The role of inflammatory responses and tumor immunity in tumor development

2014 Fiscal Year Final Research Report

• Project/Area Number: 24300325
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Carcinogenesis
• Research Institution: Kanazawa University
• Principal Investigator: OSHIMA Masanobu 金沢大学, がん進展制御研究所, 教授 (40324610)
• Co-Investigator(Renkei-kenkyūsha): OSHIMA Hiroko 金沢大学, がん進展制御研究所, 助教 (80362515) ; ISHIKAWA Tomoo 金沢大学, がん進展制御研究所, 助教 (70322162) ; NAKAYAMA Mizuho 金沢大学, がん進展制御研究所, 助教 (20398225)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 胃がん / 炎症 / 微小環境 / 腫瘍免疫 / マウスモデル

Outline of Final Research Achievements

It has been shown that inflammatory responses promote tumorigenesis. On the other hand, tumor immunity suppresses cancer development. In this project, we have examined characteristics of inflammatory microenvironment that was generated in gastric tumors of genetically engineered mouse model. Notably, infiltrated macrophages are polarized to M2 type, and CD4-positive T cells are infiltrated, which promotes tumorigenesis. Moreover, TGF-β signaling is enhanced and regulatory T cells are also infiltrated, suggesting that tumor immunity is suppressed in the inflammatory microenvironment. Importantly, depletion of Treg cells in tumor mouse model induced autoimmune gastritis by inhibition of immune suppression system, and such inflammatory responses further accelerated gastric tumorigenesis. Accordingly, these results suggest that regulation of the balance between inflammation and tumor immunity is important for direction of tumor promotion or suppression.

Free Research Field

分子病理学