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▎WuXi AppTec's content team edited previous research showing that about 75% to 90% of gastric adenocarcinomas are related to Helicobacter pylori (Hp) infection
.
In addition, about 5% to 10% of gastric adenocarcinomas are associated with Epstein-Barr virus infection
.
Although nearly 50% of the world's population is infected with H.
pylori, only 1% to 3% of the population will eventually develop into gastric adenocarcinoma due to the combined effects of H.
pylori strains, host susceptibility, and chronic inflammatory responses
.
Recently, Nature Reviews Gastroenterology & Hepatology, a sub-journal of "Nature", published a heavy review, detailing the important role of Hp in the formation of gastric adenocarcinoma
.
The paper emphasizes that early detection and eradication of H.
pylori infection are crucial in preventing chronic gastritis from developing into gastric adenocarcinoma
.
In addition, given that the host lesions may already have immunosuppressive features several years before the formation of gastric adenocarcinoma, the effective identification of relevant marker changes during the transformation of gastric atrophy into gastric metaplasia may help us improve The level of prevention and treatment of gastric adenocarcinoma! Screenshot source: Nature Reviews Gastroenterology & Hepatology Major risk factors for gastric adenocarcinoma Nearly 60% of gastric cancer patients worldwide are in East Asia, and nearly half of the patients are in China
.
Recent studies have confirmed that whether it is non-cardia gastric cancer (including gastric adenocarcinoma) or cardiac gastric cancer, Hp infection is a strong associated factor
.
In addition, other environmental risk factors for gastric adenocarcinoma include a high-salt diet as well as nitrate exposure
.
Genetic studies have shown that about 50% of gastric adenocarcinomas are chromosomally unstable gastric adenocarcinomas, and 21% of gastric adenocarcinomas are highly microsatellite unstable (MSI-H) gastric adenocarcinomas
.
The vast majority of Hp-infected patients have no obvious symptoms, and at least 20% of the infected patients are difficult to eradicate
H.
The paper emphasizes that under the combined effect of multiple risk factors, nearly 20% of H.
pylori infection may develop serious complications (including gastric atrophy, gastric metaplasia, and gastric adenocarcinoma)
.
Specifically, these factors include: environmental factors: such as smoking or tobacco exposure; dietary factors: such as higher intake of smoked foods, higher intake of high-nitrate foods, high-salt diets; host susceptibility: such as genetic variation ( Including gene polymorphisms of cytokines such as IL-1β and TNF-α), iron deficiency, and O blood type
.
How does Hp drive gastric adenocarcinoma? About 75% to 90% of gastric adenocarcinoma patients show serum Hp positivity
.
Previous studies have shown that H.
pylori infection is related to persistent immune infiltration (chronic gastritis), and the changes in the immune microenvironment caused by H.
pylori infection (changing the host's innate immunity, adaptive immunity to build an immunosuppressive environment), in the development of chronic gastritis into gastric adenocarcinoma.
played an important role in the process
.
In addition, Hp can also induce the occurrence of related pathological events by regulating vacuolar toxin-related factor A (VacA) and cytotoxin-related factor A (CagA)
.
Similar to many other solid tumors that originate from epithelial cells, different types of cells in the supporting structures surrounding gastric tumors can play multiple roles as initiators, promoters, and promoters in their growth.
These different types of supporting cells include the stroma.
cells, neuronal cells, endothelial cells, and numerous immune cells
.
The paper emphasizes that it is still unclear which immune cells are involved in the transformation of normal gastric epithelial cells into metaplasia and dysplasia in Hp-related gastric cancer
.
▲The types of immune cells recruited by Hp infection in gastric lesions (Image source: Reference [1]) The existence of Hp can be found in different stages of disease progression in patients with gastric adenocarcinoma
.
In addition to H.
pylori, studies have shown that the presence of Prevotella, Streptococcus, Pseudomonas, Sphingomonas, Bacillus and Acinetobacter can also be found in the normal mucosa adjacent to gastric tumors
.
In addition, animal studies have confirmed that Acinetobacter can induce gastritis and induce a TH1-type immune response, and there are also elevated levels of Bacteroides and Haemophilus-related markers in the blood circulation of gastric adenocarcinoma patients
.
Therefore, although Hp may mediate the initial process of gastric adenocarcinoma, the role of Hp, other bacteria and immune cells in the development of gastric metaplasia and gastric adenocarcinoma after gastric mucosal atrophy remains to be further explored
.
What is the significance of early detection and eradication of Hp? The persistence of chronic gastritis can promote the apoptosis of gastric parietal cells and cause chronic atrophic gastritis
.
The human body develops serious complications from H.
pylori infection, such as gastric atrophy, gastric metaplasia and even gastric adenocarcinoma, which can take months or years
.
During this period, the gradual reduction of oxyntic parietal cells reduces gastric acid levels and affects the composition of the stomach microbiome
.
Although only a small proportion of H.
pylori-infected individuals develop clinically significant complications
.
However, based on the fact that H.
pylori infection plays a key role in driving the occurrence of gastric adenocarcinoma, early detection, eradication and even prevention of H.
pylori infection are very important
.
Key nodes in gastric adenocarcinoma development Because tumor neoantigen expression in EBV-positive gastric adenocarcinoma and MSI-H type gastric adenocarcinoma makes it more prone to a higher degree of inflammatory response (i.
e.
, "hot tumor"), it is more likely to be treated in combination with chemotherapy and immunization.
effect under the treatment regimen
.
In contrast, most subtypes of gastric adenocarcinoma, such as diffuse gastric adenocarcinoma with genetic variation and intestinal-type gastric adenocarcinoma driven by H.
pylori infection, are immunologically "cold tumors"
.
Hp may contain immunomodulatory sequences that promote immunosuppression by inducing Treg cells
.
In addition, Hp infection-related gastric adenocarcinoma may have an immune escape mechanism, so anti-tumor immunotherapy obviously cannot work
.
The paper points out that gastric epithelial cell metaplasia (including degree and type) is a key node in the development of gastric adenocarcinoma
.
Since the immunosuppressive environment in the stomach may exist several years before the diagnosis of gastric adenocarcinoma, it is necessary to further study the inhibitory factors of the immune response in the process of H.
Molecular changes that occur during key junctions may help us develop biomarkers for early detection of epithelial changes and improve the treatment of gastric adenocarcinoma
.
In addition, on this basis, the possible risk factors of the host can be identified.
In the future, we can predict which individuals have a higher risk of complications and effectively prevent gastritis from developing into gastric adenocarcinoma
.
.
In addition, about 5% to 10% of gastric adenocarcinomas are associated with Epstein-Barr virus infection
.
Although nearly 50% of the world's population is infected with H.
pylori, only 1% to 3% of the population will eventually develop into gastric adenocarcinoma due to the combined effects of H.
pylori strains, host susceptibility, and chronic inflammatory responses
.
Recently, Nature Reviews Gastroenterology & Hepatology, a sub-journal of "Nature", published a heavy review, detailing the important role of Hp in the formation of gastric adenocarcinoma
.
The paper emphasizes that early detection and eradication of H.
pylori infection are crucial in preventing chronic gastritis from developing into gastric adenocarcinoma
.
In addition, given that the host lesions may already have immunosuppressive features several years before the formation of gastric adenocarcinoma, the effective identification of relevant marker changes during the transformation of gastric atrophy into gastric metaplasia may help us improve The level of prevention and treatment of gastric adenocarcinoma! Screenshot source: Nature Reviews Gastroenterology & Hepatology Major risk factors for gastric adenocarcinoma Nearly 60% of gastric cancer patients worldwide are in East Asia, and nearly half of the patients are in China
.
Recent studies have confirmed that whether it is non-cardia gastric cancer (including gastric adenocarcinoma) or cardiac gastric cancer, Hp infection is a strong associated factor
.
In addition, other environmental risk factors for gastric adenocarcinoma include a high-salt diet as well as nitrate exposure
.
Genetic studies have shown that about 50% of gastric adenocarcinomas are chromosomally unstable gastric adenocarcinomas, and 21% of gastric adenocarcinomas are highly microsatellite unstable (MSI-H) gastric adenocarcinomas
.
The vast majority of Hp-infected patients have no obvious symptoms, and at least 20% of the infected patients are difficult to eradicate
H.
The paper emphasizes that under the combined effect of multiple risk factors, nearly 20% of H.
pylori infection may develop serious complications (including gastric atrophy, gastric metaplasia, and gastric adenocarcinoma)
.
Specifically, these factors include: environmental factors: such as smoking or tobacco exposure; dietary factors: such as higher intake of smoked foods, higher intake of high-nitrate foods, high-salt diets; host susceptibility: such as genetic variation ( Including gene polymorphisms of cytokines such as IL-1β and TNF-α), iron deficiency, and O blood type
.
How does Hp drive gastric adenocarcinoma? About 75% to 90% of gastric adenocarcinoma patients show serum Hp positivity
.
Previous studies have shown that H.
pylori infection is related to persistent immune infiltration (chronic gastritis), and the changes in the immune microenvironment caused by H.
pylori infection (changing the host's innate immunity, adaptive immunity to build an immunosuppressive environment), in the development of chronic gastritis into gastric adenocarcinoma.
played an important role in the process
.
In addition, Hp can also induce the occurrence of related pathological events by regulating vacuolar toxin-related factor A (VacA) and cytotoxin-related factor A (CagA)
.
Similar to many other solid tumors that originate from epithelial cells, different types of cells in the supporting structures surrounding gastric tumors can play multiple roles as initiators, promoters, and promoters in their growth.
These different types of supporting cells include the stroma.
cells, neuronal cells, endothelial cells, and numerous immune cells
.
The paper emphasizes that it is still unclear which immune cells are involved in the transformation of normal gastric epithelial cells into metaplasia and dysplasia in Hp-related gastric cancer
.
▲The types of immune cells recruited by Hp infection in gastric lesions (Image source: Reference [1]) The existence of Hp can be found in different stages of disease progression in patients with gastric adenocarcinoma
.
In addition to H.
pylori, studies have shown that the presence of Prevotella, Streptococcus, Pseudomonas, Sphingomonas, Bacillus and Acinetobacter can also be found in the normal mucosa adjacent to gastric tumors
.
In addition, animal studies have confirmed that Acinetobacter can induce gastritis and induce a TH1-type immune response, and there are also elevated levels of Bacteroides and Haemophilus-related markers in the blood circulation of gastric adenocarcinoma patients
.
Therefore, although Hp may mediate the initial process of gastric adenocarcinoma, the role of Hp, other bacteria and immune cells in the development of gastric metaplasia and gastric adenocarcinoma after gastric mucosal atrophy remains to be further explored
.
What is the significance of early detection and eradication of Hp? The persistence of chronic gastritis can promote the apoptosis of gastric parietal cells and cause chronic atrophic gastritis
.
The human body develops serious complications from H.
pylori infection, such as gastric atrophy, gastric metaplasia and even gastric adenocarcinoma, which can take months or years
.
During this period, the gradual reduction of oxyntic parietal cells reduces gastric acid levels and affects the composition of the stomach microbiome
.
Although only a small proportion of H.
pylori-infected individuals develop clinically significant complications
.
However, based on the fact that H.
pylori infection plays a key role in driving the occurrence of gastric adenocarcinoma, early detection, eradication and even prevention of H.
pylori infection are very important
.
Key nodes in gastric adenocarcinoma development Because tumor neoantigen expression in EBV-positive gastric adenocarcinoma and MSI-H type gastric adenocarcinoma makes it more prone to a higher degree of inflammatory response (i.
e.
, "hot tumor"), it is more likely to be treated in combination with chemotherapy and immunization.
effect under the treatment regimen
.
In contrast, most subtypes of gastric adenocarcinoma, such as diffuse gastric adenocarcinoma with genetic variation and intestinal-type gastric adenocarcinoma driven by H.
pylori infection, are immunologically "cold tumors"
.
Hp may contain immunomodulatory sequences that promote immunosuppression by inducing Treg cells
.
In addition, Hp infection-related gastric adenocarcinoma may have an immune escape mechanism, so anti-tumor immunotherapy obviously cannot work
.
The paper points out that gastric epithelial cell metaplasia (including degree and type) is a key node in the development of gastric adenocarcinoma
.
Since the immunosuppressive environment in the stomach may exist several years before the diagnosis of gastric adenocarcinoma, it is necessary to further study the inhibitory factors of the immune response in the process of H.
Molecular changes that occur during key junctions may help us develop biomarkers for early detection of epithelial changes and improve the treatment of gastric adenocarcinoma
.
In addition, on this basis, the possible risk factors of the host can be identified.
In the future, we can predict which individuals have a higher risk of complications and effectively prevent gastritis from developing into gastric adenocarcinoma
.
