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Faculty of Medicine College Hospital Neurosurgery |
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Assistant Professor |
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MATSUMOTO Fumitaka
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Degree 【 display / non-display 】
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医学獣医学 ( 2021.11 宮崎大学 )
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医学 ( 2006.3 宮崎医科大学 )
Papers 【 display / non-display 】
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YAMASHITA Shinji, TOMONAGA Takumi, OKITA Yoshiko, SATO Yuichiro, MATSUMOTO Fumitaka, OKUYAMA Hironobu, OGASAWARA Natsuki, TAMURA Mitsuru, KAWANO Tomoki, YOKOGAMI Kiyotaka, KIWAKI Takumi, FUKUSHIMA Tsuyoshi
NMC Case Report Journal 12 ( 0 ) 369 - 375 2025
Authorship：Lead author Language：English Publishing type：Research paper (scientific journal) Publisher：The Japan Neurosurgical Society
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KADOTA Yoshihito, ODA Yoshinao, AKIYAMA Yuri, AZUMA Minako, YAMASHITA Atsushi, OKITA Yoshiko, YAMASHITA Shinji, OGURI Nobuyuki, KAWANO Tomoki, AKIZUKI Keiichi, TOMONAGA Takumi, MATSUMOTO Fumitaka
NMC Case Report Journal 12 ( 0 ) 525 - 530 2025
Authorship：Lead author Language：English Publishing type：Research paper (scientific journal) Publisher：The Japan Neurosurgical Society
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Matsumoto F., Yokogami K., Yamada A., Moritake H., Watanabe T., Yamashita S., Sato Y., Takeshima H.
Human Cell 37 ( 2 ) 523 - 530 2024.3
Authorship：Lead author Language：English Publishing type：Research paper (scientific journal) Publisher：Human Cell
Atypical teratoid/rhabdoid (AT/RT) is a rare and highly malignant tumor of the central nervous system (CNS). It is most commonly found in children less than 5 years of age and is associated with inactivation of loss of function of SMARCB1/INI1. An experimental model for AT/RT is necessary to develop new and effective therapies. We established a patient-derived new cell line (MZ611ATRT), which showed loss of BAF-47. MZ611ATRT genetically features somatic heterozygous deletion of SMARCB1 and single nucleotide deletion of the residual allele, exon 5 ([c.541delC]), resulting in a stop codon at codon 954 by frameshift. We assessed the RNA-sequencing data of the other two AT/RT cell lines with forced expression of SMARCB1 available from public databases. We found SMARCB1 overexpression significantly down-regulates the expression of a group of enzymes related to cholesterol biosynthesis. Simvastatin was highly sensitive against MZ611ATRT cells and induced apoptosis (IC50 was 3.098 µM for MZ611ATRT, 41.88uM for U-87 MG, 23.34uM for IOMM-Lee, and 18.12uM for U-251 MG.). Pathways involved in cholesterol biosynthesis may be new targets for adjuvant therapy of AT/RT.
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Ogasawara N., Yamashita S., Yamasaki K., Kawano T., Kawano T., Muta J., Matsumoto F., Watanabe T., Ohta H., Yokogami K., Fukushima T., Sato Y., Takeshima H.
Brain Tumor Pathology 40 ( 4 ) 222 - 229 2023.10
Language：English Publishing type：Research paper (scientific journal) Publisher：Brain Tumor Pathology
Malignant peripheral nerve sheath tumors (MPNSTs) arising from the trigeminal nerves are extremely rare (only 45 cases, including the present case, have been published) and have been reported to develop de novo from the peripheral nerve sheath and are not transformed from a schwannoma or neurofibroma. Here, we report a case of MPNSTs of the trigeminal nerve caused by the malignant transformation of a trigeminal schwannoma, with a particular focus on genetic considerations. After undergoing a near-total resection of a histologically typical benign schwannoma, the patient presented with regrowth of the tumor 10 years after the primary excision. Histopathologic and immunochemical examinations confirmed the recurrent tumor to be an MPNST. Comprehensive genomic analyses (FoundationOne panel-based gene assay) showed that only the recurrent MPNST sample, not the initial diagnosis of schwannoma, harbored genetic mutations, including NF1-p.R2637* and TP53-p.Y234H, candidate gene mutations associated with malignant transformation. Moreover, the results of reverse transcription polymerase chain reaction showed that the fusion of SH3PXD2A and HTRA1, which has been reported as one of the responsible genetic aberrations of schwannoma, was detected in the recurrent tumor. Taken together, we could illustrate the accumulation process of gene abnormalities for developing MPNSTs from normal cells via schwannomas.
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Rare solitary pituitary metastasis of maxillary ameloblastic carcinoma: illustrative case Reviewed
Arikawa S., Watanabe T., Yamaguchi H., Sato Y., Matsumoto F., Yokogami K., Takeshima H.
Journal of Neurosurgery: Case Lessons 6 ( 10 ) 2023.9
Language：English Publishing type：Research paper (scientific journal) Publisher：Journal of Neurosurgery: Case Lessons
BACKGROUND Ameloblastic carcinoma (AC) is a rare odontogenic carcinoma with histological features resembling ameloblastoma. Metastasis to distant organs and direct expansion into the skull base structures are associated with a poor clinical outcome. This rare case of AC metastasis to the pituitary gland presented without local recurrence at the primary focus of the maxilla. OBSERVATIONS A 47-year-old man had a 2-year history of AC in the right maxilla. Computed tomography for his regular checkup incidentally demonstrated pituitary tumor, rapidly growing over 2 months. He presented with the recent onset of panhypopituitarism and visual field defect. Magnetic resonance imaging showed a large, irregularly shaped intrasellar and suprasellar lesion with chiasmal compression. Endoscopic endonasal transsphenoidal surgery was performed for decompression of the optic apparatus to avoid intracranial spread. Histopathology confirmed metastatic AC, and a genetic panel test confirmed BRAF V600E mutation. Stereotactic radiotherapy (SRT) with the CyberKnife system was administered to the residual tumor. Remarkable tumor shrinkage was obtained, and panhypopituitarism was resolved 12 months later. LESSONS A multidisciplinary treatment strategy including maximal safe resection to avoid dissemination in combination with SRT may be crucial for local control with the preservation of pituitary and visual functions in patients with solitary pituitary metastatic AC.
DOI： 10.3171/CASE23264
Presentations 【 display / non-display 】
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悪性神経膠腫の増殖血管における上皮間転換の検出．
松元文孝
第36回日本脳腫瘍学会学術集会
Event date： 2018.12.2 - 2018.12.4
Language：Japanese Presentation type：Oral presentation (general)
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Detection of TERT promoter mutation in proliferated Vascular cells of malignant glioma.
Matsumoto F
The 15th Kyushyu and Yong-Honam Neurosurgical Joint Meeting
Event date： 2018.11
Language：English Presentation type：Oral presentation (general)
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内視鏡手術前のMRI, CT合成3Dイメージ作成の有効性について．
松元文孝、田村充、武石剛、竹島秀雄
第25回日本神経内視鏡学会
Event date： 2018.10.26 - 2018.10.27
Language：Japanese Presentation type：Oral presentation (general)
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宮崎県における10年間の原発性脳腫瘍の疫学調査．
松元文孝
日本脳神経外科学会第77回学術総会
Event date： 2018.10.10 - 2018.10.12
Language：Japanese Presentation type：Oral presentation (general)
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DIPGの憎悪に放射線再照射を併用した一例
松元文孝
第46回日本小児脳神経外科学会
Event date： 2018.6.8 - 2018.6.9
Language：English Presentation type：Oral presentation (general)
Grant-in-Aid for Scientific Research 【 display / non-display 】
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退形成乏突起神経膠腫（grade3）を乏突起神経膠腫(grade2) に逆行させる治療薬の開発
Grant number：25K19939 2025.04 - 2027.03
独立行政法人日本学術振興会 科学研究費基金 若手研究
Authorship：Principal investigator