2019 Fiscal Year Final Research Report
Development of molecular preventive therapy for oncogene-induced malignant tumors
Project/Area Number |
17K09156
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Hygiene and public health
|
Research Institution | Hyogo Medical University (2018-2019) Nagoya University (2017) |
Principal Investigator |
Sudo Makoto 兵庫医科大学, 医学部, ポストドクター (40415427)
|
Co-Investigator(Kenkyū-buntansha) |
矢嶋 伊知朗 名古屋大学, 医学系研究科, 講師 (80469022)
加藤 昌志 名古屋大学, 医学系研究科, 教授 (10281073)
|
Project Period (FY) |
2017-04-01 – 2020-03-31
|
Keywords | メラノーマ / モデルマウス / 免疫 |
Outline of Final Research Achievements |
We performed DNA microarray analysis in a benign melanocytic tumor and a melanoma from a RET-transgenic mouse. Some candidate molecules, which might regulate carcinogenesis were identified. Those transcript and protein expression levels were increased in melanoma cell lines compared with those in normal epithelial melanocytes. Depleted those molecules by siRNA or inhibitors in human melanoma cell lines showed that cell proliferation and invasion activity were decreased. Increase the molecules which are expressed by tumor associated cells and inflammatory cytokines change immune microenvironment in melanoma. The cellular and cytokine composition of the tumor microenvironment can affect the immune cell infiltration at the tumor site and escape from antitumor immune responses. Suppress the tumor associated molecules and inflammatory cytokines that supports antitumor properties. Collectively, our findings show the possibility of preventive and therapeutic strategies for melanoma.
|
Free Research Field |
腫瘍学
|
Academic Significance and Societal Importance of the Research Achievements |
現在日本は超高齢化社会になりつつあり、癌に罹患する割合が高く、癌患者数は増加し続けている。癌は遺伝的、環境的要因により、誰しもが罹患する可能性がある。癌治療により、身体的、経済的、社会的損失は大きく、癌の克服は長年の夢である。我々の研究では、発癌制御分子の探索、新規薬剤による治療方法の開発、腫瘍の免疫回避メカニズムの一端を見出した。発癌や腫瘍の免疫回避を抑制出来れば、癌治療が軽減されるだけでなく、癌予防につながる可能性がある。癌予防は新しい考え方であり、今後も研究を推進していくべき分野である。
|