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Variant ABO Blood Group Alleles, Secretor Status, and Risk of Pancreatic Cancer: Results from the Pancreatic Cancer Cohort Consortium

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Author

  • Brian M. Wolpin
  • Peter Kraft
  • Mousheng Xu
  • Emily Steplowski
  • Martin L Olsson
  • Alan A. Arslan
  • H. Bas Bueno-de-Mesquita
  • Myron Gross
  • Kathy Helzlsouer
  • Eric J. Jacobs
  • Andrea LaCroix
  • Gloria Petersen
  • Rachael Z. Stolzenberg-Solomon
  • Wei Zheng
  • Demetrius Albanes
  • Naomi E. Allen
  • Laufey Amundadottir
  • Melissa A. Austin
  • Marie-Christine Boutron-Ruault
  • Julie E. Buring
  • Federico Canzian
  • Stephen J. Chanock
  • J. Michael Gaziano
  • Edward L. Giovannucci
  • Goeran Hallmans
  • Susan E. Hankinson
  • Robert N. Hoover
  • David J. Hunter
  • Amy Hutchinson
  • Kevin B. Jacobs
  • Charles Kooperberg
  • Julie B. Mendelsohn
  • Dominique S. Michaud
  • Kim Overvad
  • Alpa V. Patel
  • Maria-Jose Sanchez
  • Leah Sansbury
  • Xiao-Ou Shu
  • Nadia Slimani
  • Geoffrey S. Tobias
  • Dimitrios Trichopoulos
  • Paolo Vineis
  • Kala Visvanathan
  • Jarmo Virtamo
  • Jean Wactawski-Wende
  • Joanne Watters
  • Kai Yu
  • Anne Zeleniuch-Jacquotte
  • Patricia Hartge
  • Charles S. Fuchs
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Summary, in English

Background: Subjects with non-O ABO blood group alleles have increased risk of pancreatic cancer. Glycosyltransferase activity is greater for the A(1) versus A(2) variant, whereas O01 and O02 variants are nonfunctioning. We hypothesized: 1) A(1) allele would confer greater risk than A(2) allele, 2) protective effect of the O allele would be equivalent for O01 and O02 variants, 3) secretor phenotype would modify the association with risk. Methods: We determined ABO variants and secretor phenotype from single nucleotide polymorphisms in ABO and FUT2 genes in 1,533 cases and 1,582 controls from 12 prospective cohort studies. Adjusted odds ratios (OR) for pancreatic cancer were calculated using logistic regression. Results: An increased risk was observed in participants with A(1) but not A(2) alleles. Compared with subjects with genotype O/O, genotypes A(2)/O, A(2)/A(1), A(1)/O, and A(1)/A(1) had ORs of 0.96 (95% CI, 0.72-1.26), 1.46 (95% CI, 0.98-2.17), 1.48 (95% CI, 1.23-1.78), and 1.71 (95% CI, 1.18-2.47). Risk was similar for O01 and O02 variant O alleles. Compared with O01/O01, the ORs for each additional allele of O02, A(1), and A(2) were 1.00 (95% CI, 0.87-1.14), 1.38 (95% CI, 1.20-1.58), and 0.96 (95% CI, 0.77-1.20); P-value, O01 versus O02 = 0.94, A(1) versus A(2) = 0.004. Secretor phenotype was not an effect modifier (P-interaction = 0.63). Conclusions: Among participants in a large prospective cohort consortium, ABO allele subtypes corresponding to increased glycosyltransferase activity were associated with increased pancreatic cancer risk. Impact: These data support the hypothesis that ABO glycosyltransferase activity influences pancreatic cancer risk rather than actions of other nearby genes on chromosome 9q34. Cancer Epidemiol Biomarkers Prev; 19(12); 3140-9. (C) 2010 AACR.

Publishing year

2010

Language

English

Pages

3140-3149

Publication/Series

Cancer Epidemiology Biomarkers & Prevention

Volume

19

Issue

12

Document type

Journal article

Publisher

American Association for Cancer Research

Topic

  • Cancer and Oncology

Status

Published

Research group

  • Transfusion Medicine

ISBN/ISSN/Other

  • ISSN: 1538-7755