Format

Send to

Choose Destination
Carcinogenesis. 2018 May 25. doi: 10.1093/carcin/bgy072. [Epub ahead of print]

Pancreatic Cancer Risk is Modulated by Inflammatory Potential of Diet and ABO Genotype: A Consortia-based Evaluation and Replication Study.

Author information

1
Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN.
2
Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN.
3
Division of Oncology, Washington University, St. Louis, MO.
4
Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT.
5
Cancer Prevention and Control Program and University of South Carolina, Columbia, SC.
6
Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC.
7
Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN.
8
Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA.
9
Unit of Epidemiology and Biostatistics, Centro di Riferimento Oncologico, Aviano (PN), Italy.
10
Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
11
Department of Oncology, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.
12
Department of Gastrointestinal Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX.
13
Department of Environmental Medicine, New York University School of Medicine, New York, New York, USA.
14
Department of Population Health, New York University School of Medicine, New York, New York, USA.
15
Department of Obstetrics and Gynecology, New York University School of Medicine, New York, NY, USA.
16
Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA.
17
Unit of Nutrition and Cancer, Bellvitge Biomedical Research Institute-IDIBELL, Catalan Institute of Oncology-ICO. L'Hospitalet de Llobregat, Barcelona, Spain.
18
International Agency for Research on Cancer, World Health Organization, Cours Albert Thomas Lyon, France.
19
Department of Public Health Solutions, National Institute for Health and Welfare, Helsinki, Finland.
20
Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, and Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, TN, USA.
21
Genomic Epidemiology Group, German Cancer Research Center (DKFZ), Heidelberg, Germany.
22
Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary's Campus, Norfolk Place, London,  London, United Kingdom.
23
Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Pantai Valley, 50603, Kuala Lumpur, Malaysia.
24
Public Health Directorate, Asturias, Spain.
25
Perlmutter Cancer Center, New York University School of Medicine, New York, NY, USA.
26
Cancer Epidemiology & Intelligence Division; Cancer Council Victoria, and Centre for Epidemiology & Biostatistics, Melbourne School of Global and Population Health, The University of Melbourne, Melbourne, Australia.

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=2,414; controls, n=4,528) in the Pancreatic Cancer Case-Control Consortium (PanC4) were analyzed, followed by replication in five nested case-control studies (cases, n=1,268; controls, n=4,215) 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 (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 vs. Q1=2.20, 95% CI=1.85-2.61, Ptrend<0.0001; ORcontinuous=1.20, 95% CI=1.17-1.24), and PanScan (ORQ5 vs. 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.

PMID:
29800239
PMCID:
PMC6067129
[Available on 2019-07-30]
DOI:
10.1093/carcin/bgy072

Supplemental Content

Full text links

Icon for Silverchair Information Systems
Loading ...
Support Center