Biotech Articles
Publish Your Research Online
Get Recognition - International Audience

Request for an Author Account   |   Login   |   Submit Article
 
 
HOME FAQ TOP AUTHORS FORUMS PUBLISH ARTICLE
 
 

Helicobacter Pylori and its Significance in Gastric Cancer

BY: Dr. Saurabha Srivastava | Category: Healthcare | Submitted: 2016-07-01 05:32:44
       Author Photo
Article Summary: "Helicobacter pylori is a emerging problem causing gastric cancer. Its pathogenesis, diagnostic and treatment is briefly described here. .."


Share with Facebook Share with Linkedin Share with Twitter Share with Pinterest Email this article
     


Helicobacter pylori and its significance in Gastric Cancer
Author: Saurabha Srivastava
National Institute of Immunology, ArunaAsaf Ali Road, New Delhi, India, 110067


Helicobacter pylori: Helicobacter pylori, or H. pylori, is a winding formed bacterium that develops in the bodily fluid layer that coats within the human stomach. To get by in the unforgiving, acidic environment of the stomach, H. pylori secretes a protein called urease, which changes over the concoction urea to smelling salts. The creation of alkali around H. pylori kills the acridity of the stomach, making it more cordial for the bacterium. What's more, the helical state of H. pylori permits it to tunnel into the bodily fluid layer, which is less acidic than within space, or lumen, of the stomach. H. pylori can likewise connect to the cells that line the internal surface of the stomach.

Albeit resistant cells that regularly perceive and assault attacking microorganisms amass close destinations of H. pylori disease, they can't achieve the stomach lining. What's more, H. pylori has created methods for meddling with nearby invulnerable reactions, making them insufficient in killing this bacterium (1, 2). Despite the fact that H. pylori contamination does not bring about sickness in most tainted individuals, it is a noteworthy danger variable for peptic ulcer malady and is in charge of the dominant part of ulcers of the stomach and upper small digestive tract.

H. pylori is thought to spread through polluted sustenance and water and through direct mouth-to-mouth contact. In many populaces, the bacterium is initially obtained amid youth. Disease is more probable in youngsters living in destitution, in swarmed conditions, and in territories with poor sanitation.

Helicobacter pylori v/s Gastric Cancer: Gastric disease, or growth of the stomach, was once viewed as a solitary substance. Presently, researchers isolate this growth into two fundamental classes: gastric cardia tumor (disease of the top inch of the stomach, where it meets the throat) and non-cardia gastric malignancy (disease in every other region of the stomach). General gastric malignancy rate is diminishing. Be that as it may, this decay is primarily in the rates of non-cardia gastric growth (3). Gastric cardia disease, which was once extremely remarkable, has ascended in rate in late decades (4).

Contamination with H. pylori is the essential recognized reason for gastric malignancy. Other danger variables for gastric growth incorporate endless gastritis; more seasoned age; male sex; an eating regimen high in salted, smoked, or ineffectively safeguarded nourishments and low in products of the soil; tobacco smoking;pernicious weakness; a background marked by stomach surgery for kindhearted conditions; and a family history of stomach disease (5, 6). H. pylori has diverse relationship with the two principle classes of gastric malignancy. While individuals contaminated with H. pylori have an expanded danger of non-cardia gastric disease, their danger of gastric cardia growth is not expanded and may even be diminished.

A few studies have distinguished an opposite relationship between H. pylori contamination and gastric cardia disease (7-9), despite the fact that the proof is not by any stretch of the imagination steady (10-11). The likelihood of an opposite relationship between the bacterium and gastric cardia disease is upheld by the comparing diminish in H. pylori contamination rates in Western nations amid the previous century—the consequence of enhanced cleanliness and across the board anti-microbial use—and the expansion in rates of gastric cardia tumor in these same districts.

Comparable epidemiologic proof recommends that H. pylori disease might be connected with a lower danger of esophageal adenocarcinoma. For instance, a huge case–control study in Sweden demonstrated that the danger of esophageal adenocarcinoma in H. pylori-contaminated people was 33% that of uninfected people (8). A meta-examination of 13 studies, including the Swedish study, found a 45 percent lessening in danger of esophageal adenocarcinoma with H. pylori disease (12). In addition, as with gastric cardia disease, sensational expansions in esophageal adenocarcinoma rates in a few Western nations parallel the decreases in H. pylori disease rates.

Despite the fact that it is not known for certain how H. pylori disease expands the danger of non-cardia gastric tumor, a few scientists conjecture that the long haul nearness of aninflammatory reaction inclines cells in the stomach coating to end up destructive. This thought is upheld by the finding that expanded articulation of a solitary cytokine (interleukin-1-beta) in the stomach of transgenic mice causes sporadic gastric irritation and growth (13). The expanded cell turnover coming about because of progressing cell harm could improve the probability that cells will create destructive changes.

One speculation that may clarify lessened dangers of gastric cardia tumor and esophageal adenocarcinoma in H. pylori-tainted people identifies with the decrease in stomach acridity that is frequently seen following quite a while of H. pylori colonization. This decrease would diminish acid reflux into the throat, a noteworthy danger variable for adenocarcinomas influencing the upper stomach and throat.

Some H. pylori microbes utilize a needle-like limb to infuse a poison created by a quality called cytotoxin-related quality A (cagA) into the intersections where cells of the stomach lining meet (14-15). This poison (known as CagA) changes the structure of stomach cells and permits the microscopic organisms to connect to them all the more effectively. Long haul presentation to the poison causes constant aggravation. Be that as it may, not all strains of H. pylori convey the cagA quality; those that do are named cagA-positive.

Epidemiologic proof proposes that contamination with cagA-positive strains is particularly connected with an expanded danger of non-cardia gastric disease and with decreased dangers of gastric cardia growth and esophageal adenocarcinoma. For instance, a meta-examination of 16 case–control contemplates led the world over demonstrated that people tainted withcagA-constructive H. pylori had double the danger of non-cardia gastric tumor than people tainted with cagA-pessimistic H. pylori (16). Then again, a case–control study led in Sweden observed that individuals tainted with cagA-positive H. pylori had a factually essentially lessened danger of esophageal adenocarcinoma. So also, another case–control study led in the United States found that disease with cagA-positive H. pylori was connected with a decreased danger of esophageal adenocarcinoma and gastric cardia malignancy joined, however that disease with cagA-negative strains was not connected with danger (17).

Late research has proposed a potential system by which CagA could add to gastric carcinogenesis. In three studies, disease with CagA-positive H. pylori was connected with inactivation of tumor silencer proteins, including p53 (18-20).

Diagnosis and treatment of an H. pylori infection

Long haul follow-up of information from a randomized clinical trial completed in Shandong, China a zone where rates of gastric disease are high found that transient treatment with antimicrobials to annihilate H. pylori lessened the rate of gastric growth. Amid an about 15-year time span after treatment, gastric tumor occurrence was lessened by very nearly 40 percent (21). At the point when the consequences of this trial were pooled with those of a few littler trials looking at the impacts on gastric growth frequency of antimicrobial treatment to destroy H. pylori, a comparable diminishment was seen (22).

As indicated by the Centers for Disease Control and Prevention (CDC), individuals who have dynamic gastric or duodenal ulcers or a recorded history of ulcers ought to be tried for H. pylori. Testing for and treating H. pylori contamination is likewise prescribed after resection of early gastric growth and for second rate gastric MALT lymphoma. Notwithstanding, most specialists concur that the accessible confirmation does not bolster across the board testing for and annihilation of H. pylori disease (22).

References

1. Atherton JC. The pathogenesis of Helicobacter pylori-induced gastro-duodenal diseases. Annual Review of Pathology 2006; 1:63–96.

2. Kusters JG, van Vliet AH, Kuipers EJ. Pathogenesis of Helicobacter pylori infection.Clinical Microbiology Reviews 2006; 19(3):449–490.

3. Anderson WF, Camargo MC, Fraumeni JF, et al. Age-specific trends in incidence of noncardia gastric cancer in US adults. JAMA 2010; 303(17):1723–1728.

4. de Martel C, Forman D, Plummer M. Gastric cancer: Epidemiology and risk factors.Gastroenterology Clinics of North America 2013; 42(2):219-240.

5. Forman D, Burley VJ. Gastric cancer: Global pattern of the disease and an overview of environmental risk factors. Best Practice & Research Clinical Gastroenterology 2006; 20(4):633–649.

6. Brenner H, Rothenbacher D, Arndt V. Epidemiology of stomach cancer. Methods in Molecular Biology 2009; 472:467–477.

7. Kamangar F, Dawsey SM, Blaser MJ, et al. Opposing risks of gastric cardia and noncardia gastric adenocarcinomas associated with Helicobacter pylori seropositivity.Journal of the National Cancer Institute 2006; 98(20):1445–1452.

8. Hansen S, Melby KK, Aase S, Jellum E, Vollset SE. Helicobacter pylori infection and risk of cardia cancer and non-cardia gastric cancer. A nested case-control study.Scandinavian Journal of Gastroenterology 1999; 34(4):353–360.

9. Ye W, Held M, Lagergren J, et al. Helicobacter pylori infection and gastric atrophy: Risk of adenocarcinoma and squamous-cell carcinoma of the esophagus and adenocarcinoma of the gastric cardia. Journal of the National Cancer Institute 2004; 96(5):388–396.

10. Kamangar F, Qiao YL, Blaser MJ, et al. Helicobacter pylori and oesophageal and gastric cancers in a prospective study in China. British Journal of Cancer 2007; 96(1):172–176.

11. Dawsey SM, Mark SD, Taylor PR, Limburg PJ. Gastric cancer and H pylori. Gut 2002; 51(3):457-458.

12. Islami F, Kamangar F. Helicobacter pylori and esophageal cancer risk: A meta-analysis.Cancer Prevention Research 2008; 1(5):329–338.

13. Tu S, Bhagat G, Cui G, et al. Overexpression of interleukin-1beta induces gastric inflammation and cancer and mobilizes myeloid-derived suppressor cells in mice.Cancer Cell 2008; 14(5):408–419.

14. Wen S, Moss SF. Helicobacter pylori virulence factors in gastric carcinogenesis. Cancer Letters 2009; 282(1):1–8.

15. Bagnoli F, Buti L, Tompkins L, Covacci A, Amieva MR. Helicobacter pylori CagA induces a transition from polarized to invasive phenotypes in MDCK cells. Proceedings of the National Academy of Science USA 2005; 102(45):16339–16344.

16. Huang JQ, Zheng GF, Sumanac K, Irvine EJ, Hunt RH. Meta-analysis of the relationship between cagA seropositivity and gastric cancer. Gastroenterology 2003; 125(6):1636–1644.

17. Chow WH, Blaser MJ, Blot WJ, et al. An inverse relation between cagA+ strains ofHelicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma. Cancer Research 1998; 58(4):588–590.

18. André AR, Ferreira MV, Mota RM, et al. Gastric adenocarcinoma and Helicobacter pylori: Correlation with p53 mutation and p27 immunoexpression. Cancer Epidemiology 2010; 34(5):618–625.

19. Wei J, Nagy TA, Vilgelm A, et al. Regulation of p53 tumor suppressor by Helicobacter pylori in gastric epithelial cells. Gastroenterology 2010; 139(4):1333–1343.

20. Tsang YH, Lamb A, Romero-Gallo J, et al. Helicobacter pylori CagA targets gastric tumor suppressor RUNX3 for proteasome-mediated degradation. Oncogene 2010; 29(41):5643–5650.

21. Ma JL, Zhang L, Brown LM, et al. Fifteen-year effects of Helicobacter pylori, garlic, and vitamin treatments on gastric cancer incidence and mortality. Journal of the National Cancer Institute 2012; 104(6):488-492.

22. Kamangar F, Sheikhattari P, Mohebtash M. Helicobacter pylori and its effects on human health and disease. Archives of Iranian Medicine 2011; 14(3):192-199.




About Author / Additional Info:
I am working as Research Associate in National Institute of Immunology, New Delhi

Search this site & forums
Share this article with friends:



Share with Facebook Share with Linkedin Share with Twitter Share with Pinterest Email this article

More Social Bookmarks (Digg etc..)


Comments on this article: (0 comments so far)

Comment By Comment

Leave a Comment   |   Article Views: 746



Additional Articles:

•   DNAzymes: Introduction and DNAzymes in Cancer Treatment

•   Issues Related to Suspension Animal Cell Culture

•   Nanophotonics: A Branch of Optical Engineering

•   Biocontrol Potential of Compost




Latest Articles in "Healthcare" category:
•   Health Care and WHO

•   Current Scenario Of Gene Therapy

•   Targeted Cancer Therapy

•   Custom Made Medicine - Pharmacogenomics

•   Nanotechnology and its Application in Medicine - What are Nanoparticles?

•   Red Biotechnology and Cure of Tuberculosis

•   Patho-Biotechnology: Solution to Fight Antibiotic Resistance Bacteria?

•   A Baby Please With a Cheek Dimple...

•   Ribonucleic Acid Interference

•   Biomarker in Cancer Prognosis, Detection and Treatment

•   Adjuvant Therapy For Treating Cancer

•   DNA Microarray and Protein Microarray

•   DNA Vaccine: Vaccine of Next Generation

•   Cancer Immunotherapy Using Monoclonal Antibodies

•   Vaccines to Treat Cancer!

•   Tumor Marker and Cancer Detection

•   Targeted Therapy and Cancer Treatment

•   Enzyme Linked Immunosorbent Assay : A Biotechnology Technique

•   Lycopene as Anti-cancer Agent



Important Disclaimer: All articles on this website are for general information only and is not a professional or experts advice. We do not own any responsibility for correctness or authenticity of the information presented in this article, or any loss or injury resulting from it. We do not endorse these articles, we are neither affiliated with the authors of these articles nor responsible for their content. Please see our disclaimer section for complete terms.
Page copy protected against web site content infringement by Copyscape
Copyright © 2010 biotecharticles.com - Do not copy articles from this website.

ARTICLE CATEGORIES :
Agriculture Bioinformatics Applications Biotech Products Biotech Research
Biology Careers College/Edu DNA Environmental Biotech
Genetics Healthcare Industry News Issues Nanotechnology
Others Stem Cells Press Release Toxicology  


  |   Disclaimer/Privacy/TOS   |   Submission Guidelines   |   Contact Us