Serologic Response to Helicobacter pylori Proteins Associated With Risk of Colorectal Cancer Among Diverse Populations in the United States.
Adolescent
Adult
Aged
Aged, 80 and over
Antibodies, Bacterial
/ blood
Bacterial Proteins
/ immunology
Biomarkers
/ blood
Case-Control Studies
Colorectal Neoplasms
/ blood
Female
Helicobacter Infections
/ blood
Helicobacter pylori
/ immunology
Host-Pathogen Interactions
Humans
Incidence
Male
Middle Aged
Prospective Studies
Risk Factors
Seroepidemiologic Studies
United States
/ epidemiology
Virulence
Young Adult
Cohort Studies
Epidemiology
Gastrointestinal Cancers
Journal
Gastroenterology
ISSN: 1528-0012
Titre abrégé: Gastroenterology
Pays: United States
ID NLM: 0374630
Informations de publication
Date de publication:
01 2019
01 2019
Historique:
received:
29
06
2018
revised:
12
09
2018
accepted:
27
09
2018
pubmed:
9
10
2018
medline:
29
1
2019
entrez:
9
10
2018
Statut:
ppublish
Résumé
Previous studies reported an association of the bacteria Helicobacter pylori, the primary cause of gastric cancer, and risk of colorectal cancer (CRC). However, these findings have been inconsistent, appear to vary with population characteristics, and may be specific for virulence factor VacA. To more thoroughly evaluate the potential association of H pylori antibodies with CRC risk, we assembled a large consortium of cohorts representing diverse populations in the United States. We used H pylori multiplex serologic assays to analyze serum samples from 4063 incident cases of CRC, collected before diagnosis, and 4063 matched individuals without CRC (controls) from 10 prospective cohorts for antibody responses to 13 H pylori proteins, including virulence factors VacA and CagA. The association of seropositivity to H pylori proteins, as well as protein-specific antibody level, with odds of CRC was determined by conditional logistic regression. Overall, 40% of controls and 41% of cases were H pylori-seropositive (odds ratio [OR], 1.09; 95% CI, 0.99-1.20). H pylori VacA-specific seropositivity was associated with an 11% increased odds of CRC (OR, 1.11; 95% CI, 1.01-1.22), and this association was particularly strong among African Americans (OR, 1.45; 95% CI, 1.08-1.95). Additionally, odds of CRC increased with level of VacA antibody in the overall cohort (P = .008) and specifically among African Americans (P = .007). In an analysis of a large consortium of cohorts representing diverse populations, we found serologic responses to H pylori VacA to associate with increased risk of CRC risk, particularly for African Americans. Future studies should seek to understand whether this marker is related to virulent H pylori strains carried in these populations.
Sections du résumé
BACKGROUND & AIMS
Previous studies reported an association of the bacteria Helicobacter pylori, the primary cause of gastric cancer, and risk of colorectal cancer (CRC). However, these findings have been inconsistent, appear to vary with population characteristics, and may be specific for virulence factor VacA. To more thoroughly evaluate the potential association of H pylori antibodies with CRC risk, we assembled a large consortium of cohorts representing diverse populations in the United States.
METHODS
We used H pylori multiplex serologic assays to analyze serum samples from 4063 incident cases of CRC, collected before diagnosis, and 4063 matched individuals without CRC (controls) from 10 prospective cohorts for antibody responses to 13 H pylori proteins, including virulence factors VacA and CagA. The association of seropositivity to H pylori proteins, as well as protein-specific antibody level, with odds of CRC was determined by conditional logistic regression.
RESULTS
Overall, 40% of controls and 41% of cases were H pylori-seropositive (odds ratio [OR], 1.09; 95% CI, 0.99-1.20). H pylori VacA-specific seropositivity was associated with an 11% increased odds of CRC (OR, 1.11; 95% CI, 1.01-1.22), and this association was particularly strong among African Americans (OR, 1.45; 95% CI, 1.08-1.95). Additionally, odds of CRC increased with level of VacA antibody in the overall cohort (P = .008) and specifically among African Americans (P = .007).
CONCLUSIONS
In an analysis of a large consortium of cohorts representing diverse populations, we found serologic responses to H pylori VacA to associate with increased risk of CRC risk, particularly for African Americans. Future studies should seek to understand whether this marker is related to virulent H pylori strains carried in these populations.
Identifiants
pubmed: 30296434
pii: S0016-5085(18)35088-1
doi: 10.1053/j.gastro.2018.09.054
pmc: PMC6309494
mid: NIHMS1508988
pii:
doi:
Substances chimiques
Antibodies, Bacterial
0
Bacterial Proteins
0
Biomarkers
0
VacA protein, Helicobacter pylori
0
Types de publication
Journal Article
Multicenter Study
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
175-186.e2Subventions
Organisme : NCI NIH HHS
ID : P30 CA016087
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201600002C
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201600018C
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA190428
Pays : United States
Organisme : NCI NIH HHS
ID : UM1 CA186107
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI118932
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201600001C
Pays : United States
Organisme : NCI NIH HHS
ID : UM1 CA167552
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA040360
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA077955
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA087969
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL034595
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK058404
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA092447
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA167552
Pays : United States
Organisme : NCI NIH HHS
ID : UM1 CA182934
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201600003C
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA116087
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA057726
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201600004C
Pays : United States
Organisme : BLRD VA
ID : I01 BX000627
Pays : United States
Organisme : NCI NIH HHS
ID : K99 CA215314
Pays : United States
Organisme : NCI NIH HHS
ID : R00 CA215314
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI039657
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK058587
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA202979
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA097193
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA164973
Pays : United States
Commentaires et corrections
Type : CommentIn
Type : CommentIn
Informations de copyright
Copyright © 2019 AGA Institute. Published by Elsevier Inc. All rights reserved.
Références
J Gastrointest Oncol. 2014 Dec;5(6):463-8
pubmed: 25436126
mBio. 2016 Jan 26;7(1):e01869-15
pubmed: 26814181
Cancer Prev Res (Phila). 2014 Jul;7(7):758-65
pubmed: 24824037
Gastroenterology. 1993 Jul;105(1):22-30
pubmed: 8514038
Gut. 2011 Nov;60(11):1479-86
pubmed: 21471567
J Clin Med Res. 2012 Jun;4(3):172-6
pubmed: 22719803
Nat Rev Cancer. 2005 May;5(5):388-96
pubmed: 15864280
J Infect Dis. 1997 May;175(5):1240-2
pubmed: 9129095
J Natl Cancer Inst. 2005 Nov 16;97(22):1688-94
pubmed: 16288122
Helicobacter. 2018 Jun;23(3):e12477
pubmed: 29600573
Infect Immun. 1997 Apr;65(4):1181-8
pubmed: 9119449
Lancet Glob Health. 2016 Sep;4(9):e609-16
pubmed: 27470177
J Cancer Res Ther. 2016 Oct;12(Supplement):15-18
pubmed: 27721244
Cancer Epidemiol Biomarkers Prev. 2013 Nov;22(11):1964-74
pubmed: 24045925
Cancer Epidemiol Biomarkers Prev. 2011 May;20(5):826-34
pubmed: 21357376
Cancer. 2002 Jan 15;94(2):500-11
pubmed: 11900235
Best Pract Res Clin Gastroenterol. 2014 Dec;28(6):1003-15
pubmed: 25439067
Mol Carcinog. 2016 Aug;55(8):1251-61
pubmed: 26333108
Control Clin Trials. 1998 Feb;19(1):61-109
pubmed: 9492970
Chin J Cancer Res. 2017 Apr;29(2):127-136
pubmed: 28536491
J Surg Res. 2008 May 1;146(1):149-58
pubmed: 17720195
Control Clin Trials. 2000 Dec;21(6 Suppl):349S-355S
pubmed: 11189687
CA Cancer J Clin. 2018 Jan;68(1):7-30
pubmed: 29313949
Am J Epidemiol. 2012 Jan 1;175(1):54-9
pubmed: 22085628
Cancer Causes Control. 2012 Apr;23(4):537-45
pubmed: 22367721
Toxins (Basel). 2017 Oct 12;9(10):
pubmed: 29023421
Regul Pept. 2000 Sep 25;93(1-3):13-9
pubmed: 11033048
Gastroenterology. 2005 May;128(5):1512-5
pubmed: 15887132
J Natl Cancer Inst. 1995 Feb 1;87(3):190-7
pubmed: 7707406
Helicobacter. 2016 Dec;21(6):488-492
pubmed: 27006167
Helicobacter. 2017 Sep;22 Suppl 1:
pubmed: 28891133
PLoS Pathog. 2017 Oct 5;13(10):e1006573
pubmed: 28982167
Helicobacter. 2009 Dec;14(6):525-35
pubmed: 19889070
Gastroenterology. 1998 Aug;115(2):275-80
pubmed: 9679032
BMC Cancer. 2014 Apr 28;14:296
pubmed: 24774100
J Clin Oncol. 2006 Nov 1;24(31):5010-6
pubmed: 17075120
Am J Epidemiol. 2000 Feb 15;151(4):346-57
pubmed: 10695593
Am J Epidemiol. 2003 Feb 15;157(4):335-44
pubmed: 12578804
Gastroenterology. 2017 Aug;153(2):420-429
pubmed: 28456631
Helicobacter. 2006 Apr;11(2):75-80
pubmed: 16579836
J Proteomics. 2016 Jan 1;130:94-107
pubmed: 26363098