2023 Fiscal Year Final Research Report
Analysis of the mechanism of pancreatic cancer progression via immune nerve signaling regulated by gut microbiota
| Project/Area Number |
21K07907
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Review Section |
Basic Section 53010:Gastroenterology-related
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
伊地知 秀明 東京大学, 医学部附属病院, 講師 (70463841)
|
|---|
| Project Period (FY) |
2021-04-01 – 2024-03-31
|
| Keywords | 膵臓癌 / 腸内細菌叢 / 神経 |
|---|
| Outline of Final Research Achievements |
We conducted research to elucidate the mechanism of pancreatic cancer development from chronic pancreatitis, in relation to immune cells and nerve signaling in the tumor microenvironment utilizing genetically modified mouse models. We also analyzed the effect of gut microbiota on tumor microenvironment. We found distinct pattern of microbiota, tumor innervation by sympathetic neuron, tumor progression and anti-tumor immune suppression by sympathetic signaling in the mouse model of pancreatic cancer with chronic pancreatitis. Intervention to gut microbiota suppressed tumor development in the mouse model with chronic pancreatitis, suggesting the possibility of a novel prevention therapy.
|
| Free Research Field |
消化器内科学
|
| Academic Significance and Societal Importance of the Research Achievements |
慢性膵炎は膵臓癌の危険因子として知られているが、慢性膵炎からの発癌機序や危険因子、発癌予防の方法については明らかになっていない。本研究では腸内細菌叢や腫瘍内の交感神経シグナルという新しい視点から研究を行い、腸内細菌叢への介入により抗腫瘍免疫の低下や交感神経シグナルを介した発癌を抑制できる可能性が示唆された。これは慢性膵炎のコントロールや慢性膵炎からの発癌抑制法の新規開発につながる可能性のある研究成果であると考えられる。
|
