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World J Gastroenterol. Jan 21, 2014; 20(3): 684-698
Published online Jan 21, 2014. doi: 10.3748/wjg.v20.i3.684
Role of Helicobacter pylori in gastric mucosa-associated lymphoid tissue lymphomas
Marta-Isabel Pereira, José Augusto Medeiros
Marta-Isabel Pereira, Clinical Hematology Department, Coimbra University Hospital Center, 3000-075 Coimbra, Portugal
Marta-Isabel Pereira, José Augusto Medeiros, Institute of Physiology, Faculty of Medicine, University of Coimbra, Azinhaga de Santa Comba, 3000-548 Coimbra, Portugal
Author contributions: Pereira MI and Medeiros JA contributed equally to this work.
Correspondence to: José Augusto Medeiros, MD, PhD, Institute of Physiology, Faculty of Medicine, University of Coimbra, Azinhaga de Santa Comba, 3000-548 Coimbra, Portugal. jmedeiros@fmed.uc.pt
Telephone: +351-919-502495 Fax: +351-239-855051
Received: September 29, 2013
Revised: November 19, 2013
Accepted: December 5, 2013
Published online: January 21, 2014
Processing time: 142 Days and 20.9 Hours
Core Tip

Core tip: Mucosa-associated lymphoid tissue (MALT) lymphomas are indolent B-cell lymphomas, originating in acquired MALT induced as a response to a chronic immunoinflammatory stimulus, notably infection by Helicobacter pylori (H. pylori). Antigenic stimulation determines lymphoid hyperplasia; additional genetic aberrations activate survival pathways, with the emergence of a malignant clone. The digestive system (predominantly the stomach) is the most frequent location, reflecting contact with foreign antigens, mucosal permeability and intrinsic lymphoid system. Early-stage gastric MALT lymphoma can regress through the eradication of H. pylori. Immortalizing genetic abnormalities, advanced disease or eradication-refractoriness require treatment alternatives, presently not consensual. Representative clinical trials are needed to optimize patient care.