Abstract
It is widely accepted that carcinogenesis is a multistep process in which regulation of both cell proliferation and apoptosis is disturbed. p53, which is considered the cellular gatekeeper for growth and division, induces apoptosis. Helicobacter pylori(Hp) infection is an accepted risk factor for the development of gastric cancer, but not all infected individuals develop gastric cancer. Because CagA+ Hp induces increased cell proliferation, the CagA+ strain is believed to play an important role in the pathogenesis of gastric cancer. We have reported that p53 alteration were more frequently found in the CagA+ Hp infection in gastric cancer patients. In this chapter, we summarized recent findings of the relation among p53, CagA and cag PAI.
| Original language | English |
|---|---|
| Pages (from-to) | 41-45 |
| Number of pages | 5 |
| Journal | Nippon rinsho. Japanese journal of clinical medicine |
| Volume | 61 |
| Issue number | 1 |
| Publication status | Published - 01-2003 |
| Externally published | Yes |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
-
SDG 3 Good Health and Well-being
All Science Journal Classification (ASJC) codes
- General Medicine
Fingerprint
Dive into the research topics of 'cag PAI and gastric carcinogenesis-association with p53 gene mutation'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver