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Related Concept Videos

Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Gastritis-I: Introduction and Types01:27

Gastritis-I: Introduction and Types

Gastritis, defined by the inflammation or irritation of the stomach lining or gastric mucosa, manifests in several distinct forms: acute, chronic, reactive, and a specific subtype known as autoimmune metaplastic atrophic gastritis.
Acute gastritis presents as a sudden inflammation triggered by various stressors to the stomach lining, such as exposure to corrosive agents, local irritants like aspirin and other NSAIDs, alcohol consumption, radiation therapy, physical trauma, severe burns, sepsis,...
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
Mucosal Barrier of the Stomach01:25

Mucosal Barrier of the Stomach

The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Stomach Histology01:26

Stomach Histology

The stomach comprises several layers that work together to facilitate digestion and protect the organ. The outermost layer is called the serosa, which provides support and protection to the stomach. The muscularis externa layer is responsible for the mechanical breakdown of food by contracting and moving the stomach. The submucosa layer, located beneath the muscularis externa, contains connective tissue, blood vessels, nerves, and glands that secrete mucus and other substances essential for...

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Related Experiment Video

Updated: Jun 20, 2026

Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia
03:05

Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia

Published on: February 16, 2024

Basic aspects of gastric cancer.

Marta Correia1, José Carlos Machado, Ari Ristimäki

  • 1Institute of Molecular Pathology and Immunology of the University of Porto, Rua Dr. Roberto Frias s/n, Porto, Portugal.

Helicobacter
|August 29, 2009
PubMed
Summary
This summary is machine-generated.

Gastric cancer remains a major global health challenge. This review highlights advances in understanding its molecular basis, including genetic factors, inflammation, and stem cell roles, to improve survival rates.

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Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT
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Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT

Published on: January 22, 2018

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Last Updated: Jun 20, 2026

Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia
03:05

Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia

Published on: February 16, 2024

Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT
10:28

Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT

Published on: January 22, 2018

Area of Science:

  • Oncology
  • Molecular Biology
  • Gastroenterology

Background:

  • Gastric cancer is a leading cause of cancer deaths globally.
  • Long-term survival rates for gastric cancer have seen limited improvement.
  • Understanding the molecular mechanisms of gastric cancer is crucial for developing new therapies.

Purpose of the Study:

  • To review recent advancements in understanding the molecular nature of gastric cancer.
  • To highlight progress in the research of gastric cancer precursor lesions.
  • To provide insights into genetic susceptibility, inflammation, and stem cell involvement.

Main Methods:

  • Review of current scientific literature on gastric cancer molecular biology.
  • Analysis of host-related genetic factors, including inflammation and carcinogen metabolism genes.
  • Examination of the roles of specific molecules like interleukin-1 beta and E-cadherin in experimental models.
  • Inclusion of research on the role of stem cells in gastric carcinogenesis.

Main Results:

  • Identified host genetic factors influencing susceptibility to gastric cancer.
  • Demonstrated the role of interleukin-1 beta overexpression and E-cadherin deletion in gastric carcinogenesis using mouse models.
  • Highlighted the significance of stem cells in the development of gastric cancer.

Conclusions:

  • Advances in understanding gastric cancer's molecular underpinnings are significant.
  • Genetic susceptibility, inflammatory pathways, and stem cell biology are key areas for future research.
  • Further investigation into these molecular aspects holds promise for improving gastric cancer treatment and patient outcomes.