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World J Gastroenterol. Dec 7, 2013; 19(45): 8219-8226
Published online Dec 7, 2013. doi: 10.3748/wjg.v19.i45.8219
Role of Helicobacter pylori virulence factor cytotoxin-associated gene A in gastric mucosa-associated lymphoid tissue lymphoma
Hong-Ping Wang, Yong-Liang Zhu, Wei Shao
Hong-Ping Wang, Yong-Liang Zhu, Gastroenterology Laboratory, the Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310009, Zhejiang Province, China
Wei Shao, Department of Gastroenterology, People’s Hospital of Putuo District, Zhoushan 316000, Zhejiang Province, China
Author contributions: Wang HP and Shao W searched the literature and wrote the manuscript; Zhu YL conceived the topic and was involved in writing the manuscript; all authors revised the manuscript.
Supported by Foundation of Scientific Technology Bureau of Zhejiang Province, No. 2010C33118
Correspondence to: Wei Shao, MD, Department of Gastroenterology, People’s Hospital of Putuo District, 24F Xincheng District, Zhoushan 316000, Zhejiang Province, China. 667318_won@sina.com
Telephone: +86-580-3019686 Fax: +86-580-3019686
Received: September 27, 2013
Revised: November 4, 2013
Accepted: November 12, 2013
Published online: December 7, 2013
Abstract

Helicobacter pylori (H. pylori) infection might initiate and contribute to the progression of lymphoma from gastric mucosa-associated lymphoid tissue (MALT). Increasing evidence shows that eradication of H. pylori with antibiotic therapy can lead to regression of gastric MALT lymphoma and can result in a 10-year sustained remission. The eradication of H. pylori is the standard care for patients with gastric MALT lymphoma. Cytotoxin-associated gene A (CagA) protein, one of the most extensively studied H. pylori virulence factors, is strongly associated with the gastric MALT lymphoma. CagA possesses polymorphisms according to its C-terminal structure and displays different functions among areas and races. After being translocated into B lymphocytes via type IV secretion system, CagA deregulates intracellular signaling pathways in both tyrosine phosphorylation-dependent and -independent manners and/or some other pathways, and thereby promotes lymphomagenesis. A variety of proteins including p53 and protein tyrosine phosphatases-2 are involved in the malignant transformation induced by CagA. Mucosal inflammation is the foundational mechanism underlying the occurrence and development of gastric MALT lymphoma.

Keywords: Helicobacter pylori, Cytotoxin-associated gene A, Gastric mucosa-associated lymphoid tissue lymphoma, Lymphomagenesis, Molecular mechanism

Core tip: Cytotoxin-associated gene A (CagA) protein encoded by cag pathogenicity island of Helicobacter pylori is a bacterium-derived oncoprotein and is strongly associated with the gastric mucosa-associated lymphoid tissue (MALT) lymphoma. After being translocated into B cells via type IV secretion system in ATP-dependent manner, CagA deregulates several pathways in both tyrosine phosphorylation-dependent and -independent manners, and thereby promotes lymphomagenesis. Two important proteins, p53 and protein tyrosine phosphatases-2, are involved in the malignant transformation induced by CagA. In addition, mucosal inflammation is the foundational mechanism underlying the occurrence and development of gastric MALT lymphoma. However, the exact mechanism by which CagA promotes oncogenesis needs further clarification.