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
. 2014 Mar;8(2):131-9.
doi: 10.5009/gnl.2014.8.2.131. Epub 2014 Mar 11.

Immune response and the tumor microenvironment: how they communicate to regulate gastric cancer

Affiliations
Review

Immune response and the tumor microenvironment: how they communicate to regulate gastric cancer

Keunwook Lee et al. Gut Liver. 2014 Mar.

Abstract

Gastric cancer is the second most common cause of cancer-related death in the world. A growing body of evidence indicates that inflammation is closely associated with the initiation, progression, and metastasis of many tumors, including those of gastric cancer. In addition, approximately 60% of the world's population is colonized by Helicobacter pylori, which accounts for more than 50% of gastric cancers. While the role of inflammation in intestinal and colonic cancers is relatively well defined, its role in stomach neoplasia is still unclear because of the limited access of pathogens to the acidic environment and the technical difficulties isolating and characterizing immune cells in the stomach, especially in animal models. In this review, we will provide recent updates addressing how inflammation is involved in gastric malignancies, and what immune characteristics regulate the pathogenesis of stomach cancer. Also, we will discuss potential therapeutics that target the immune system for the efficient treatment of gastric cancer.

Keywords: Helicobacter pylori; Immune cells; Inflammation; Stomach neoplasms.

PubMed Disclaimer

Conflict of interest statement

No potential conflict of interest relevant to this article was reported.

Figures

Fig. 1
Fig. 1
Innate immune cells associated with gastric pathogenesis. NO, nitric oxide; MMP, matrix metalloproteinase; IL, interleukin; TIL, tissue infiltrating lymphocyte; MDSC, myeloid-derived suppressor cell; CAF, carcinoma-associated fibroblast.
Fig. 2
Fig. 2
Helper T cell subsets and gastric neoplasia. IL, interleukin; TGF, transforming growth factor; IFN, interferon.

References

    1. Parkin DM. The global health burden of infection-associated cancers in the year 2002. Int J Cancer. 2006;118:3030–3044. - PubMed
    1. Yuasa Y. Control of gut differentiation and intestinal-type gastric carcinogenesis. Nat Rev Cancer. 2003;3:592–600. - PubMed
    1. Balkwill F, Mantovani A. Inflammation and cancer: back to Virchow? Lancet. 2001;357:539–545. - PubMed
    1. Koebel CM, Vermi W, Swann JB, et al. Adaptive immunity maintains occult cancer in an equilibrium state. Nature. 2007;450:903–907. - PubMed
    1. Correa P. Human gastric carcinogenesis: a multistep and multifactorial process. First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention. Cancer Res. 1992;52:6735–6740. - PubMed

Publication types

MeSH terms