Cellular and molecular aspects of gastric cancer.
Journal: 2006/July - World Journal of Gastroenterology
ISSN: 1007-9327
PUBMED: 16718776
Abstract:
Gastric cancer remains a global killer with a shifting burden from the developed to the developing world. The cancer develops along a multistage process that is defined by distinct histological and pathophysiological phases. Several genetic and epigenetic alterations mediate the transition from one stage to another and these include mutations in oncogenes, tumour suppressor genes and cell cycle and mismatch repair genes. The most significant advance in the fight against gastric cancer came with the recognition of the role of Helicobacter pylori (H pylori) as the most important acquired aetiological agent for this cancer. Recent work has focussed on elucidating the complex host/microbial interactions that underlie the neoplastic process. There is now considerable insight into the pathogenesis of this cancer and the prospect of preventing and eradicating the disease has become a reality. Perhaps more importantly, the study of H pylori-induced gastric carcinogenesis offers a paradigm for understanding more complex human cancers. In this review, we examine the molecular and cellular events that underlie H pylori-induced gastric cancer.
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World J Gastroenterol 12(19): 2979-2990

Cellular and molecular aspects of gastric cancer

Malcolm G Smith, Georgina L Hold, Eiichi Tahara, Emad M El-Omar, Department of Medicine and Therapeutics, Aberdeen University, Foresterhill, Aberdeen AB25 2ZD, Scotland, United Kingdom
Author contributions: All authors contributed equally to the work

Correspondence to: Professor Emad M El-Omar, Department of Medicine and Therapeutics, Institute of Medical Sciences, Aberdeen University, Foresterhill, Aberdeen AB25 2ZD, Scotland, United Kingdom. ku.ca.ndba@ramo-le.e

Telephone: +44-1224-553021 Fax: +44-1224-555766

Malcolm G Smith, Georgina L Hold, Eiichi Tahara, Emad M El-Omar, Department of Medicine and Therapeutics, Aberdeen University, Foresterhill, Aberdeen AB25 2ZD, Scotland, United Kingdom
Author contributions: All authors contributed equally to the work

Correspondence to: Professor Emad M El-Omar, Department of Medicine and Therapeutics, Institute of Medical Sciences, Aberdeen University, Foresterhill, Aberdeen AB25 2ZD, Scotland, United Kingdom. ku.ca.ndba@ramo-le.e

Telephone: +44-1224-553021 Fax: +44-1224-555766

Received 2005 Aug 3; Revised 2005 Oct 20; Accepted 2005 Oct 26.

Abstract

Gastric cancer remains a global killer with a shifting burden from the developed to the developing world. The cancer develops along a multistage process that is defined by distinct histological and pathophysiological phases. Several genetic and epigenetic alterations mediate the transition from one stage to another and these include mutations in oncogenes, tumour suppressor genes and cell cycle and mismatch repair genes. The most significant advance in the fight against gastric caner came with the recognition of the role of Helicobacter pylori (H pylori) as the most important acquired aetiological agent for this cancer. Recent work has focussed on elucidating the complex host/microbial interactions that underlie the neoplastic process. There is now considerable insight into the pathogenesis of this cancer and the prospect of preventing and eradicating the disease has become a reality. Perhaps more importantly, the study of H pylori-induced gastric carcinogenesis offers a paradigm for understanding more complex human cancers. In this review, we examine the molecular and cellular events that underlie H pylori-induced gastric cancer.

Keywords: Gastric cancer, Helicobacter pylori, Host-microbial interactions, Inflammation, Molecular mechanisms, Host genetics
Abstract

Footnotes

S- Editor Wang J E- Editor Ma WH

Footnotes

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