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- Material Type
- 文書・図像類
- Author/Editor
- 上野, 真一
- Author Heading
- Publication, Distribution, etc.
- Alternative Title
- Basic and clinical sudies regarding to the idenification of inflammatory factors promoting the malignant transformation mechanism in digestive organ cancer
- Text Language Code
- jpn
- Target Audience
- 一般
- Note (General)
- 2011-2013年度科学研究費助成事業（基盤研究（C））研究成果報告書 課題番号：23591992 研究代表者：上野真一（鹿児島大学・医歯（薬）学総合研究科・特任教授）炎症遷延化を引き起こすHMGB1と呼応するTLR-4、マクロファージ/TAMの動態、またEMTの存在について、ヒト肝癌（HCC）を用いて検討し、TAMに対する独自の抗FRβイムノトキシンによる制御を検討した。HMGB1レベルとTAM数、またTAM数と予後の相関がみられた。EMTに関する知見では、転写因子ZEB-1も関与した。一方、TAMの制御に関して、抗FRβイムノトキシンをヌードマウスHepG2皮下移植モデルに投与したところ、著明な腫瘍増殖抑制効果が認められた。以上の結果より、組織HMGB1とこれらにより誘導されるTAMによる腫瘍組織悪性化（形質転換）への可能性の関連が強く示唆された。To investigate the cancer transformation of human hepatocellular carcinoma (HCC), the change of HMGB1 and its receptor TLR-4 with tissue macrophage (TAM) were analyzed. Moreover, the usefulness of FrB immunotoxin against TAM was studied if it could diminish tumor's malignant transformation. In HCC, correlations of HMGB1 level and number of TAM, and the number of TAM and patients prognosis were seen. For the knowledge about EMT, transcription factor ZEB-1 participated, too. On the other hand, after giving FrB immunotoxin to nude mouse HepG2 transplant model under skin, a clear effect of tumor promotion was seen. With these considerations, it was suggested that HMGB1 and derived TAM would contribute to the malignant transformation of HCCs, and FrB immunotoxin could be a treatment strategy.