Details of a Researcher - Ishikawa, Takaaki

Ishikawa, Takaaki

写真a

Affiliation: Faculty of Pharmacy, Department of Pharmacy Division of Pharmacotherapeutics ( Shiba-Kyoritsu )

Position: Research Associate/Assistant Professor/Instructor

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Academic Background 【 Display / hide 】

2003.04

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2007.03

Keio University, Faculty of Science and Technology, Department of Applied Physics and Phsico-Infomatics

University, Graduated
2007.04

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2010.03

Keio University, Graduate school of Science and Technology, School of Fundamental Science and Technology

Graduate School, Completed, Master's course
2010.04

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2015.03

University of Tsukuba, School of Medicine and Health Sciences, School of Medicine

University, Graduated
2020.04

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2025.03

University of Tsukuba, Graduate School of Comprehensive Human Sciences, Doctoral Program in Medical Sciences

Graduate School, Completed, Doctoral course

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Academic Degrees 【 Display / hide 】

Bachelor(Engineering), Keio University, Coursework, 2007.03
Master(Engineering), Keio University, Coursework, 2010.03
Bachelor(Medicine), University of Tsukuba, Coursework, 2015.03
Ph.D(Medicine), University of Tsukuba, Coursework, 2025.03

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Licenses and Qualifications 【 Display / hide 】

Medical License, 2015.04
Board-Certified Neurosurgeon, 2022.04

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Papers 【 Display / hide 】

Esophageal cancer cells exhibit heterogeneity in DNA double-strand break repair and G2/M checkpoint arrest associated with cell viability after ionizing radiation

Tateno K, Okuda K, Haruna S, Isono M, Ishikawa T, Okumura H, Hayashi R, Suzuki R, Takahashi T, Saito T, Yokobori T, Uchihara Y, Suzuki K, Yamauchi M, Shirabe K, Saeki H, Shibata A

Advances in Radiation Oncology 2026

Research paper (scientific journal), Accepted
Carbon ion stimulation therapy reverses iron deposits and microglia driven neuroinflammation and induces cognitive improvement in an Alzheimer’s disease mouse model

Lee W.S., Kokubo T., Choi Y., Hamano T., Zaboronok A., Ishikawa T., Kwon O.D., Kim E.H., Kim J.K.

Scientific Reports 15 ( 1 ) 2025.12

Research paper (scientific journal), Joint Work, Accepted

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Insoluble iron deposits often exist as iron oxide nanoparticles in protein aggregates, impaired ferritin, or activated microglia and have been implicated as major causes of neuroinflammation in Alzheimer’s disease. However, no crucial evidence has been reported to support the therapeutic effects of current iron chelators on the deposition of various molecular forms of insoluble iron. We investigated the therapeutic effect of carbon ion stimulation (CIS) via a transmission beam on insoluble iron deposits, iron inclusion bodies, and the associated biological response in 5xFAD AD mouse brains. Compared with no treatment, CIS dose-dependently induced a 33–60% reduction in the amount of ferrous-containing iron species and associated inclusion bodies in the brains of AD mice. CIS induced considerable neuroinflammation downregulation and, conversely, anti-inflammatory upregulation, which was associated with improved memory and enhanced hippocampal neurogenesis. In conclusion, our results suggest that the effective degradation of insoluble iron deposits in combination with pathogenic inclusion bodies promotes AD-modifying properties and offers a potential CIS treatment option for AD.
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Hemagglutinating virus of Japan envelope encapsulating microRNA-34a-5p robustly induces apoptosis of malignant meningioma cells by suppressing survivin

Ishikawa T., Matsuda M., Kaneda Y., Ishikawa E.

Journal of Neuro Oncology 175 ( 2 ) 753 - 762 2025.11

Research paper (scientific journal), Lead author, Accepted, ISSN 0167594X

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Purpose: Malignant meningiomas are characterized by high recurrence rates and limited therapeutic options beyond surgery and radiation. This study aimed to develop a novel nucleic acid-based therapeutic approach for malignant meningiomas and to evaluate its efficacy both in vitro and in vivo. Methods: IOMM-Lee and HKBMM cell lines were used as models of malignant meningioma. Inhibitory effects of hemagglutinating virus of Japan envelope (HVJ-E) and microRNA-34a-5p (miR-34a-5p) were assessed using cell viability assays, apoptosis assays, RT-qPCR, and western blotting. Finally, the tumor suppressive effect of HVJ-E encapsulating miR-34a-5p was evaluated using a subcutaneous xenograft model in nude mice. Result: HVJ-E significantly reduced viability of malignant meningioma cells. Furthermore, HVJ-E encapsulating miR-34a-5p demonstrated enhanced anti-tumor activity by inducing apoptosis through downregulation of survivin expression. This tumor-suppressive effect was also confirmed in a subcutaneous mouse model. Conclusion: Our findings indicate that HVJ-E encapsulating miR-34a-5p effectively inhibits the growth of malignant meningioma cells both in vitro and in vivo. This novel combination therapy holds promise as a potential treatment strategy for malignant meningiomas.
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Establishment of a novel benign meningioma cell line spontaneously immortalized under hypoxic conditions

Ishikawa T., Matsuda M., Ishikawa H., Toyomura J., Ohyama A., Sakamoto N., Zaboronok A., Ishikawa E.

Human Cell 38 ( 1 ) 2025.01

Research paper (scientific journal), Lead author, Accepted, ISSN 09147470

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Meningiomas are the most frequent brain tumors, typically benign and curable by surgery. However, some patients experience repeated recurrences from residual tumors. To address such cases, the development of novel therapeutic options is crucial. For this purpose, the availability of cell lines that possess the characteristics of benign meningiomas is essential. Here, we established a benign meningioma cell line under 3% O<inf>2</inf> hypoxic conditions without the induction of immortalization genes. This cell line, named TKB-MEN2, has been stably grown for over two years with more than 20 passages. There were no hotspot telomerase reverse transcriptase (TERT) promoter mutations or cyclin-dependent kinase inhibitor 2A/2B (CDKN2A/2B) homozygous deletions, which are genetic features typical of malignant meningiomas. Cultured under hypoxic conditions, this cell line showed fewer characteristics of cellular senescence, such as morphological changes, IL-6 secretion, and lower senescence-associated b-galactosidase activity, compared to the same cell line cultured under 20% O<inf>2</inf> conditions. This immortalized non-transgenic cell line appears to reflect the characteristics of a genuine benign meningioma, potentially allowing the identification of new therapeutic targets and the development of novel therapies for benign meningiomas.
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Intraosseous schwannoma in the clivus mimicking chordoma treated with endoscopic endonasal surgery: A case report

Ishikawa T., Akutsu H., Hara T., Tanaka S., Masumoto T., Ishikawa E.

Surgical Neurology International 13 2022

Research paper (scientific journal), Lead author, Accepted

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Background: Intraosseous schwannomas are extremely rare and they have not yet been reported to occur in the clivus. We report a schwannoma in the clivus mimicking chordoma and review intraosseous schwannomas of the skull. Case Description: A 62-year-old man presented with gradually worsening hoarseness with dysphagia and atrophy of the left tongue, trapezius muscle, and sternocleidomastoid muscle. Magnetic resonance imaging showed that the tumor was mainly located in the clivus, and a computed tomography (CT) scan revealed an osteolytic lesion with expansion of the clivus and preservation of the bony cortex. Endoscopic endonasal surgery was performed to diagnose and treat symptoms. The tumor was subtotally removed without any complications. The histopathological findings revealed typical schwannoma, which showed Antoni A and Antoni B patterns positive for S100 protein. Based on the preoperative imaging, intraoperative and histopathological findings, the tumor was considered to be an intraosseous schwannoma in the clivus, and no recurrence was observed after 1 year of postoperative follow-up. Conclusion: Even though the intraosseous schwannoma in the clivus is uncommon, it should be considered as a differential diagnosis if an expansive lesion without destruction of the cortical bone is shown on CT as well as iso-hyperintensity on T2-weighted magnetic resonance imaging.
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