Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2006 May 21;12(19):2979-90.
doi: 10.3748/wjg.v12.i19.2979.

Cellular and molecular aspects of gastric cancer

Malcolm-G Smith  1 , Georgina-L Hold, Eiichi Tahara, Emad-M El-Omar
Affiliations
Review

Cellular and molecular aspects of gastric cancer

Malcolm-G Smith et al. World J Gastroenterol. .

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.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Divergent responses to H pylori infection.
Figure 2
Figure 2
H pylori induced gastric epithelial inflammation.
Figure 3
Figure 3
Intestinal type gastric cancer: Genetic and epigenetic alterations during carcinogenesis.
Figure 4
Figure 4
Diffuse type gastric cancer: Genetic and epigenetic alterations during carcinogenesis.
Figure 5
Figure 5
Cancer-stromal interaction in gastric cancer through growth factors and cytokines.
See this image and copyright information in PMC

References

    1. Black RJ, Bray F, Ferlay J, Parkin DM. Cancer incidence and mortality in the European Union: cancer registry data and estimates of national incidence for 1990. Eur J Cancer. 1997;33:1075–1107. - PubMed
    1. Correa P. Helicobacter pylori and gastric cancer: state of the art. Cancer Epidemiol Biomarkers Prev. 1996;5:477–481. - PubMed
    1. Parkin DM. Global cancer statistics in the year 2000. Lancet Oncol. 2001;2:533–543. - PubMed
    1. Kuniyasu H, Yasui W, Yokozaki H, Tahara E. Helicobacter pylori infection and carcinogenesis of the stomach. Langenbecks Arch Surg. 2000;385:69–74. - PubMed
    1. LAUREN P. THE TWO HISTOLOGICAL MAIN TYPES OF GASTRIC CARCINOMA: DIFFUSE AND SO-CALLED INTESTINAL-TYPE CARCINOMA. AN ATTEMPT AT A HISTO-CLINICAL CLASSIFICATION. Acta Pathol Microbiol Scand. 1965;64:31–49. - PubMed

MeSH terms