2020 Fiscal Year Final Research Report
To build new method of angiogenesis inhibitor for oral squamous cell cancer targeting CXCR4
Project/Area Number |
19K24094
|
Research Category |
Grant-in-Aid for Research Activity Start-up
|
Allocation Type | Multi-year Fund |
Review Section |
0907:Oral science and related fields
|
Research Institution | Okayama University |
Principal Investigator |
Omori Haruka 岡山大学, 大学病院, 医員 (30850424)
|
Project Period (FY) |
2019-08-30 – 2021-03-31
|
Keywords | 扁平上皮癌 / 口腔癌 / 癌微小環境 / 腫瘍血管 / CXCR4 |
Outline of Final Research Achievements |
CXCR4-SDF1(stromal cell derived factor 1) axis is reported it played a role in growth and survival with angiogenesis. We discovered well differentiated oral squamous cell carcinoma had blood vessels express CXCR4. Furthermore, we transplanted well differentiated human oral squamous cell carcinoma cell line (HSC2) to under the skin in the back of the mouse and administer AMD 3100 is CXCR4 inhibitor intraperitoneally. We compared group inhibited CXCR4 with control histologically and measured running and shape of blood vessel so we discovered group inhibited CXCR was inhibited angiogenesis of tumor, became hypoxia and made tumor necrosis.
|
Free Research Field |
口腔病理学
|
Academic Significance and Societal Importance of the Research Achievements |
CXCR4-SDF1 axisの血管新生経路は、既存の血管新生阻害薬として知られているVEGFによる血管新生の経路とは異なるため、腫瘍血管におけるCXCR4の役割が明らかとなれば、新たなアプローチの抗腫瘍血管治療の開発につながる可能性がある。また、CXCR4阻害剤であるAMD3100はFDA(アメリカ食品医薬品局)、EMA(欧州医薬品庁)により、「造血幹細胞を末梢血に動員する薬剤」として承認を受けた薬剤である。本研究で抗腫瘍効果が認められれば、既存の抗癌剤や分子標的剤との併用療法や、VEGF阻害剤への薬剤耐性化患者に対する新たな治療の選択肢として、臨床応用が期待できる。
|