| Budget Amount *help |
¥121,810,000 (Direct Cost: ¥93,700,000、Indirect Cost: ¥28,110,000)
Fiscal Year 2014: ¥22,620,000 (Direct Cost: ¥17,400,000、Indirect Cost: ¥5,220,000)
Fiscal Year 2013: ¥23,790,000 (Direct Cost: ¥18,300,000、Indirect Cost: ¥5,490,000)
Fiscal Year 2012: ¥25,090,000 (Direct Cost: ¥19,300,000、Indirect Cost: ¥5,790,000)
Fiscal Year 2011: ¥24,830,000 (Direct Cost: ¥19,100,000、Indirect Cost: ¥5,730,000)
Fiscal Year 2010: ¥25,480,000 (Direct Cost: ¥19,600,000、Indirect Cost: ¥5,880,000)
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| 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.
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