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Accumulation of somatic mutations in TP53 in gastric epithelium with Helicobacter pylori infection
Takahiro Shimizu1, Hiroyuki Marusawa1, Yuko Matsumoto1
1Department of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Gastroenterology
|May 3, 2014
Summary
Helicobacter pylori infection causes genetic mutations in the stomach lining, increasing gastric cancer risk. Activation-induced cytidine deaminase (AID) activity promotes these mutations, driving cancer development.
Area of Science:
- Gastroenterology
- Oncology
- Genetics
Background:
- Helicobacter pylori infection is a known risk factor for gastric cancer.
- Gastric cancer develops in inflamed gastric mucosa.
- Genetic aberrations accumulate in non-tumorous gastric epithelium with H. pylori infection.
Purpose of the Study:
- To investigate the genetic basis of gastric cancer in H. pylori-infected individuals.
- To identify genetic aberrations in non-tumorous gastric epithelium.
- To explore the role of inflammation in gastric carcinogenesis.
Main Methods:
- Whole-exome sequencing of gastric tumors and noncancerous tissues.
- Deep-sequencing of tumor-related genes in 34 gastritis samples.
- Deep sequencing in mouse models with TP53 and activation-induced cytidine deaminase (AICDA or AID) expression.
Main Results:
- Somatic mutations were found to accumulate in various genes within inflamed gastric tissues.
- Low-abundance mutations in TP53 (44.1%) and ARID1A (14.7%) were confirmed in gastritis tissues.
- Mutations predominantly showed C:G>T:A transitions, a marker of AID-induced cytidine deamination.
Conclusions:
- Somatic mutations accumulate in gastric mucosal tissues infected with H. pylori.
- Increased cytidine deaminase activity in these tissues promotes mutation accumulation.
- This process may contribute to gastric carcinogenesis in H. pylori-infected patients.
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