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HANEDA Hiroshi

    Graduate School of Medical Sciences Department of Oncology, Immunology and Surgery
Last Updated :2026/09/04

Researcher Information

J-Global ID

Research Interests

  • Immunotherapy   Minimally Invasive Surgery   Perioperative Chemo-immunotherapy   Mediastinal Tumor   Lung Cancer   

Research Areas

  • Life sciences / Respiratory surgery

Academic & Professional Experience

  • 2014/04 - 2019/03  名古屋市立大学大学院医学系研究科 呼吸器・小児外科学
  • 2003/07 - 2006/03  Nagoya City UniversityGraduate School of Medical Sciences Department of Oncology, Immunology and Surgery

Published Papers

Research Grants & Projects

  • 日本学術振興会：科学研究費助成事業
    Date (from‐to) : 2005 -2006 
    Author : 羽田 裕司
     
    1.p53誘導性アポトーシス・スクリーニングシステムの確立 Clontec社tet-onシステムを用いて、内在性p53の欠失したsaos2細胞株にテトラサイクリン(tet)の濃度依存的にp53を過剰発現する細胞(saos2/tet-on-p53)を作成。この細胞はドキシサイクリン(tetアナログ)の添加によりその濃度依存的にp53の過剰発現が誘導、アポトーシスとなる。しかし本研究でのスクリーニングにはtetによる誘導後に生存する細胞はすべて偽陽性として拾われてしまうため、全ての細胞死が誘導されるラインを選別中である。 2.レトロウイルスshRNA発現システムの確立 RNAiは2本鎖RNA (dsRNA)を細胞内に導入することでそのRNA配列に特異的な発現抑制がかかる手法で、哺乳類細胞へは21ヌクレオチド前後の短いdsRNAを形質導入することで標的遺伝子の発現を抑制できる。近年ではdsRNAの代わりに、プラスミドベクターを用いて2つの相補的配列をとる21ヌクレオチドの配列の間に短い配列をはさんだ1本鎖のRNAを転写させ細胞内で、dsRNAと同様の効果を安定して発揮するベクターが開発されており、本研究ではClontec社のpSIREN-RetroQ vectorを用いた。ランダムライブラリー作成の準備段階として、関連因子として解析が進んでいるBax, Puma, Noxa等に対するベクターをpositive controlとして作成、1,のsaos2/tet-on-p53細胞に導入し、アポトーシス抑制能の解析を試みた。 3、ランダムshRNAライブラリーの作成 本研究で作成を目指したランダムshRNAライブラリーは21ヌクレオチドをランダムに作成するため理論上4^<21>=4×10^<12>のスクリーニングが可能であるが、まず一次スクリーニングのため少数のライブラリーの作成に取りかかった。
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research
    Date (from‐to) : 2005 -2006 
    Author : YANO Motoki; HANEDA Hiroshi; ENDO Katsuhiko
     
    We have established the endostatin transfection systems which showed the impact of antiangiogenesis and suppression of tumor growth. However the effect was not maintained for a long time. Finally the endostatin-tranfected animals died without tumor dormancy. There, also, have been no reports of effective clinical trials. We hypothesized the reasons he short effect of endostatin depended on up-regulation of some kinds of angiogenic factors. In the present study we have transfected mice lungs with endostatin gene and analyzed the VEGF gene expression. We used quantitative RT-PCR method to quantify the VEGF mRNA using GAPDH mRNA as an internal control. The both expression of Endostatin and VEGF mRNAs in the lung were apparent and the expression of VEGF mRNA in trasfection group (n=6) was higher than in cntol group (n=6) (p=0.0755 in Schffe's method in ANOVA, p=0.055 in Mann-Whitney U test). This mechanism was not unclear but the data was very important. This data may suggest that suppression of VEGF induced prolongation of effect of endostatin. Next we can try endostatin gene transfection with suppression of VEGF to prove the present data and achieve the tumor dormancy.
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research
    Date (from‐to) : 2005 -2006 
    Author : FUJII Yoshitaka; YANO Motoki; SASAKI Hidefumi; HANEDA Hiroshi; ENDO Katsuhiko
     
    1. Using probes for the 13 different mutations including 11 that have already been reported, we have genotyped the EGFR mutation status in 400 non small cell lung cancer patients operated between 2000-2006 at Nagoya City University Hospital using the TaqMan PCR assay. We have evaluated the relationships among the EGFR mutation, clinical-pathologic factors, gefitinib sensitivity, and overall survival. We show in our previous paper that the TaqMan PCR assay is sensitive enough to detect the mutation in samples contaminated with 9 fold excess of wild type samples. Therefore, we have analyzed small samples obtained from CT guided biopsy or trans-bronchial biopsy. 2. Some studies reported that downstream signaling molecules, EGFR gene amplification, and the expression of the other ErbB receptors were the other predictors of gefitinib sensitivity. Therefore, we have analyzed the other biomarkers, as the EGFR copy number, the ErbB2 copy number and PIK3CA gene mutation and have evaluated the relationship between their biomarkers and clinical-pathologic factors. 3. We have reported these studies at the annual meetings and have published them as an article. 4. In the future, we hope that EGFR mutation status using TaqMan PCR assay contributes to made-to-order treatment

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