徳島大学 / 教育研究者総覧 --- 原慶次郎

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徳島大学 ⟩ 病院 ⟩ 中央診療施設等 ⟩ 地域脳神経外科診療部 ⟩
徳島大学 ⟩ 病院 ⟩ 診療科 ⟩ 脳·神経·精神科 ⟩ 脳神経外科 ⟩

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研究活動

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研究テーマ

著書・論文

学術論文(審査論文):

1.	Kohei Muto, Ryosuke Miyamoto, Yuka Terasawa, Yoshimitsu Shimatani, Keijiro Hara, Takumi Kakimoto, Tatsuya Fukumoto, Yusuke Osaki, Koji Fujita, Masafumi Harada, Hisanori Uehara, Yasushi Takagi and Yuishin Izumi : A novel COL4A1 variant associated with recurrent epistaxis and glioblastoma, Human Genome Variation, Vol.8, No.1, 18, 2021. (徳島大学機関リポジトリ) ● Metadata: 116530 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41439-021-00150-0 (文献検索サイトへのリンク) ● Summary page in Scopus @ Elsevier: 2-s2.0-85105944271 (徳島大学機関リポジトリ: 116530, DOI: 10.1038/s41439-021-00150-0, Elsevier: Scopus)
2.	Toshitaka Fujihara, Yoshifumi Mizobuchi, Kohhei Nakajima, Teruyoshi Kageji, Kazuhito Matsuzaki, KT Kitazato, Ryotaro Otsuka, Keijiro Hara, Hideo Mure, Toshiyuki Okazaki, Kazuyuki Kuwayama, Shinji Nagahiro and Yasushi Takagi : Down-regulation of MDR1 by Ad-DKK3 via Akt/NFB pathways augments the anti-tumor effect of temozolomide in glioblastoma cells and a murine xenograft model, Journal of Neuro-Oncology, Vol.139, No.2, 323-332, 2018. (要約) Glioblastoma multiforme (GBM) is the most malignant of brain tumors. Acquired drug resistance is a major obstacle for successful treatment. Earlier studies reported that expression of the multiple drug resistance gene (MDR1) is regulated by YB-1 or NFκB via the JNK/c-Jun or Akt pathway. Over-expression of the Dickkopf (DKK) family member DKK3 by an adenovirus vector carrying DKK3 (Ad-DKK3) exerted anti-tumor effects and led to the activation of the JNK/c-Jun pathway. We investigated whether Ad-DKK3 augments the anti-tumor effect of temozolomide (TMZ) via the regulation of MDR1. GBM cells (U87MG and U251MG), primary TGB105 cells, and mice xenografted with U87MG cells were treated with Ad-DKK3 or TMZ alone or in combination. Ad-DKK3 augmentation of the anti-tumor effects of TMZ was associated with reduced MDR1 expression in both in vivo and in vitro studies. The survival of Ad-DKK3-treated U87MG cells was inhibited and the expression of MDR1 was reduced. This was associated with the inhibition of Akt/NFκB but not of YB-1 via the JNK/c-Jun- or Akt pathway. Our results suggest that Ad-DKK3 regulates the expression of MDR1 via Akt/NFκB pathways and that it augments the anti-tumor effects of TMZ in GBM cells. (徳島大学機関リポジトリ) ● Metadata: 112895 (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s11060-018-2894-5 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29779087 ● Summary page in Scopus @ Elsevier: 2-s2.0-85047143200 (徳島大学機関リポジトリ: 112895, DOI: 10.1007/s11060-018-2894-5, PubMed: 29779087, Elsevier: Scopus)
3.	Keijiro Hara, Teruyoshi Kageji, Yoshifumi Mizobuchi, Keiko T. Kitazato, Toshiyuki Okazaki, Toshitaka Fujihara, Kohhei Nakajima, Hideo Mure, Kazuyuki Kuwayama, Tomoyo Hara and Shinji Nagahiro : Blocking of the interaction between Wnt proteins and their co-receptors contributes to the anti-tumor effects of adenovirus-mediated DKK3 in glioblastoma, Cancer Letters, Vol.356, 496-505, 2015. (要約) The effect of the third member of the Dickkopf family (DKK3) in the Wnt pathway in glioblastoma remains unclear. We first demonstrated the non-specific interaction of Wnt3a and Wnt5a with the receptors LRP6 and ROR2 and the up-regulation of the Wnt pathway in glioblastoma cells. We used an adenovirus vector and found that an increase in DKK3 protein attenuated the expression of Wnt3a, Wnt5a and LRP6, but not of ROR2, and their interaction, thereby affecting both canonical- and non-canonical Wnt downstream cascades. This produced anti-tumor effects in GBM xenograft models. The suppression of Wnt pathways upstream by DKK3 may have promise for the treatment of glioblastoma. (キーワード) Adenoviridae / Animals / アポトーシス (apoptosis) / Blotting, Western / 細胞増殖·分化 (cell proliferation and differentiation) / Flow Cytometry / Genetic Vectors / Glioblastoma / Humans / Immunoenzyme Techniques / Immunoprecipitation / Intercellular Signaling Peptides and Proteins / Low Density Lipoprotein Receptor-Related Protein-6 / 男性 (male) / Mice / Mice, Inbred BALB C / Mice, Nude / Proto-Oncogene Proteins / RNA, Messenger / Real-Time Polymerase Chain Reaction / Receptor Tyrosine Kinase-like Orphan Receptors / Reverse Transcriptase Polymerase Chain Reaction / Tumor Cells, Cultured / Wnt Proteins / Wnt3A Protein / Xenograft Model Antitumor Assays (徳島大学機関リポジトリ) ● Metadata: 106342 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.canlet.2014.09.045 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25301448 ● Summary page in Scopus @ Elsevier: 2-s2.0-84919491383 (徳島大学機関リポジトリ: 106342, DOI: 10.1016/j.canlet.2014.09.045, PubMed: 25301448, Elsevier: Scopus)
4.	Toshiyuki Okazaki, Teruyoshi Kageji, Kazuyuki Kuwamura, Keiko T. Kitazato, Hideo Mure, Keijiro Hara, Ryoma Morigaki, Yoshifumi Mizobuchi, Kazuhito Matsuzaki and Shinji Nagahiro : Up-regulation of endogenous PML induced by a combination of interferon-beta and temozolomide enhances p73/YAP-mediated apoptosis in glioblastoma, Cancer Letters, Vol.323, No.2, 199-207, 2012. (要約) Interferon-beta (IFN-) is reported to augment anti-tumor effects by temozolomide in glioblastoma via down-regulation of MGMT. Promyelocytic leukemia (PML), a gene induced by IFN-, is a tumor suppressor. Here, we report for the first time that in combination therapy, an IFN--induced increase in endogenous PML contributes to anti-tumor effects in p53 wild- and mutant glioma cells in a xenograft mice model. The increased PML promoted the accumulation of p73, a structural and functional homolog of p53, to fuse the coactivator Yes-associated-protein in the PML nuclear bodies. The adjuvant therapy targeted at PML may be a promising therapeutic strategy for glioblastoma. (キーワード) Apoptosis / Base Sequence / Blotting, Western / Brain Neoplasms / Cell Line, Tumor / DNA Primers / DNA-Binding Proteins / Dacarbazine / Glioblastoma / Humans / Interferon-beta / Nuclear Proteins / Real-Time Polymerase Chain Reaction / Transcription Factors / Tumor Suppressor Proteins / Up-Regulation (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.canlet.2012.04.013 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22542810 ● Search Scopus @ Elsevier (PMID): 22542810 ● Search Scopus @ Elsevier (DOI): 10.1016/j.canlet.2012.04.013 (DOI: 10.1016/j.canlet.2012.04.013, PubMed: 22542810)

国際会議:

1.	Toshitaka Fujihara, Teruyoshi Kageji, Yoshifumi Mizobuchi, Keijiro Hara, Kenji Shouno, Kohhei Nakajima, Hideo Mure, Kazuyuki Kuwayama and Shinji Nagahiro : Down-regulation of MDR1 by DKK3 attenuates chemoresistance to temozolomide, and potentiates its anti-tumor effects, 20th Annual Socientific Meeting and Education Day of the Society for Neuro-Oncology, Nov. 2015.
2.	Yoshifumi Mizobuchi, T Okazaki, Teruyoshi Kageji, Kazuyuki Kuwayama, KT Kitazato, Hideo Mure, Keijiro Hara, Ryoma Morigaki, Kazuhito Matsuzaki, Kohhei Nakajima, T Fujihara and Shinji Nagahiro : A combination of interferon-beta and temozolomide augments anti-tumor effects through p73/YAP-mediated apoptosis by PML in glioblastoma, The 4th Quadrennial Meeting of the World Federation of Neuro-Oncology held in conjunction with the 2013 SNO Scientific Meeting and Education Day, San Francisco, Nov. 2013.
3.	Keijiro Hara, Teruyoshi Kageji, Yoshifumi Mizobuchi, T Okazaki, T Fujihara, Kohhei Nakajima, Hideo Mure, Kazuyuki Kuwayama, T Hara and Shinji Nagahiro : REIC/Dkk-3, one of Dickkopf(Dkk)family members, contributes to the anti-tumor effects in glioblastoma through regulation of both Wnt signal pathways, The 4th Quadrennial Meeting of the World Federation of Neuro-Oncology held in conjunction with the 2013 SNO Scientific Meeting and Education Day, San Francisco, Nov. 2013.
4.	Kohhei Nakajima, Keijiro Hara, Teruyoshi Kageji, Yoshifumi Mizobuchi, KT KItazato, T Fujihara, Kazuyuki Kuwayama, R Otsuka, DK Kung and Shinji Nagahiro : Down-regulation of MDR by Ad-REIC contributes to augment the chemotherapy by temozolomide, The 4th Quadrennial Meeting of the World Federation of Neuro-Oncology held in conjunction with the 2013 SNO Scientific Meeting and Education Day, San Francisco, Nov. 2013.

国内講演発表:

1.	藤原敏孝, 中島公平, 原慶次郎, 安積麻衣, 松田拓, 多田恵曜, 髙木康志 : 脳腫瘍生検術におけるStealth Autoguideの初期使用経験, 日本脳神経外科学会第82回学術集会, 2023年10月.
2.	中島公平, 安積麻衣, 藤原敏孝, 原慶次郎, 髙木康志 : Sellar atypical teratoid/rhabdoid tumor の1例, 第28回日本脳腫瘍の外科学会, 2023年9月.
3.	手島奈津美, 安積麻衣, 中島公平, 松田知大, 山口泉, 藤原敏孝, 曽我部周, 原慶次郎, 髙木康志 : 術後管理に難渋した頭蓋咽頭腫の1例, 第95回日本脳神経外科学会中国四国支部学術集会, 2023年4月.
4.	安積麻衣, 藤原敏孝, 原慶次郎, 中島公平, 溝渕佳史, 髙木康志 : 術後脳腫瘍患者における転院時転帰予測因子についての検討, 日本脳神経外科学会第81回学術総会, 2022年9月.
5.	原慶次郎, 溝渕佳史, 安積麻衣, 曽我部周, 藤原敏孝, 中島公平, 髙木康志 : Hyper vascularityを呈した松果体部腫瘍の1例, 第93回日本脳神経外科学会中国四国支部学術集会, 2022年4月.
6.	藤原敏孝, 多田恵曜, 溝渕佳史, 中島公平, 原慶次郎, 安積麻衣, 髙木康志 : テント上髄膜腫手術症例におけるてんかん及び周術期発作管理の検討, 日本脳神経外科学会第80回学術総会, 2021年10月.
7.	安積麻衣, 宮本健志, 藤原敏孝, 中島公平, 原慶次郎, 溝渕佳史, 髙木康志 : 特発性頭蓋内圧亢進様の症状のみで発症した小児脳腫瘍の1例, 第35回中国四国脳腫瘍研究会, 2021年9月.
8.	原慶次郎, 溝渕佳史, 安積麻衣, 中島公平, 髙木康志 : AIDS関連トキソプラズマ脳症の1例, 第91回(一社)日本脳神経外科学会中国四国支部学術集会, 2021年4月.
9.	原慶次郎, 西京子, 里見淳一郎, 永廣信治 : High flow bypassとdistal occlusionを行った中大脳動脈血栓化紡錘状動脈瘤の一例, 第76回(一社)日本脳神経外科学会中国四国支部学術集会, 2013年12月.
10.	原慶次郎, 溝渕佳史, 北里慶子, 岡﨑敏之, 影治照喜, 永廣信治, 公文裕巳 : 悪性神経膠腫におけるREIC/Dkk-3遺伝子導入によるWnt蛋白制御の意義, 第13回日本分子脳神経外科学会, 2012年9月.
11.	岡﨑敏之, 松﨑和仁, 溝渕佳史, 北里慶子, 影治照喜, 原慶次郎, 永廣信治 : 膠芽腫に対するテモゾロミドとインターフェロンβ併用療法におけるPMLの役割, 徳島脳腫瘍セミナー2010, 2010年2月.

その他・研究会:

1.	安積麻衣, 中島公平, 藤原敏孝, 原慶次郎, 髙木康志 : リツシマブ併用大量療法が奏功した難治性中枢神経原発悪性リンパ腫の1例, 第37回中四国脳腫瘍研究会, 2023年9月.

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

脳内微量出血模倣モデルにおける認知症関連蛋白発現機序の解明と制御 (研究課題/領域番号: 22K16662 )
悪性神経膠腫に対するAd-REICの抗腫瘍効果とWntシグナル制御の分子機構 (研究課題/領域番号: 25462264 )
研究者番号（60710340）による検索