研究者詳細 - 石川　隆昭

石川　隆昭（イシカワ　タカアキ）

Ishikawa, Takaaki

写真a

所属（所属キャンパス）: 薬学部薬学科薬物治療学講座（芝共立）

職名: 助教

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免許・資格【表示／非表示】

医師免許, 2015年04月
脳神経外科専門医, 2022年04月

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Genomic landscape and clinical impact of BRCA1/2 pathogenic variants in metastatic castration-resistant prostate cancer.

Iida K, Urabe F, Matsui Y, Tashiro K, Yoshihara K, Urabe Y, Ishikawa T, Matsuzaki J, Kimura T, Saito Y

NPJ precision oncology 2026年02月

ISSN 2397-768X
- Access to Document (DOI)
Primary subdural tumor mimicking subdural hematoma: illustrative case.

Ishikawa T, Tsurubuchi T, Nagatomo K, Hosaka S, Fukushima H, Sakamoto N, Hirato J, Inoue Y, Ichimura K, Mizumoto M, Muroi A, Takada H, Ishikawa E

Journal of neurosurgery. Case lessons 11 （ 5 ） 2026年02月
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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 11 （ 3 ） 101987 2026年

研究論文（学術雑誌）, 査読有り, ISSN 2452-1094
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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年12月

研究論文（学術雑誌）, 共著, 査読有り

　概要を見る

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年11月

研究論文（学術雑誌）, 筆頭著者, 査読有り, ISSN 0167594X

　概要を見る

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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