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

被引：70

作者：

Wolpin, Brian M. ^{[1
,2
]}

Kraft, Peter ^{[4
,5
]}

Xu, Mousheng ^{[4
]}

Steplowski, Emily ^{[6
]}

Olsson, Martin L. ^{[7
]}

Arslan, Alan A. ^{[8
,9
]}

Bueno-de-Mesquita, H. Bas ^{[10
,11
]}

Gross, Myron ^{[12
]}

Helzlsouer, Kathy ^{[13
,14
]}

Jacobs, Eric J. ^{[15
,16
]}

LaCroix, Andrea ^{[17
]}

Petersen, Gloria ^{[18
]}

Stolzenberg-Solomon, Rachael Z. ^{[19
]}

Zheng, Wei ^{[20
]}

Albanes, Demetrius ^{[20
]}

Allen, Naomi E. ^{[21
,22
]}

Amundadottir, Laufey ^{[20
,23
]}

Austin, Melissa A. ^{[24
]}

Boutron-Ruault, Marie-Christine ^{[25
,26
]}

Buring, Julie E. ^{[27
,28
]}

Canzian, Federico ^{[3
]}

Chanock, Stephen J. ^{[20
,24
]}

Gaziano, J. Michael ^{[32
]}

Giovannucci, Edward L. ^{[2
,4
,29
,30
,31
,33
]}

Hallmans, Goeran ^{[34
]}

Hankinson, Susan E. ^{[2
,4
]}

Hoover, Robert N. ^{[20
]}

Hunter, David J. ^{[2
,4
]}

Hutchinson, Amy ^{[20
,35
]}

Jacobs, Kevin B. ^{[20
,36
]}

Kooperberg, Charles ^{[18
]}

Mendelsohn, Julie B. ^{[20
]}

Michaud, Dominique S. ^{[4
,36
]}

Overvad, Kim ^{[37
]}

Patel, Alpa V. ^{[17
]}

Sanchez, Maria-Jose ^{[38
]}

Sansbury, Leah

Shu, Xiao-Ou ^{[21
,22
]}

Slimani, Nadia ^{[39
]}

Tobias, Geoffrey S. ^{[20
]}

Trichopoulos, Dimitrios ^{[4
,40
]}

Vineis, Paolo ^{[41
]}

Visvanathan, Kala ^{[15
,16
]}

Virtamo, Jarmo ^{[42
]}

Wactawski-Wende, Jean ^{[43
]}

Watters, Joanne ^{[39
]}

Yu, Kai ^{[20
]}

Zeleniuch-Jacquotte, Anne ^{[9
,10
]}

Hartge, Patricia ^{[20
]}

Fuchs, Charles S. ^{[1
,2
]}

机构：

[1] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA

[2] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA

[3] Harvard Univ, Sch Med, Dept Ambulatory Care & Prevent, Boston, MA USA

[4] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA

[5] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA

[6] Informat Management Serv Inc, Silver Spring, MD USA

[7] Lund Univ, Div Hematol & Transfus Med, Dept Lab Med, Lund, Sweden

[8] NYU, Dept Obstet & Gynecol, Sch Med, New York, NY 10016 USA

[9] NYU, Dept Environm Med, Sch Med, New York, NY 10016 USA

[10] NYU, Inst Canc, New York, NY 10016 USA

[11] Natl Inst Publ Hlth & Environm RIVM, Bilthoven, Netherlands

[12] Univ Med Ctr Utrecht, Dept Gastroenterol & Hepatol, Utrecht, Netherlands

[13] Univ Minnesota, Sch Med, Dept Lab Med Pathol, Minneapolis, MN 55455 USA

[14] St Johns Mercy Med Ctr, Prevent & Res Ctr, Baltimore, MD USA

[15] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA

[16] Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA

[17] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA

[18] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA

[19] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA

[20] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA

[21] Vanderbilt Univ, Div Epidemiol, Dept Med, Vanderbilt Epidemiol Ctr, Nashville, TN USA

[22] Vanderbilt Univ, Vanderbilt Ingram Canc Ctr, Nashville, TN USA

[23] Univ Oxford, Canc Epidemiol Unit, Oxford, England

[24] NCI, Lab Translat Genom, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA

[25] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA

[26] Univ Washington, Inst Publ Hlth Genet, Sch Publ Hlth, Seattle, WA 98195 USA

[27] INSERM, Villejuif, France

[28] Inst Gustave Roussy, Villejuif, France

[29] Brigham & Womens Hosp, Dept Med, Div Prevent Med, Phys Hlth Study, Boston, MA 02115 USA

[30] Brigham & Womens Hosp, Dept Med, Div Aging, Phys Hlth Study, Boston, MA 02115 USA

[31] Brigham & Womens Hosp, Dept Med, Div Cardiovasc Med, Phys Hlth Study, Boston, MA 02115 USA

[32] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany

[33] Vet Affairs Boston Healthcare Syst, Massachusetts Vet Epidemiol Res & Informat Ctr, Boston, MA USA

[34] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA

[35] Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden

[36] NCI, Core Genotyping Facil, SAIC Frederick Inc, Frederick, MD 21701 USA

[37] Univ London Imperial Coll Sci Technol & Med, Div Epidemiol Publ Hlth & Primary Care, London, England

[38] Aarhus Univ, Dept Epidemiol, Sch Publ Hlth, Aalborg, Denmark

[39] NCI, Div Canc Control & Populat Sci, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA

[40] Int Agcy Res Canc, F-69372 Lyon, France

[41] Acad Athens, Bur Epidemiol Res, Athens, Greece

[42] Univ London Imperial Coll Sci Technol & Med, MRC HPA Ctr Environm & Hlth, Sch Publ Hlth, London, England

[43] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland

来源：

CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION | 2010年 / 19卷 / 12期

基金：

美国国家卫生研究院; 英国惠康基金; 英国医学研究理事会;

关键词：

VON-WILLEBRAND-FACTOR; GENOME-WIDE ASSOCIATION; GENETIC-VARIANTS; GROUP ANTIGENS; A-TRANSFERASE; SUSCEPTIBILITY; MUTATIONS; SEQUENCE; LOCUS; FUT2;

D O I：

10.1158/1055-9965.EPI-10-0751

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：3140 / 3149

页数：10

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