| Literature DB >> 28032715 |
Jiaqi Huang1, Ulrika Zagai1, Göran Hallmans2, Olof Nyrén1, Lars Engstrand3, Rachael Stolzenberg-Solomon4, Eric J Duell5, Kim Overvad6, Verena A Katzke7, Rudolf Kaaks7, Mazda Jenab8, Jin Young Park8, Raul Murillo8, Antonia Trichopoulou9,10, Pagona Lagiou9,10,11, Christina Bamia9,10, Kathryn E Bradbury12, Elio Riboli13, Dagfinn Aune13, Konstantinos K Tsilidis13,14, Gabriel Capellá15, Antonio Agudo16, Vittorio Krogh17, Domenico Palli18, Salvatore Panico19, Elisabete Weiderpass1,20,21,22, Anne Tjønneland23, Anja Olsen23, Begoña Martínez24, Daniel Redondo-Sanchez24,25,26, Maria-Dolores Chirlaque27,25,28, Petra Hm Peeters29, Sara Regnér30, Björn Lindkvist31, Alessio Naccarati32, Eva Ardanaz25,33, Nerea Larrañaga25,34, Marie-Christine Boutron-Ruault35,36,37, Vinciane Rebours38, Amélie Barré39, H B As Bueno-de-Mesquita40,41,42,43, Weimin Ye1,44.
Abstract
The association between H. pylori infection and pancreatic cancer risk remains controversial. We conducted a nested case-control study with 448 pancreatic cancer cases and their individually matched control subjects, based on the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, to determine whether there was an altered pancreatic cancer risk associated with H. pylori infection and chronic corpus atrophic gastritis. Conditional logistic regression models were applied to calculate odds ratios (ORs) and corresponding 95% confidence intervals (CIs), adjusted for matching factors and other potential confounders. Our results showed that pancreatic cancer risk was neither associated with H. pylori seropositivity (OR = 0.96; 95% CI: 0.70, 1.31) nor CagA seropositivity (OR = 1.07; 95% CI: 0.77, 1.48). We also did not find any excess risk among individuals seropositive for H. pylori but seronegative for CagA, compared with the group seronegative for both antibodies (OR = 0.94; 95% CI: 0.63, 1.38). However, we found that chronic corpus atrophic gastritis was non-significantly associated with an increased pancreatic cancer risk (OR = 1.35; 95% CI: 0.77, 2.37), and although based on small numbers, the excess risk was particularly marked among individuals seronegative for both H. pylori and CagA (OR = 5.66; 95% CI: 1.59, 20.19, p value for interaction < 0.01). Our findings provided evidence supporting the null association between H. pylori infection and pancreatic cancer risk in western European populations. However, the suggested association between chronic corpus atrophic gastritis and pancreatic cancer risk warrants independent verification in future studies, and, if confirmed, further studies on the underlying mechanisms.Entities:
Keywords: EPIC cohort; H. pylori infection; chronic corpus atrophic gastritis; nested case-control study; pancreatic cancer risk
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Year: 2017 PMID: 28032715 PMCID: PMC5930360 DOI: 10.1002/ijc.30590
Source DB: PubMed Journal: Int J Cancer ISSN: 0020-7136 Impact factor: 7.396