Molecular characterization of helicobacter pylori and gastric cancer
Article written by Master, Doctor Mai Vien Phuong- Gastrointestinal endoscopist - Department of Medical Examination & Internal Medicine - Vinmec Central Park International General Hospital
H. pylori is a spiral-shaped bacterium that lives in the lining of the human stomach. This type of bacteria is directly related to stomach cancer. Currently, the prevalence of H. pylori infection is recorded in our country and in the world at a relatively high rate.
1. Biological characteristics of bacteria H.Pylori
H. pylori infection is a strong and well known risk factor for stomach cancer classified as a group 1 carcinogen by the International Agency for Research on Cancer (IARC). Pathophysiological mechanisms have been proposed to explain why H. pylori infection may increase the risk of gastric cancer, but most authors suggest that chronic inflammation is the main mechanism.
H. pylori is thought to be spread through contaminated food and water, through direct mouth-to-mouth contact. In the majority of the population, bacterial infection occurs primarily in children, especially in poor countries, where housing is cramped and unsanitary.
2. What is the current rate of H. pylori infection in Vietnam?
In Vietnam, the prevalence of H.pylori infection in the population is about 80%. According to reports from 2002 - 2006, the rate of H. pylori infection in children is quite high, from 78.7% to 85.7%. A recent study at the Department of Gastroenterology - Children's Hospital 1, Ho Chi Minh City, in 2015, the rate of H.pylori infection determined by endoscopy and histopathology was 67.1% for children aged 15 years and older. go down. In the past 20 years, there have been many publications and warnings about H. pylori infection in the same family, especially parents or grandparents, which are the main cause of disease transmission to children. The prevalence of H. pylori infection in perforation complications due to peptic ulcers in Vietnam and around the world is about 80-100%. In bleeding complications due to peptic ulcer, this rate is about 60-85%. In gastric cancer, H.pylori infection rate is about 80% of cases.
3. What is stomach cancer and what are the symptoms?
Stomach cancer was previously considered a single entity. Scientists now divide them into two main classes: gastric cardia (cancer of the first inch of the stomach, where it joins the esophagus) and non-cardiac stomach cancer (cancer of the stomach). in all remaining regions of the stomach). H. pylori infection was the first identified cause of stomach cancer. Other risk factors include: chronic gastritis, old age, male; eating a lot of salt, smoking, using poorly preserved foods, eating less fruits and vegetables, pernicious anemia, having a history of gastric bypass surgery for benign diseases, having cancer in the family stomach letter.
The association rate of H. pylori with the two main classes of gastric cancer is not the same. While people infected with H. pylori have an increased risk for non-cardiac stomach cancer, the risks for cardiatric cancer are not increased and may even decrease.
4. What are the symptoms of stomach disease caused by H.pylori bacteria?
>> See more: Photodynamic therapy and vaccines in the treatment of helicobacter pylori - Posted by Master, Doctor Mai Vien Phuong - Gastroenterologist - Department of Examination & Internal Medicine - General Hospital Vinmec Central Park International Faculty
5. What is a positive H. pylori cagA and how do they affect the risk of stomach and esophageal cancer?
A small number of H. pylori bacteria use a needle-like appendage to inject a toxin produced by a gene called cagA (cytotoxin-associated gene A) into the cells. the junction between the cells lining the stomach. The cagA toxin alters the structure of stomach cells and makes it easier for bacteria to attach to them. Long-term exposure to the toxin induces chronic inflammation. About 60% of H. pylori in Western countries and most of H. pylori in East Asian countries are cagA-positive. Epidemiological evidence suggests that cagA-positive infection is specifically associated with an increased risk of non-cardiac gastric cancer and a reduced risk of gastric carcinoma as well as carcinoma. esophageal gland. For example, a meta-analysis of 16 case-control studies conducted around the world found that H.pylori cagA-positive individuals had twice the risk of non-cardiac stomach cancer compared with those with H. pylori cagA-negative people.
In contrast, a case-control study conducted in Sweden showed that H.pylori cagA-positive individuals had a statistically significant reduction in the risk of esophageal adenocarcinoma. Similarly, another case-control study in the United States showed that H. pylori cagA-positive infection was associated with a reduced risk of esophageal adenocarcinoma and combined gastric cancer, but infection with cagA strains - negative is no risk. A recent study has suggested a likely mechanism by which CagA may be involved in gastric carcinogenesis. In three studies, CagA-positive H. pylori infection was associated with inactivation of tumor suppressor proteins, including p53.
H. pylori has a special adaptability to live in the hostile acidic environment of the stomach and colonization of H. pylori causes gastritis in most subjects infected with this bacterium. Bacterial adhesion to epithelial cells induces an inflammatory response, with the concentration of neutrophils followed by B and T lymphocytes, macrophages and plasma cells, most of which produce generate large amounts of oxygen or nitrogen groups that react with free radicals, causing epithelial cell damage and carcinogenesis. Damage to the gastric mucosa from H. pylori infection is also possible because of bacterial virulence factors encoded by the “cag pathogenicity island” [Full name is cytotoxin-associated gene pathogenicity island (cag-PAI) , a special type IV secretion system (T4SS), encoded by Helicobacter pylori type 1 strains. T4SS is used by bacteria to exchange metabolites, DNA or proteins with the external environment (ND).], such as vacuo-forming cytotoxin A (VacA) and protein CagA (CagA). VacA is a toxin secreted by bacteria and penetrates epithelial cell membranes, creates vacuoles and affects mitochondria, leading to apoptosis [Galmiche A et al., 2000; Kuck D et al., 2001]. In contrast, CagA, upon entering epithelial cells, induces proliferative and motility signaling, as well as the production of cytokines [Keates S, and CS. 1999]. CagA induces morphological changes in host cells through interaction with protein SHP-2, a cytoplasmic tyrosin phosphatase [Higashi H et al., 2002]. Indeed, after entering the cell, CagA is first tyrosin-phosphorylated by the Src family of kinases, and then bound to SHP-2. Because SHP-2 plays an important role in the transduction phenomena performed by various tyrosin kinase receptors, CagA induces cellular dysfunction by downregulating SHP-2. , inhibited cytoskeleton rearrangement, proliferation and increased motility in gastric epithelial cells. In addition, it has been hypothesized that cag polymorphisms, which are part of the tyrosine coding sequence, may be essential variables of clinical outcomes when infected with different strains of H. pylori cag+. Indeed, H. pylori can be divided into two main subtypes based on structurally different tyrosin-phosphorylation/SHP-2 binding sites: East Asian cag+ strains and Western cag+ strains. Specifically, patients infected with East Asian strains had an increased inflammatory response, higher levels of gastric precancerous lesions, and a greater risk of gastric cancer compared with patients infected with Western strains.
Increasing evidence confirms the importance of genetic variation in the pathogenesis of gastric cancer and precancerous lesions. The multifunctionality of TLR4, a cell surface lipopolysaccharide (LPS) receptor involved in H. pylori recognition and host response, is associated with increased levels of inflammation with tissue damage severe in people infected with H. pylori. Specifically, individuals with TLR4+896A>G polymorphism are more likely to have gastric atrophy and severe inflammation and also have an increased risk of ectopic gastric cancer. Finally, the genetic diversity and variability of essential pathogenesis factors such as cagA, TRL4 and SHP2 genes appear to influence the oncogenic potential of H. pylori strains. Therefore, it is important to recognize and differentiate carcinogenic H. pylori strains and to identify genetically high-risk populations predisposed to gastric cancer. Although there are many molecular mechanisms that confirm the role of H. pylori in gastric cancer, H. pylori infection is not considered to be a “sufficient condition” for the development of cancer [Fock KM et al., 2008]. Indeed, only a minority of subjects infected with bacteria develop gastric cancer, as many host and environmental factors act synergistically in this multifactorial disease.
H. pylori bacteria is a type of bacteria that has different characteristics from many other bacteria, one of the basic factors that help H. pylori can survive for a long time in the acidic environment of the stomach is H bacteria. pylori can secrete the enzyme urease, and urease has the ability to neutralize acids to help create a suitable environment for H. pylori bacteria not to be destroyed by stomach acid.
Currently, Vinmec International General Hospital, using 13C carbon isotope in the breath test to diagnose H. pylori bacteria with the top-class machine with 02 airbags, both gives very high diagnostic value. (> 95%) both ensure safety for patients. Accordingly, patients can perform a combination of screening and early detection of gastric cancer to protect their health, because H. pylori bacteria is the main cause of stomach diseases, especially especially stomach cancer. When the diagnosis results are available, customers will be consulted for effective treatment to ensure the best health.
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