The mechanisms of immune-mediated tumor progression triggered by cancer metabolism

2015 Fiscal Year Final Research Report

• Project/Area Number: 26670183
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Experimental pathology
• Research Institution: Keio University
• Principal Investigator: Jinushi Masahisa 慶應義塾大学, 医学部, 准教授 (40318085)
• Research Collaborator: Kitabayashi Isho 国立がん研究センター, 研究所, 造血腫瘍分野長 ; Kimohara Yoshihiro 熊本大学, 大学院医学研究科細胞病理学, 准教授 ; Taku syuichiro 熊本大学, 大学院医学研究科脳神経外科学, 講師 ; Akita Hirotoshi 北海道大学, 大学院医学研究科腫瘍内科学, 教授 ; Yagita Hideo 順天堂大学, 医学部免疫学, 先任准教授
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: 腫瘍代謝

Outline of Final Research Achievements

I focused the role of most notable cancer metabolic pathway, IDH1/2 mutation in gliomas on tumor immunogenic phenotypes, I found that IDH1/2 in glioma cells contribute to generation of immunosuppressive microenvironments, which are manifested by the infiltration of M2 macrophages, MDSCs, and PD-1-positive T cells with transformation of PD-L1-positive glioma cells from PD-L1-bnegative ones. Thus, IDH-1/2 mutation triggers "inflamed phanotypes" of gliomas, and our study provides scientific rationale that immunochenckpoint blackade may be useful for targeting IDH-mutated tumors.

Free Research Field

腫瘍免疫