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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,...
Barrett Esophagus-I: Introduction01:21

Barrett Esophagus-I: Introduction

Barrett's esophagus is a medical condition where the esophageal mucosa is significantly damaged by stomach acid or other digestive fluids, often due to long-term exposure associated with gastroesophageal reflux disease (GERD). In GERD, a weakened or abnormally relaxed lower esophageal sphincter allows stomach acid to flow persistently into the esophagus.
This constant acid exposure transforms the esophagus's pink mucosal lining (stratified squamous epithelium) into a type of lining more similar...
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...
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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Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia
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Published on: February 16, 2024

Gastric cancer: basic aspects.

Carlos Resende1, Alexandra Thiel, José C Machado

  • 1IPATIMUP, Institute of Molecular Pathology and Immunology of the University of Porto, Porto, Portugal.

Helicobacter
|September 8, 2011
PubMed
Summary
This summary is machine-generated.

Gastric cancer (GC) risk is influenced by genetic variants and epigenetic changes. This review highlights key genes and molecular pathways involved in gastric carcinogenesis, including inflammatory mediators like cyclooxygenase-2 (COX-2).

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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 of Gastric Cancer Patient-derived Xenograft Models and Primary Cell Lines
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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Gastric cancer (GC) is a leading cause of cancer mortality globally.
  • GC development involves complex interactions between environmental factors, genetic predispositions, and molecular alterations.
  • Recent advances in molecular oncobiology have identified numerous genes critical to gastric carcinogenesis.

Purpose of the Study:

  • To review recently identified basic aspects and key genes involved in gastric carcinogenesis.
  • To discuss genetic variants that modify GC risk.
  • To explore newly associated genes in oncogenic activation and tumor suppressor inactivation pathways.

Main Methods:

  • Literature review of molecular oncobiology studies.
  • Analysis of genetic and epigenetic alterations in gastric cancer.
  • Focus on recently described genes and molecular mediators.

Main Results:

  • Genetic variants in IL-10, IL-17, MUC1, MUC6, DNMT3B, SMAD4, and SERPINE1 are linked to modified GC risk.
  • New associations include oncogenic activation of GSK3β, CD133, DSC2, P-Cadherin, CDH17, CD168, CD44, MMP7, MMP11, and miRNAs.
  • Tumor suppressor gene inactivation involves TFF1, PDX1, BCL2L10, XRCC, psiTPTE-HERV, HAI-2, GRIK2, and RUNX3.
  • Cyclooxygenase-2 (COX-2) plays a role in gastric carcinogenesis and is a potential therapeutic target.

Conclusions:

  • Gastric carcinogenesis is a multifactorial process driven by genetic and epigenetic alterations.
  • Numerous genes, including those involved in inflammation and cell adhesion, are implicated in GC development.
  • Understanding these molecular mechanisms offers potential targets for novel gastric cancer therapies, such as targeting COX-2.