Elucidation of mechanism of tumor associated macrophage in mandibular bone invasion by oral squamous cell carcinoma cells and a research for new treatment

2017 Fiscal Year Final Research Report

• Project/Area Number: 26463024
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Surgical dentistry
• Research Institution: Tokyo Medical University
• Principal Investigator: SATOMI TAKAFUMI 東京医科大学, 医学部, 臨床准教授 (70276921)
• Co-Investigator(Kenkyū-buntansha): 河野 通秀 東京医科大学, 医学部, 助教 (00421066) ; 近津 大地 東京医科大学, 医学部, 教授 (30343122) ; 渡辺 正人 東京医科大学, 医学部, 臨床講師 (40349460) ; 虻川 東嗣 明海大学, 歯学部, 准教授 (50453717) ; 藤川 考 東京医科大学, 医学部, 兼任助教 (60322468) ; 長尾 俊孝 東京医科大学, 医学部, 主任教授 (90276709)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: 顎骨浸潤 / 腫瘍関連マクロファージ / 口腔癌

Outline of Final Research Achievements

The cytokine colony stimulating factor-1(CSF-1) is an important factor of tumor associated macrophage (TAM) recruitment and differentiation and several pharmacological agents targeting the CSF-1 receptor (CSF-1R) have been developed to regulate TAM in solid cancers. Although single CSF-1R inhibition only modestly delayed tumor growth, combination with mTOR promoted the control of tumor outgrowth. The mTOR decreased VEGFR mRNA expression and the mRNA expressions RANKL and CSF-1R decreased in CSF-1R inhibition in bone invasion by oral squamous cell carcinoma (OSCC). CSF-1R inhibition can suppress osteoclast mediated bone invasion by OSCC.
We suggest that combination treatment of mTOR with CSF-1R inhibition might be expected to be a therapeutic target to prevent bone invasion by OSCC. Our data support further development of treatments combining mTOR with TAM targeting agents.

Free Research Field

口腔外科学