations

Abstract

Diets with high inflammatory potential are suspected to increase risk for pancreatic cancer (PC). Using pooled analyses, we examined whether this association applies to populations from different geographic regions and population subgroups with varying risks for PC, including variation in ABO blood type. Data from six case-control studies (cases, n = 2414; controls, n = 4528) in the Pancreatic Cancer Case-Control Consortium (PanC4) were analyzed, followed by replication in five nested case-control studies (cases, n = 1268; controls, n = 4215) from the Pancreatic Cancer Cohort Consortium (PanScan). Two polymorphisms in the ABO locus (rs505922 and rs8176746) were used to infer participants' blood types. Dietary questionnaire-derived nutrient/food intake was used to compute energy-adjusted dietary inflammatory index (E-DII) scores to assess inflammatory potential of diet. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable-adjusted logistic regression. Higher E-DII scores, reflecting greater inflammatory potential of diet, were associated with increased PC risk in PanC4 [ORQ5 versus Q1=2.20, 95% confidence interval (CI) = 1.85-2.61, Ptrend < 0.0001; ORcontinuous = 1.20, 95% CI = 1.17-1.24], and PanScan (ORQ5 versus Q1 = 1.23, 95% CI = 0.92-1.66, Ptrend = 0.008; ORcontinuous = 1.09, 95% CI = 1.02-1.15). As expected, genotype-derived non-O blood type was associated with increased PC risk in both the PanC4 and PanScan studies. Stratified analyses of associations between E-DII quintiles and PC by genotype-derived ABO blood type did not show interaction by blood type (Pinteraction = 0.10 in PanC4 and Pinteraction=0.13 in PanScan). The results show that consuming a pro-inflammatory diet and carrying non-O blood type are each individually, but not interactively, associated with increased PC risk.

Original language	English (US)
Pages (from-to)	1056-1067
Number of pages	12
Journal	Carcinogenesis
Volume	39
Issue number	8
DOIs	https://doi.org/10.1093/carcin/bgy072
State	Published - Jul 30 2018

Bibliographical note

Funding Information:
This PanC4 studies were supported by funding from multiple sources. The Mayo Clinic Biospecimen Resource for Pancreas Research was supported by The National Institutes of Health (NIH)/National Cancer Institute (NCI) grant (P50 CA102701 and R25 CA092049). The University of Minnesota Study was supported by NIH/ NCI grant (RO1 CA58697). The MD Anderson Pancreatic Cancer study was supported by the NIH Research Project Grant Program (RO1 CA98380). The University of California, San Francisco (UCSF) study was supported in part by NCI grants (RO1s CA59706, CA108370, CA109767, CA89726, and CA098889), and by the Rombauer Pancreatic Cancer Research Fund. Cancer incidence data collection in the UCSF study was supported by the California Department of Public Health, the NCI’s Surveillance, Epidemiology and End Results Program (contract N01-PC-35136) awarded to the Northern California Cancer Center. The Yale University Pancreatic Cancer Study was supported by NIH/NCI grant (5R01CA098870). The Italy and Milan studies were supported by the Italian Association for Cancer Research (AIRC, project N. 13203) and within the COST Action (BM1214) EU-Pancreas. N.S. and J.R.H. were supported by the United States National Institute of Diabetes and Digestive and Kidney Diseases (R44DK103377). The Prostate, Lung, Colorectal, Ovarian Cancer Screening Trial was sponsored by National Cancer Institute’s Division of Cancer Prevention, in collaboration with the Division of Cancer Epidemiology and Genetics and supported by contracts from the National Cancer Institute [University of Colorado Denver, NO1-CN-25514, Georgetown University NO1-CN-25522, Pacific Health Research Institute NO1-CN-25515, Henry Ford Health System NO1-CN-25512, University of Minnesota, NO1-CN-25513, Washington University NO1-CN-25516, University of Pittsburgh NO1-CN-25511, University of Utah NO1-CN-25524 Marshfield Clinic Research Foundation NO1-CN-25518, University of Alabama at Birmingham NO1-CN-75022, Westat, Inc. NO1-CN-25476, University of California, Los Angeles NO1-CN-25404]. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Trial was supported by funding provided by the Intramural Research Program of the National Cancer Institute, and the U.S. Public Health Service contracts [(N01-CN-45165, N01-RC-45035, N01-RC-37004]. The New York University Women’s Health Study is supported by the National Cancer Institute research grants (R01CA034588,R01CA098661, P30CA016087) and the National Institute of Environmental Health Sciences Center grant (ES000260). The European Prospective Investigation into Cancer and Nutrition was supported by the European Commission: Public Health and Consumer Protection Directorate 1993–2004; Research Directorate-General 2005; Ligue contre le Cancer; Societé 3 M; Mutuelle Générale de l’Education Nationale; Institut National de la Santé et de la Recherche Médicale (INSERM) (France); German Cancer Aid, German Cancer Research Center, Federal Ministry of Education and Research (Germany); Danish Cancer Society (Denmark); Health Research Fund (FIS) of the Spanish Ministry of Health, The participating regional governments and institutions (Spain); Cancer Research UK, Medical Research Council, Stroke Association, British Heart Foundation, Department of Health, Food Standards Agency, the Wellcome Trust (United Kingdom); Greek Ministry of Health and Social Solidarity, Hellenic Health Foundation and Stavros Niarchos Foundation (Greece); Italian Association for Research on Cancer (AIRC) (Italy); Dutch Ministry of Public Health, Welfare and Sports, Dutch Prevention Funds, LK Research Funds, Dutch ZON (Zorg Onderzoek Nederland) (the Netherlands); Swedish Cancer Society, Swedish Scientific Council, Regional Government of Skane and Västerbotten (Sweden); World Cancer Research Fund (WCRF). The Shanghai Men’s and Women’s Health Studies were supported by the National Cancer Institute extramural research grants (R01CA82729, R01CA70867, R01CA124908). The PanScan project is supported by the Intramural Research Program of the National Institutes of Health, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Department of Health and Human Services.

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Antwi, S. O., Bamlet, W. R., Pedersen, K. S., Chaffee, K. G., Risch, H. A., Shivappa, N., Steck, S. E., Anderson, K. E., Bracci, P. M., Polesel, J., Serraino, D., La Vecchia, C., Bosetti, C., Li, D., Oberg, A. L., Arslan, A. A., Albanes, D., Duell, E. J., Huybrechts, I., ... Petersen, G. M. (2018). Pancreatic cancer risk is modulated by inflammatory potential of diet and ABO genotype: A consortia-based evaluation and replication study. Carcinogenesis, 39(8), 1056-1067. https://doi.org/10.1093/carcin/bgy072

Antwi, SO, Bamlet, WR, Pedersen, KS, Chaffee, KG, Risch, HA, Shivappa, N, Steck, SE, Anderson, KE, Bracci, PM, Polesel, J, Serraino, D, La Vecchia, C, Bosetti, C, Li, D, Oberg, AL, Arslan, AA, Albanes, D, Duell, EJ, Huybrechts, I, Amundadottir, LT, Hoover, R, Mannisto, S, Chanock, SJ, Zheng, W, Shu, XO, Stepien, M, Canzian, F, Bueno-De-Mesquita, B, Quirós, JR, Zeleniuch-Jacquotte, A, Bruinsma, F, Milne, RL, Giles, GG, Hébert, JR, Stolzenberg-Solomon, RZ & Petersen, GM 2018, 'Pancreatic cancer risk is modulated by inflammatory potential of diet and ABO genotype: A consortia-based evaluation and replication study', Carcinogenesis, vol. 39, no. 8, pp. 1056-1067. https://doi.org/10.1093/carcin/bgy072

@article{61ec7a3155be4bfd9d96ab05665d6f07,

title = "Pancreatic cancer risk is modulated by inflammatory potential of diet and ABO genotype: A consortia-based evaluation and replication study",

abstract = "Diets with high inflammatory potential are suspected to increase risk for pancreatic cancer (PC). Using pooled analyses, we examined whether this association applies to populations from different geographic regions and population subgroups with varying risks for PC, including variation in ABO blood type. Data from six case-control studies (cases, n = 2414; controls, n = 4528) in the Pancreatic Cancer Case-Control Consortium (PanC4) were analyzed, followed by replication in five nested case-control studies (cases, n = 1268; controls, n = 4215) from the Pancreatic Cancer Cohort Consortium (PanScan). Two polymorphisms in the ABO locus (rs505922 and rs8176746) were used to infer participants' blood types. Dietary questionnaire-derived nutrient/food intake was used to compute energy-adjusted dietary inflammatory index (E-DII) scores to assess inflammatory potential of diet. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable-adjusted logistic regression. Higher E-DII scores, reflecting greater inflammatory potential of diet, were associated with increased PC risk in PanC4 [ORQ5 versus Q1=2.20, 95% confidence interval (CI) = 1.85-2.61, Ptrend < 0.0001; ORcontinuous = 1.20, 95% CI = 1.17-1.24], and PanScan (ORQ5 versus Q1 = 1.23, 95% CI = 0.92-1.66, Ptrend = 0.008; ORcontinuous = 1.09, 95% CI = 1.02-1.15). As expected, genotype-derived non-O blood type was associated with increased PC risk in both the PanC4 and PanScan studies. Stratified analyses of associations between E-DII quintiles and PC by genotype-derived ABO blood type did not show interaction by blood type (Pinteraction = 0.10 in PanC4 and Pinteraction=0.13 in PanScan). The results show that consuming a pro-inflammatory diet and carrying non-O blood type are each individually, but not interactively, associated with increased PC risk.",

author = "Antwi, {Samuel O.} and Bamlet, {William R.} and Pedersen, {Katrina S.} and Chaffee, {Kari G.} and Risch, {Harvey A.} and Nitin Shivappa and Steck, {Susan E.} and Anderson, {Kristin E.} and Bracci, {Paige M.} and Jerry Polesel and Diego Serraino and {La Vecchia}, Carlo and Cristina Bosetti and Donghui Li and Oberg, {Ann L.} and Arslan, {Alan A.} and Demetrius Albanes and Duell, {Eric J.} and Inge Huybrechts and Amundadottir, {Laufey T.} and Robert Hoover and Satu Mannisto and Chanock, {Stephen J.} and Wei Zheng and Shu, {Xiao Ou} and Magdalena Stepien and Federico Canzian and Bas Bueno-De-Mesquita and Quir{\'o}s, {Jos{\'e} Ramon} and Anne Zeleniuch-Jacquotte and Fiona Bruinsma and Milne, {Roger L.} and Giles, {Graham G.} and H{\'e}bert, {James R.} and Stolzenberg-Solomon, {Rachael Z.} and Petersen, {Gloria M.}",

note = "Funding Information: This PanC4 studies were supported by funding from multiple sources. The Mayo Clinic Biospecimen Resource for Pancreas Research was supported by The National Institutes of Health (NIH)/National Cancer Institute (NCI) grant (P50 CA102701 and R25 CA092049). The University of Minnesota Study was supported by NIH/ NCI grant (RO1 CA58697). The MD Anderson Pancreatic Cancer study was supported by the NIH Research Project Grant Program (RO1 CA98380). The University of California, San Francisco (UCSF) study was supported in part by NCI grants (RO1s CA59706, CA108370, CA109767, CA89726, and CA098889), and by the Rombauer Pancreatic Cancer Research Fund. Cancer incidence data collection in the UCSF study was supported by the California Department of Public Health, the NCI{\textquoteright}s Surveillance, Epidemiology and End Results Program (contract N01-PC-35136) awarded to the Northern California Cancer Center. The Yale University Pancreatic Cancer Study was supported by NIH/NCI grant (5R01CA098870). The Italy and Milan studies were supported by the Italian Association for Cancer Research (AIRC, project N. 13203) and within the COST Action (BM1214) EU-Pancreas. N.S. and J.R.H. were supported by the United States National Institute of Diabetes and Digestive and Kidney Diseases (R44DK103377). The Prostate, Lung, Colorectal, Ovarian Cancer Screening Trial was sponsored by National Cancer Institute{\textquoteright}s Division of Cancer Prevention, in collaboration with the Division of Cancer Epidemiology and Genetics and supported by contracts from the National Cancer Institute [University of Colorado Denver, NO1-CN-25514, Georgetown University NO1-CN-25522, Pacific Health Research Institute NO1-CN-25515, Henry Ford Health System NO1-CN-25512, University of Minnesota, NO1-CN-25513, Washington University NO1-CN-25516, University of Pittsburgh NO1-CN-25511, University of Utah NO1-CN-25524 Marshfield Clinic Research Foundation NO1-CN-25518, University of Alabama at Birmingham NO1-CN-75022, Westat, Inc. NO1-CN-25476, University of California, Los Angeles NO1-CN-25404]. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Trial was supported by funding provided by the Intramural Research Program of the National Cancer Institute, and the U.S. Public Health Service contracts [(N01-CN-45165, N01-RC-45035, N01-RC-37004]. The New York University Women{\textquoteright}s Health Study is supported by the National Cancer Institute research grants (R01CA034588,R01CA098661, P30CA016087) and the National Institute of Environmental Health Sciences Center grant (ES000260). The European Prospective Investigation into Cancer and Nutrition was supported by the European Commission: Public Health and Consumer Protection Directorate 1993–2004; Research Directorate-General 2005; Ligue contre le Cancer; Societ{\'e} 3 M; Mutuelle G{\'e}n{\'e}rale de l{\textquoteright}Education Nationale; Institut National de la Sant{\'e} et de la Recherche M{\'e}dicale (INSERM) (France); German Cancer Aid, German Cancer Research Center, Federal Ministry of Education and Research (Germany); Danish Cancer Society (Denmark); Health Research Fund (FIS) of the Spanish Ministry of Health, The participating regional governments and institutions (Spain); Cancer Research UK, Medical Research Council, Stroke Association, British Heart Foundation, Department of Health, Food Standards Agency, the Wellcome Trust (United Kingdom); Greek Ministry of Health and Social Solidarity, Hellenic Health Foundation and Stavros Niarchos Foundation (Greece); Italian Association for Research on Cancer (AIRC) (Italy); Dutch Ministry of Public Health, Welfare and Sports, Dutch Prevention Funds, LK Research Funds, Dutch ZON (Zorg Onderzoek Nederland) (the Netherlands); Swedish Cancer Society, Swedish Scientific Council, Regional Government of Skane and V{\"a}sterbotten (Sweden); World Cancer Research Fund (WCRF). The Shanghai Men{\textquoteright}s and Women{\textquoteright}s Health Studies were supported by the National Cancer Institute extramural research grants (R01CA82729, R01CA70867, R01CA124908). The PanScan project is supported by the Intramural Research Program of the National Institutes of Health, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Department of Health and Human Services. Publisher Copyright: {\textcopyright} The Author(s) 2018.",

year = "2018",

month = jul,

day = "30",

doi = "10.1093/carcin/bgy072",

language = "English (US)",

volume = "39",

pages = "1056--1067",

journal = "Carcinogenesis",

issn = "0143-3334",

publisher = "Oxford University Press",

number = "8",

}

TY - JOUR

T1 - Pancreatic cancer risk is modulated by inflammatory potential of diet and ABO genotype

T2 - A consortia-based evaluation and replication study

AU - Antwi, Samuel O.

AU - Bamlet, William R.

AU - Pedersen, Katrina S.

AU - Chaffee, Kari G.

AU - Risch, Harvey A.

AU - Shivappa, Nitin

AU - Steck, Susan E.

AU - Anderson, Kristin E.

AU - Bracci, Paige M.

AU - Polesel, Jerry

AU - Serraino, Diego

AU - La Vecchia, Carlo

AU - Bosetti, Cristina

AU - Li, Donghui

AU - Oberg, Ann L.

AU - Arslan, Alan A.

AU - Albanes, Demetrius

AU - Duell, Eric J.

AU - Huybrechts, Inge

AU - Amundadottir, Laufey T.

AU - Hoover, Robert

AU - Mannisto, Satu

AU - Chanock, Stephen J.

AU - Zheng, Wei

AU - Shu, Xiao Ou

AU - Stepien, Magdalena

AU - Canzian, Federico

AU - Bueno-De-Mesquita, Bas

AU - Quirós, José Ramon

AU - Zeleniuch-Jacquotte, Anne

AU - Bruinsma, Fiona

AU - Milne, Roger L.

AU - Giles, Graham G.

AU - Hébert, James R.

AU - Stolzenberg-Solomon, Rachael Z.

AU - Petersen, Gloria M.

N1 - Funding Information: This PanC4 studies were supported by funding from multiple sources. The Mayo Clinic Biospecimen Resource for Pancreas Research was supported by The National Institutes of Health (NIH)/National Cancer Institute (NCI) grant (P50 CA102701 and R25 CA092049). The University of Minnesota Study was supported by NIH/ NCI grant (RO1 CA58697). The MD Anderson Pancreatic Cancer study was supported by the NIH Research Project Grant Program (RO1 CA98380). The University of California, San Francisco (UCSF) study was supported in part by NCI grants (RO1s CA59706, CA108370, CA109767, CA89726, and CA098889), and by the Rombauer Pancreatic Cancer Research Fund. Cancer incidence data collection in the UCSF study was supported by the California Department of Public Health, the NCI’s Surveillance, Epidemiology and End Results Program (contract N01-PC-35136) awarded to the Northern California Cancer Center. The Yale University Pancreatic Cancer Study was supported by NIH/NCI grant (5R01CA098870). The Italy and Milan studies were supported by the Italian Association for Cancer Research (AIRC, project N. 13203) and within the COST Action (BM1214) EU-Pancreas. N.S. and J.R.H. were supported by the United States National Institute of Diabetes and Digestive and Kidney Diseases (R44DK103377). The Prostate, Lung, Colorectal, Ovarian Cancer Screening Trial was sponsored by National Cancer Institute’s Division of Cancer Prevention, in collaboration with the Division of Cancer Epidemiology and Genetics and supported by contracts from the National Cancer Institute [University of Colorado Denver, NO1-CN-25514, Georgetown University NO1-CN-25522, Pacific Health Research Institute NO1-CN-25515, Henry Ford Health System NO1-CN-25512, University of Minnesota, NO1-CN-25513, Washington University NO1-CN-25516, University of Pittsburgh NO1-CN-25511, University of Utah NO1-CN-25524 Marshfield Clinic Research Foundation NO1-CN-25518, University of Alabama at Birmingham NO1-CN-75022, Westat, Inc. NO1-CN-25476, University of California, Los Angeles NO1-CN-25404]. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Trial was supported by funding provided by the Intramural Research Program of the National Cancer Institute, and the U.S. Public Health Service contracts [(N01-CN-45165, N01-RC-45035, N01-RC-37004]. The New York University Women’s Health Study is supported by the National Cancer Institute research grants (R01CA034588,R01CA098661, P30CA016087) and the National Institute of Environmental Health Sciences Center grant (ES000260). The European Prospective Investigation into Cancer and Nutrition was supported by the European Commission: Public Health and Consumer Protection Directorate 1993–2004; Research Directorate-General 2005; Ligue contre le Cancer; Societé 3 M; Mutuelle Générale de l’Education Nationale; Institut National de la Santé et de la Recherche Médicale (INSERM) (France); German Cancer Aid, German Cancer Research Center, Federal Ministry of Education and Research (Germany); Danish Cancer Society (Denmark); Health Research Fund (FIS) of the Spanish Ministry of Health, The participating regional governments and institutions (Spain); Cancer Research UK, Medical Research Council, Stroke Association, British Heart Foundation, Department of Health, Food Standards Agency, the Wellcome Trust (United Kingdom); Greek Ministry of Health and Social Solidarity, Hellenic Health Foundation and Stavros Niarchos Foundation (Greece); Italian Association for Research on Cancer (AIRC) (Italy); Dutch Ministry of Public Health, Welfare and Sports, Dutch Prevention Funds, LK Research Funds, Dutch ZON (Zorg Onderzoek Nederland) (the Netherlands); Swedish Cancer Society, Swedish Scientific Council, Regional Government of Skane and Västerbotten (Sweden); World Cancer Research Fund (WCRF). The Shanghai Men’s and Women’s Health Studies were supported by the National Cancer Institute extramural research grants (R01CA82729, R01CA70867, R01CA124908). The PanScan project is supported by the Intramural Research Program of the National Institutes of Health, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Department of Health and Human Services. Publisher Copyright: © The Author(s) 2018.

PY - 2018/7/30

Y1 - 2018/7/30

N2 - Diets with high inflammatory potential are suspected to increase risk for pancreatic cancer (PC). Using pooled analyses, we examined whether this association applies to populations from different geographic regions and population subgroups with varying risks for PC, including variation in ABO blood type. Data from six case-control studies (cases, n = 2414; controls, n = 4528) in the Pancreatic Cancer Case-Control Consortium (PanC4) were analyzed, followed by replication in five nested case-control studies (cases, n = 1268; controls, n = 4215) from the Pancreatic Cancer Cohort Consortium (PanScan). Two polymorphisms in the ABO locus (rs505922 and rs8176746) were used to infer participants' blood types. Dietary questionnaire-derived nutrient/food intake was used to compute energy-adjusted dietary inflammatory index (E-DII) scores to assess inflammatory potential of diet. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable-adjusted logistic regression. Higher E-DII scores, reflecting greater inflammatory potential of diet, were associated with increased PC risk in PanC4 [ORQ5 versus Q1=2.20, 95% confidence interval (CI) = 1.85-2.61, Ptrend < 0.0001; ORcontinuous = 1.20, 95% CI = 1.17-1.24], and PanScan (ORQ5 versus Q1 = 1.23, 95% CI = 0.92-1.66, Ptrend = 0.008; ORcontinuous = 1.09, 95% CI = 1.02-1.15). As expected, genotype-derived non-O blood type was associated with increased PC risk in both the PanC4 and PanScan studies. Stratified analyses of associations between E-DII quintiles and PC by genotype-derived ABO blood type did not show interaction by blood type (Pinteraction = 0.10 in PanC4 and Pinteraction=0.13 in PanScan). The results show that consuming a pro-inflammatory diet and carrying non-O blood type are each individually, but not interactively, associated with increased PC risk.

AB - Diets with high inflammatory potential are suspected to increase risk for pancreatic cancer (PC). Using pooled analyses, we examined whether this association applies to populations from different geographic regions and population subgroups with varying risks for PC, including variation in ABO blood type. Data from six case-control studies (cases, n = 2414; controls, n = 4528) in the Pancreatic Cancer Case-Control Consortium (PanC4) were analyzed, followed by replication in five nested case-control studies (cases, n = 1268; controls, n = 4215) from the Pancreatic Cancer Cohort Consortium (PanScan). Two polymorphisms in the ABO locus (rs505922 and rs8176746) were used to infer participants' blood types. Dietary questionnaire-derived nutrient/food intake was used to compute energy-adjusted dietary inflammatory index (E-DII) scores to assess inflammatory potential of diet. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable-adjusted logistic regression. Higher E-DII scores, reflecting greater inflammatory potential of diet, were associated with increased PC risk in PanC4 [ORQ5 versus Q1=2.20, 95% confidence interval (CI) = 1.85-2.61, Ptrend < 0.0001; ORcontinuous = 1.20, 95% CI = 1.17-1.24], and PanScan (ORQ5 versus Q1 = 1.23, 95% CI = 0.92-1.66, Ptrend = 0.008; ORcontinuous = 1.09, 95% CI = 1.02-1.15). As expected, genotype-derived non-O blood type was associated with increased PC risk in both the PanC4 and PanScan studies. Stratified analyses of associations between E-DII quintiles and PC by genotype-derived ABO blood type did not show interaction by blood type (Pinteraction = 0.10 in PanC4 and Pinteraction=0.13 in PanScan). The results show that consuming a pro-inflammatory diet and carrying non-O blood type are each individually, but not interactively, associated with increased PC risk.

UR - http://www.scopus.com/inward/record.url?scp=85054962963&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85054962963&partnerID=8YFLogxK

U2 - 10.1093/carcin/bgy072

DO - 10.1093/carcin/bgy072

M3 - Article

C2 - 29800239

AN - SCOPUS:85054962963

SN - 0143-3334

VL - 39

SP - 1056

EP - 1067

JO - Carcinogenesis

JF - Carcinogenesis

IS - 8

ER -

Pancreatic cancer risk is modulated by inflammatory potential of diet and ABO genotype: A consortia-based evaluation and replication study

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