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Related Concept Videos

Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

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

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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...
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Tumor Progression02:07

Tumor Progression

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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
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Gastritis-I: Introduction and Types01:27

Gastritis-I: Introduction and Types

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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,...
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Cancers Originate from Somatic Mutations in a Single Cell02:21

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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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Author Spotlight: Advancing Early Detection and Treatment of Gastrointestinal Tumors
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Gastric cancer pathogenesis.

Hilmar Berger1, Miguel S Marques2,3,4, Rike Zietlow1

  • 1Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.

Helicobacter
|August 18, 2016
PubMed
Summary
This summary is machine-generated.

This review covers recent advances in understanding gastric cancer (GC) development, focusing on the cell of origin, Helicobacter pylori genotoxicity, and long noncoding RNAs. Improved knowledge aids in identifying new targets for GC prevention and treatment.

Keywords:
Helicobacter pylorigastric cancergenotoxicitylong noncoding RNAsstem cells

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Area of Science:

  • Oncology
  • Molecular Biology
  • Gastroenterology

Background:

  • Gastric cancer (GC) arises from a complex, multistep process involving genetic and epigenetic alterations.
  • Key factors include Helicobacter pylori infection, host genetic susceptibility, and environmental influences.
  • These alterations dysregulate cell signaling, disrupting the balance between cell proliferation and apoptosis.

Purpose of the Study:

  • To review recent advancements in understanding gastric cancer development.
  • To focus on three critical areas: the cell of origin, H. pylori genotoxicity, and long noncoding RNAs in GC transformation.
  • To highlight the importance of molecular insights for novel therapeutic and preventive strategies.

Main Methods:

  • Review of the latest research published within the last year.
  • Synthesis of findings related to the cellular origins of gastric malignancy.
  • Analysis of mechanisms underlying direct genotoxicity caused by H. pylori infection.
  • Examination of the role of aberrant long noncoding RNA expression in GC pathogenesis.

Main Results:

  • Advances in identifying the specific cell types that initiate gastric cancer.
  • Elucidation of how H. pylori directly damages DNA, contributing to cancer development.
  • Demonstration of the significant role of dysregulated long noncoding RNAs in the multistep process of GC transformation.
  • Consolidation of knowledge on molecular pathways disrupted in gastric cancer.

Conclusions:

  • Understanding the molecular underpinnings of GC is crucial for developing effective prevention and treatment strategies.
  • Recent research provides critical insights into the cell of origin, H. pylori's genotoxic effects, and the role of noncoding RNAs.
  • Continued investigation into these areas holds promise for identifying novel therapeutic targets for gastric cancer.