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Annals of Oncology Advance Access originally published online on March 27, 2008
Annals of Oncology 2008 19(7):1299-1303; doi:10.1093/annonc/mdn055
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© The Author 2008. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

gastrointestinal tumors

Analysis of Pro12Ala PPAR gamma polymorphism and Helicobacter pylori infection in gastric adenocarcinoma and peptic ulcer disease

K. N. Prasad1,*, A. Saxena1, U. C. Ghoshal2, M. R. Bhagat4 and N. Krishnani3

1 Department of Microbiology
2 Department of Gastroenterology
3 Department of Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow
4 Department of Gastroenterology, Central Command Hospital, Lucknow, India

* Correspondence to: Dr K. N. Prasad, Department of Microbiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226 014, India. Tel: +91-522-2668631; Fax: +91-522-2668017; E-mail: knprasad{at}sgpgi.ac.in

Background: Peroxisome proliferator-activated receptor gamma (PPAR{gamma}) is a ligand-dependent transcription factor involved in various disease processes including inflammation and carcinogenesis. We investigated the association of Pro12Ala PPAR{gamma} polymorphism and Helicobacter pylori infection with gastric cancer and peptic ulcer disease (PUD).

Patients and methods: In total, 348 adult patients [62 gastric adenocarcinoma, 45 PUD and 241 nonulcer dyspepsia (NUD)] who underwent an upper gastrointestinal endoscopy were enrolled. PPAR{gamma} polymorphism was analyzed by PCR-based restriction fragment length polymorphism. H. pylori infection was diagnosed by rapid urease test, culture, histopathology and PCR.

Results: PPAR{gamma} G carrier had significant association with gastric adenocarcinoma [P = 0.023, odds ratio (OR) = 2.136, 95% CI = 1.112–4.104] and PUD (P = 0.028, OR = 2.165, 95% CI = 1.008–4.306) when compared with NUD. Combination of G carrier and H. pylori infection further increased the risk of gastric adenocarcinoma (OR = 3.054, 95% CI = 1.195–7.807) and PUD (OR = 11.161, 95% CI = 3.495–35.644). PPAR{gamma} polymorphism did not increase the risk of gastric adenocarcinoma and PUD in H. pylori-negative subjects.

Conclusions: The study suggests that Pro12Ala PPAR{gamma} polymorphism is associated with gastric adenocarcinoma and PUD, and is a potential marker for genetic susceptibility to these two diseases in the presence of H. pylori infection.

Key words: gastric adenocarcinoma, Helicobacter pylori infection, peptic ulcer disease, PPAR{gamma} polymorphism

Received for publication January 4, 2008. Revision received February 3, 2008. Accepted for publication February 4, 2008.


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