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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-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...
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,...
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...
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...

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Related Experiment Video

Updated: May 17, 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

Gastric carcinogenesis.

Ismail Gomceli1, Baris Demiriz, Mesut Tez

  • 1Department of Gastroenterologic Surgery, Antalya Education and Research Hospital, 07070 Antalya, Turkey.

World Journal of Gastroenterology
|October 16, 2012
PubMed
Summary

Gastric cancer remains a leading cause of cancer deaths globally. This research explores chronic inflammation

Area of Science:

  • Oncology
  • Gastroenterology
  • Cancer Research

Background:

  • Gastric cancer is the second leading cause of cancer deaths worldwide, with poor survival rates (28% 5-year relative survival).
  • Current treatments for advanced gastric cancer have limited impact on overall survival, with over 80% of patients dying within a year.
  • Chronic inflammation, injury, and repair processes are implicated in neoplasia development, potentially stimulating tumor growth.

Purpose of the Study:

  • To investigate the role of chronic inflammation in gastric carcinogenesis.
  • To highlight recent advancements in understanding gastric cancer precursor lesions.
  • To explore the cellular events initiating gastric metaplasia.

Main Methods:

  • Review of documented processes in neoplasia, including cellular metaplasia.
Keywords:
Cancer Stem CellCarcinogenesisGastric CancerOncogenesisTumorigenesis

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Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform
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Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform

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

Published on: February 16, 2024

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform
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Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform

Published on: May 10, 2024

  • Analysis of pathways involved in gastric carcinogenesis.
  • Consideration of the role of peritumoral stroma in gastrointestinal cancers.

    • Main Results:

    • Chronic inflammation appears critical in initiating, sustaining, and advancing tumor growth.
    • Gastric carcinogenesis involves pathways such as intestinal metaplasia and spasmolytic polypeptide-expressing metaplasia.
    • The initiating cellular event in gastric metaplasia remains a subject of ongoing research.

    Conclusions:

    • Understanding gastric carcinogenesis and precursor lesions is crucial for improving patient outcomes.
    • Further research into the cellular mechanisms of gastric metaplasia is warranted.
    • Targeting inflammatory pathways may offer new therapeutic strategies for gastric cancer.