Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • News & Views
  • Published:

Helicobacter pylori

Pathogenic enablers — toxic relationships in the stomach

Chronic infection with Helicobacter pylori is the strongest known risk factor for the development of gastric cancer. Saju et al. shed new light on mechanisms by which Epstein–Barr virus, a viral initiator of gastric cancer, potentiates the oncogenic effects of Helicobacter pylori in the stomach.

This is a preview of subscription content, access via your institution

Access options

Buy this article

Prices may be subject to local taxes which are calculated during checkout

Figure 1: Co-infection with Helicobacter pylori and EBV in gastric epithelial cells promotes the oncogenic activity of CagA.

References

  1. Parkin, D. M., Bray, F., Ferlay, J. & Pisani, P. Global cancer statistics, 2002. CA Cancer J. Clin. 55, 74–108 (2005).

    Article  Google Scholar 

  2. Correa, P. Human gastric carcinogenesis: a multistep and multifactorial process — first American Cancer Society award lecture on cancer epidemiology and prevention. Cancer Res. 52, 6735–6740 (1992).

    CAS  PubMed  Google Scholar 

  3. The Cancer Genome Atlas Research Network. Comprehensive molecular characterization of gastric adenocarcinoma. Nature 513, 202–209 (2014).

  4. Amieva, M. & Peek, R. M. Jr. Pathobiology of Helicobacter pylori-induced gastric cancer. Gastroenterology 150, 64–78 (2016).

    Article  CAS  Google Scholar 

  5. Mueller, D. et al. c-Src and c-Abl kinases control hierarchic phosphorylation and function of the CagA effector protein in Western and East Asian Helicobacter pylori strains. J. Clin. Invest. 122, 1553–1566 (2012).

    Article  CAS  Google Scholar 

  6. Murphy, G., Pfeiffer, R., Camargo, M. C. & Rabkin, C. S. Meta-analysis shows that prevalence of Epstein–Barr virus-positive gastric cancer differs based on sex and anatomic location. Gastroenterology 137, 824–833 (2009).

    Article  Google Scholar 

  7. Saju, P. M.-K. et al. Host SHP1 phosphatase antagonizes Helicobacter pylori CagA and can be downregulated by Epstein–Barr virus. Nat. Microbiol. 1, 16026 (2016).

    Article  CAS  Google Scholar 

  8. Lofgren, J. L. et al. Lack of commensal flora in Helicobacter pylori-infected INS-GAS mice reduces gastritis and delays intraepithelial neoplasia. Gastroenterology 140, 210–220 (2011).

    Article  Google Scholar 

  9. Lertpiriyapong, K. et al. Gastric colonisation with a restricted commensal microbiota replicates the promotion of neoplastic lesions by diverse intestinal microbiota in the Helicobacter pylori INS-GAS mouse model of gastric carcinogenesis. Gut 63, 54–63 (2014).

    Article  CAS  Google Scholar 

  10. Tsugawa, H. et al. Reactive oxygen species-induced autophagic degradation of Helicobacter pylori CagA is specifically suppressed in cancer stem-like cells. Cell Host Microbe 12, 764–777 (2012).

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Richard M. Peek Jr.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

PowerPoint slides

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Wroblewski, L., Peek, R. Pathogenic enablers — toxic relationships in the stomach. Nat Rev Gastroenterol Hepatol 13, 317–318 (2016). https://doi.org/10.1038/nrgastro.2016.68

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nrgastro.2016.68

This article is cited by

Search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing