Genomic instability and mechanisms of carcinogenesis due to infection and inflammation

2014 Fiscal Year Final Research Report

• Project Area: Conversion of tumor-regulation vector to intercept oncogenic spiral accelerated by infection and inflammation
• Project/Area Number: 22114006
• Research Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
• Allocation Type: Single-year Grants
• Review Section: Biological Sciences
• Research Institution: Kobe University
• Principal Investigator: AZUMA Takeshi 神戸大学, 医学(系)研究科(研究院), 教授 (60221040)
• Co-Investigator(Kenkyū-buntansha): MARUSAWA Hiroyuki 京都大学, 医学研究科, 講師 (80324630)
• Project Period (FY): 2010-04-01 – 2015-03-31
• Keywords: ヘリコバクターピロリ / 胃がん / AID / ヘリコバクタースイス / 胃MALTリンパ腫 / CXCL13 / インターフェロンガンマ

Outline of Final Research Achievements

It is well recognized that cancer develops via a stepwise accumulation of genetic aberrations. We revealed that pathogenic bacterial or viral factors and the subsequent inflammatory reactions lead to the aberrant expression of a DNA mutator-enzyme, activation-induced cytidine deaminase (AID), in various epithelial cells, causing the accumulation of genetic damages. Indeed, aberrant AID expression is widely observed in gastrointestinal tissues underlying chronic inflammation, such as chronic viral hepatitis and H. pylori-related gastritis.
It has been known that gastric mucosa-associated lymphoid tissue lymphomas can be induced by H. suis infection. We revealed that the inflammatory cytokine; interferon γ and B lymphocyte chemoattractant; CXCL13 were dramatically upregulated in the stomach of H. suis infected mice, suggesting that they are crucial for the development of gastric MALT lymphomas after H. suis infection.

Free Research Field

消化器内科学、細菌学