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Aberrant AID expression and human cancer development.
1Department of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan. maru@kuhp.kyoto-u.ac.jp
The International Journal of Biochemistry & Cell Biology
|March 11, 2008
Summary
Activation-induced cytidine deaminase (AID) may drive cancer by causing mutations in non-immune cells. Aberrant AID expression, linked to inflammation, could be a key factor in tumor development.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Cancer arises from accumulated somatic mutations in genes controlling cell growth and death.
- The origin of genetic changes leading to malignant transformation remains unclear.
- Activation-induced cytidine deaminase (AID) is known for generating diversity in immunoglobulin genes through mutations and recombination.
Purpose of the Study:
- To investigate the potential role of Activation-induced cytidine deaminase (AID) as a mutagen in non-lymphoid tissues.
- To explore the link between aberrant AID expression, inflammation, and cancer development.
Main Methods:
- The study focuses on the known functions of AID and its potential off-target effects.
- It examines conditions triggering aberrant AID expression in epithelial cells, such as infections and inflammatory stimuli.
Main Results:
- AID's function as a genome mutator could extend to host genes in non-lymphoid tissues, potentially contributing to tumorigenesis.
- Aberrant AID expression is observed in human epithelial cells under inflammatory conditions (e.g., Helicobacter pylori infection, cytokine stimulation).
- AID expression is typically absent in epithelial cells under normal physiological conditions.
Conclusions:
- Aberrant AID activity in epithelial tissues presents a potential mechanism linking inflammation to somatic mutations and subsequent cancer development.
- This finding suggests AID could be a critical factor in inflammation-driven carcinogenesis.
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