Abstract

Background: Helicobacter pylori (H.P.) is a very common bacteria that affect half of the population. It has been incriminated in cancer stomach and gastric lymphoma.

Objective: This work aims to discuss the relation and mechanism of H.P. in causing gastric carcinoma.

Review of Literature: H.P. has different methods of transmission like oral-oral, fecal-oral, gastro-oral and gastro gastric. The microbiological features of H.P. support its growth and protect it from oxidative damage that enhancing its survival rate. H.P. is now determined as one of the most critical carcinogenic infectious agents because it's a high risk of developing stomach cancer. Gastric cancer is the third type of cancer leading to death and it is due to different causes and risk factors. There are many factors affect the outcome of patients who had infected with H.P. and increase the risk of developing cancer. These are environmental, host-related and virulence factors. All of these factors participate in the development of gastric cancer by two mechanisms, direct inflammatory effects and indirect through mutations in the cell-cycle regulating genes.

Conclusion: H.P. infection has an important carcinogenic role in the development of cancer stomach. Eradication of H.P. will decrease the risk of developing stomach cancer.

Keywords: Helicobacter pylori; Gastric Cancer; Transmission; Infection; Relation

References

1. Kusters J., et al. “Pathogenesis of Helicobacter pylori Infection”. Clinical Microbiology Reviews 3 (2006): 449-490.
2. Hasosah M., et al. “Prevalence and risk factors of Helicobacter pylori infection in Saudi children" a three-year prospective controlled study”. Helicobacter1 (2015): 56-63.
3. McColl KEL. “Helicobacter pylori infection”. The New England Journal of Medicine 17 (2010): 1597-1604.
4. Hunt RH e. “Helicobacter pylori in developing countries. World Gastroenterology Organization Global Guideline”. Journal of Gastrointestinal and Liver Diseases 3 (2011): 299-304.
5. Bytzer P., et al. “Diagnosis and treatment of Helicobacter pylori infection”. Danish Medical Bulletin 4 (2011): C4271.
6. Plummer M. “Global burden of cancers attributable to infections in 2012: a synthetic analysis”. The Lancet Global Health's 9 (2016): e609-e616.
7. Chang, AH and Parsonnet J. "Role of Bacteria in Oncogenesis". Clinical Microbiology Reviews4 (2010): 837-857.
8. Fock KM. “Review article: the epidemiology and prevention of gastric cancer”. Alimentary Pharmacology and Therapeutics 40 (2014): 250-260.
9. “Saudi Cancer Registry Cancer Incidence Report in Saudi Arabia 2010”. Riyadh (KSA): Saudi Cancer Registry 16 (2014): 54-56.
10. Watts G. “Nobel prize is awarded to doctors who discovered H pylori”. British Medical Journal 7520 (2005): 795.
11. JE E. “Recent developments in the epidemiology of Helicobacter pylori”. Gastroenterology Clinics of North America 3 (2000): 559-578.
12. LM Brown. “Helicobacter pylori: epidemiology and routes of transmission”. Epidemiologic Reviews 2 (2000): 283-297.
13. Sauid Ishaq L. “Helicobacter pylori and gastric cancer: a state-of-the-art review. PubMed Central (PMC)”. Gastroenterology and Hepatology from Bed to Bench 1 (2015): S6-S14.
14. Tursi A., et al. “[The modes of transmission of Helicobacter pylori infection]”. Recenti Progressi in Medicina 5 (1997): 232-236.
15. DR Cave. “How is Helicobacter pylori transmitted?” Gastroenterology6 (1997): S9-S14.
16. Y Kivi. “Helicobacter pylori occurrence and transmission: a family affair?” Scandinavian Journal of Infectious Diseases 6-7(2006): 407-417.
17. M Hill. “Microbiology of Helicobacter pylori”. Gastroenterology Clinics of North America 1 (1993): 5-19.
18. Hazell SL., et al. “Helicobacter pylori catalase”. Journal of General Microbiology 1 (1991): 57-61.
19. HL Mobley R. “Microbial ureases: significance, regulation, and molecular characterization”. Microbiological Reviews 1 (1989): 85-108.
20. El-Omar EM., et al. “Interleukin-1 polymorphisms associated with increased risk of gastric cancer”. Nature 404 (2000): 398-402.
21. Ikeda F., et al. “Hyperglycemia increases risk of gastric cancer posed by Helicobacter pylori infection: A population-based cohort study”. Gastroenterology136 (2009): 1234-1241.
22. Honarmand-Jahromy S. “Reciprocal impact of host factors and Helicobacter pylori genotypes on gastric diseases”. World Journal of Gastroenterology31 (2015): 9317-9327.
23. Figueiredo C. “Cytokines, cytokine gene polymorphisms and Helicobacter pylori infection: Friend or foe?” World Journal of Gastroenterology18 (2014): 5235-5243.
24. Yamaoka Y. “Mechanisms of disease: Helicobacter pylori virulence factors”. World Journal of Gastroenterology Nature Reviews Gastroenterology and Hepatology 11 (2010): 629-641.
25. Renzo Suriani M. “CagA and VacA Helicobacter pylori antibodies in gastric cancer”. Canadian Journal of Gastroenterology and Hepatology 3 (2008): 255-258.
26. Blaser MJ e. “Infection with Helicobacter pylori strains possessing cagA is associated with an increased risk of developing adenocarcinoma of the stomach”. Cancer Research 10 (1995): 2111-2115.
27. Yong X., et al. “Helicobacter pylori virulence factor CagA promotes tumorigenesis of gastric cancer via multiple signaling pathways”. Cell Communication and Signaling 13 (2015): 30.
28. Tan S., et al. “Helicobacter pylori Perturbs Iron Trafficking in the Epithelium to Grow on the Cell Surface”. PLOS Pathogens 5 (2011): e1002050.
29. Neal J., et al. “ pylori virulence factor CagA increases intestinal cell proliferation by Wnt pathway activation in a transgenic zebrafish model”. Disease Models and Mechanisms 2013 6 (2013): 802-810.
30. Tan S., et al. “Helicobacter pylori Usurps Cell Polarity to Turn the Cell Surface into a Replicative Niche”. PLOS Pathogens5 (2009): e1000407.
31. Bronte-Tinkew D., et al. “Helicobacter pylori Cytotoxin-Associated Gene A Activates the Signal Transducer and Activator of Transcription 3 Pathway In vitro and In vivo”. Cancer Research 2 (2009): 632-639.
32. Algood H and Cover T. “Helicobacter pylori Persistence: An Overview of Interactions between pylori and Host Immune Defenses”. Clinical Microbiology Reviews 19.4 (2006): 597-613.
33. Chaturvedi R e. “Induction of polyamine oxidase 1 by Helicobacter pylori causes macrophage apoptosis by hydrogen peroxide release and mitochondrial membrane depolarization”. Journal of Biological Chemistry 38 (2004): 40161-40173.
34. Gobert AP e. “Helicobacter pylori induces macrophage apoptosis by activation of arginase II”. Journal of Immunology 9 (2002): 4692-4700.
35. Palframan S., et al. “Vacuolating cytotoxin A (VacA), a key toxin for Helicobacter pylori pathogenesis”. Frontiers in Cellular and Infection Microbiology 2 (2012): 92.
36. Wroblewski L., et al. “Helicobacter pylori and Gastric Cancer: Factors That Modulate Disease Risk”. Clinical Microbiology Reviews 4 (2010): 713-739.
37. Uemura N., et al. “Helicobacter pylori infection and the development of gastric cancer". The New England Journal of Medicine 345 (2001): 784-789.
38. Lee YY and Derakhshan MH. “Environmental and lifestyle risk factors of gastric cancer”. Archives of Iranian Medicine 6 (2013): 358-365.
39. Hakimeh Zali M., et al. “Gastric cancer: prevention, risk factors and treatment”. Gastroenterology and Hepatology from Bed to Bench 4 (2011): 175-185.
40. Ma J., et al. “Fifteen-Year Effects of Helicobacter pylori, Garlic, and Vitamin Treatments on Gastric Cancer Incidence and Mortality”. Journal of the National Cancer Institute 6 (2012): 488-492.
41. Fuccio L., et al. “Meta-analysis: can Helicobacter pylori eradication treatment reduce the risk for gastric cancer?” Annals of Internal Medicine 2 (2009): 121-128.
42. Bin Lu and Meng Li. “Helicobacter pylori eradication for preventing gastric cancer”. World Journal of Gastroenterology 19 (2014): 5660-5665.
43. Li P., et al. “Association between dietary antioxidant vitamins intake/blood level and risk of gastric cancer”. International Journal of Cancer 6 (2014): 1444-1453.
44. Li W., et al. “Effects of Helicobacter pylori Treatment on Gastric Cancer Incidence and Mortality in Subgroups”. Journal of the National Cancer Institute7 (2014): 116.
45. Correa P. “Human gastric carcinogenesis: A multistep and multifactorial process - First American Cancer Society Award lecture on cancer epidemiology and prevention”. Cancer Research 52 (1992): 6735-6740.
46. Correa P., et al. “A model for gastric cancer epidemiology”. Lancet 2 (1975): 58-59.
47. Bartchewsky W Jr., et al. “Effect of Helicobacter pylori infection on IL-8, IL-1beta and COX-2 expression in patients with chronic gastritis and gastric cancer”. Scandinavian Journal of Gastroenterology 44 (2009): 153-161.
48. Niwa T., et al. “Inflammatory processes triggered by Helicobacter pylori infection cause aberrant DNA methylation in gastric epithelial cells”. Cancer Research 70 (2010): 1430-1440.
49. Baghaei K., et al. “Determination of Helicobacter pylori virulence by analysis of the cag pathogenicity island isolated from Iranian patients”. Digestive and Liver Disease 41 (2009): 634-638.
50. Gonzalez CA., et al. “Helicobacter pylori cagA and vacA genotypes as predictors of progression of gastric preneoplastic lesions: A longterm follow-up in a high-risk area in Spain”. The American Journal of Gastroenterology 106 (2011): 867-874.
51. Huang JQ., et al. “Meta-Analysis of the relationship between cagA seropositivity and gastric cancer”. Gastroenterology 125 (2003): 1636-1644.

Citation

Citation: Bassam Oudh Al Johny.,et al. “The Relation of Helicobacter pylori Infection to Gastric Cancer Acta Scientific Medical Sciences 4.5 (2020): 54-59.

Copyright

Copyright: © 2020 Bassam Oudh Al Johny.,et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.