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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,...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Gastritis III: Clinical Manifestations and Management01:23

Gastritis III: Clinical Manifestations and Management

The clinical manifestations of gastritis can vary depending on the cause and type of gastritis, but some common symptoms may include the following.
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...
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: Jun 18, 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

Gastrin, inflammation, and carcinogenesis.

Celia Chao1, Mark R Hellmich

  • 1Department of Surgery, Sealy Center for Cancer Cell Biology, University of Texas Medical Branch, Galveston, Texas 77555-0722, USA.

Current Opinion in Endocrinology, Diabetes, and Obesity
|November 13, 2009
PubMed
Summary
This summary is machine-generated.

Gastrin peptides and cholecystokinin (CCK2) receptors promote gastrointestinal cancer progression during inflammation. Targeting these pathways may offer new therapeutic strategies for inflammation-related cancers.

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Area of Science:

  • Gastroenterology and Oncology
  • Molecular Biology
  • Immunology

Background:

  • Helicobacter pylori infection is a key risk factor for gastric cancer, establishing a model for inflammation-associated cancers.
  • Gastrin peptides and their receptors (CCK2 receptors) play a critical role in potentiating gastrointestinal malignancies.

Purpose of the Study:

  • To review current clinical and experimental evidence on the role of gastrin peptides and CCK2 receptors in gastrointestinal cancer.
  • To elucidate the mechanisms by which gastrin influences cancer progression in inflammatory conditions.

Main Methods:

  • Review of recent clinical and experimental studies.
  • Analysis of molecular and cellular signaling pathways.
  • Examination of immune cell and fibroblast modulation.

Main Results:

  • Gastrin and CCK2 receptor expression are upregulated during inflammation and cancer.
  • Gastrin promotes inflammation by inducing cyclooxygenase-2 (COX-2) and interleukin-8 (IL-8).
  • Gastrin and CCK2 receptors modulate immune cells and fibroblasts in cancer progression.

Conclusions:

  • Future research should focus on gastrin's role in intercellular signaling within the tumor microenvironment.
  • Understanding inflammation-cancer pathways can lead to novel therapies targeting the inflammatory microenvironment.