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  1. Article ; Online: Drug Repositioning for Refractory Benign Tumors of the Central Nervous System.

    Tamura, Ryota

    International journal of molecular sciences

    2023  Volume 24, Issue 16

    Abstract: Drug repositioning (DR) is the process of identifying novel therapeutic potentials for already-approved drugs and discovering new therapies for untreated diseases. DR can play an important role in optimizing the pre-clinical process of developing novel ... ...

    Abstract Drug repositioning (DR) is the process of identifying novel therapeutic potentials for already-approved drugs and discovering new therapies for untreated diseases. DR can play an important role in optimizing the pre-clinical process of developing novel drugs by saving time and cost compared with the process of de novo drug discovery. Although the number of publications related to DR has rapidly increased, most therapeutic approaches were reported for malignant tumors. Surgical resection represents the definitive treatment for benign tumors of the central nervous system (BTCNS). However, treatment options remain limited for surgery-, chemotherapy- and radiation-refractory BTCNS, as well as malignant tumors. Meningioma, pituitary neuroendocrine tumor (PitNET), and schwannoma are the most common BTCNS. The treatment strategy using DR may be applied for refractory BTCNS, such as Grade 2 meningiomas, neurofibromatosis type 2-related schwannomatosis, and PitNETs with cavernous sinus invasion. In the setting of BTCNS, stable disease can provide significant benefit to the patient. DR may provide a longer duration of survival without disease progression for patients with refractory BTCNS. This article reviews the utility of DR for refractory BTCNS.
    MeSH term(s) Humans ; Drug Repositioning ; Central Nervous System ; Meningioma/drug therapy ; Neurilemmoma/drug therapy ; Pituitary Neoplasms ; Meningeal Neoplasms/drug therapy
    Language English
    Publishing date 2023-08-20
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms241612997
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  2. Article ; Online: Current Understanding of Neurofibromatosis Type 1, 2, and Schwannomatosis.

    Tamura, Ryota

    International journal of molecular sciences

    2021  Volume 22, Issue 11

    Abstract: Neurofibromatosis (NF) is a neurocutaneous syndrome characterized by the development of tumors of the central or peripheral nervous system including the brain, spinal cord, organs, skin, and bones. There are three types of NF: NF1 accounting for 96% of ... ...

    Abstract Neurofibromatosis (NF) is a neurocutaneous syndrome characterized by the development of tumors of the central or peripheral nervous system including the brain, spinal cord, organs, skin, and bones. There are three types of NF: NF1 accounting for 96% of all cases, NF2 in 3%, and schwannomatosis (SWN) in <1%. The NF1 gene is located on chromosome 17q11.2, which encodes for a tumor suppressor protein, neurofibromin, that functions as a negative regulator of Ras/MAPK and PI3K/mTOR signaling pathways. The NF2 gene is identified on chromosome 22q12, which encodes for merlin, a tumor suppressor protein related to ezrin-radixin-moesin that modulates the activity of PI3K/AKT, Raf/MEK/ERK, and mTOR signaling pathways. In contrast, molecular insights on the different forms of SWN remain unclear. Inactivating mutations in the tumor suppressor genes SMARCB1 and LZTR1 are considered responsible for a majority of cases. Recently, treatment strategies to target specific genetic or molecular events involved in their tumorigenesis are developed. This study discusses molecular pathways and related targeted therapies for NF1, NF2, and SWN and reviews recent clinical trials which involve NF patients.
    MeSH term(s) Animals ; Biomarkers, Tumor ; Clinical Trials as Topic ; Disease Models, Animal ; Disease Susceptibility ; Genes, Neurofibromatosis 1 ; Genes, Neurofibromatosis 2 ; Genetic Predisposition to Disease ; Humans ; Models, Biological ; Molecular Targeted Therapy ; Mutation ; Neurilemmoma/diagnosis ; Neurilemmoma/etiology ; Neurilemmoma/therapy ; Neurofibromatoses/diagnosis ; Neurofibromatoses/etiology ; Neurofibromatoses/therapy ; Neurofibromatosis 1/diagnosis ; Neurofibromatosis 1/etiology ; Neurofibromatosis 1/therapy ; Neurofibromatosis 2/diagnosis ; Neurofibromatosis 2/etiology ; Neurofibromatosis 2/therapy ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Skin Neoplasms/diagnosis ; Skin Neoplasms/etiology ; Skin Neoplasms/therapy ; Treatment Outcome
    Chemical Substances Biomarkers, Tumor ; Protein Kinase Inhibitors
    Language English
    Publishing date 2021-05-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22115850
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Current Understanding of Neurofibromatosis Type 1, 2, and Schwannomatosis

    Ryota Tamura

    International Journal of Molecular Sciences, Vol 22, Iss 5850, p

    2021  Volume 5850

    Abstract: Neurofibromatosis (NF) is a neurocutaneous syndrome characterized by the development of tumors of the central or peripheral nervous system including the brain, spinal cord, organs, skin, and bones. There are three types of NF: NF1 accounting for 96% of ... ...

    Abstract Neurofibromatosis (NF) is a neurocutaneous syndrome characterized by the development of tumors of the central or peripheral nervous system including the brain, spinal cord, organs, skin, and bones. There are three types of NF: NF1 accounting for 96% of all cases, NF2 in 3%, and schwannomatosis (SWN) in <1%. The NF1 gene is located on chromosome 17q11.2, which encodes for a tumor suppressor protein, neurofibromin, that functions as a negative regulator of Ras/MAPK and PI3K/mTOR signaling pathways. The NF2 gene is identified on chromosome 22q12, which encodes for merlin, a tumor suppressor protein related to ezrin-radixin-moesin that modulates the activity of PI3K/AKT, Raf/MEK/ERK, and mTOR signaling pathways. In contrast, molecular insights on the different forms of SWN remain unclear. Inactivating mutations in the tumor suppressor genes SMARCB1 and LZTR1 are considered responsible for a majority of cases. Recently, treatment strategies to target specific genetic or molecular events involved in their tumorigenesis are developed. This study discusses molecular pathways and related targeted therapies for NF1, NF2, and SWN and reviews recent clinical trials which involve NF patients.
    Keywords neurofibromatosis type 1 ; neurofibromatosis type 2 ; schwannomatosis ; molecular targeted therapy ; clinical trial ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 572
    Language English
    Publishing date 2021-05-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article: Preparation and Characterization of Crosslinked Electrospun Gelatin Fabrics via Maillard Reactions.

    Dechojarassri, Duangkamol / Kaneshige, Ryota / Tamura, Hiroshi / Furuike, Tetsuya

    Materials (Basel, Switzerland)

    2023  Volume 16, Issue 11

    Abstract: In this study, nonwoven gelatin (Gel) fabrics crosslinked ... ...

    Abstract In this study, nonwoven gelatin (Gel) fabrics crosslinked using
    Language English
    Publishing date 2023-05-30
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2487261-1
    ISSN 1996-1944
    ISSN 1996-1944
    DOI 10.3390/ma16114078
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: [Schwannoma:Update on Molecular Profiling and Therapeutic Advances].

    Tamura, Ryota / Toda, Masahiro

    No shinkei geka. Neurological surgery

    2022  Volume 50, Issue 1, Page(s) 162–170

    Abstract: Schwannoma is a tumor that develops from the Schwann cells in the peripheral nervous system or cranial nerves. Gamma Knife radiosurgery has become an accepted treatment for schwannoma, with a high rate of tumor control. For sporadic or neurofibromatosis ... ...

    Abstract Schwannoma is a tumor that develops from the Schwann cells in the peripheral nervous system or cranial nerves. Gamma Knife radiosurgery has become an accepted treatment for schwannoma, with a high rate of tumor control. For sporadic or neurofibromatosis type 2-associated schwannoma resistant to radiotherapy, vascular endothelial growth factor(VEGF)-A/VEGF receptor(VEGFR)-targeted therapy(e.g., bevacizumab)may become the first-line therapy. However, some aspects of treatment with bevacizumab are problematic, such as the need for frequent parenteral administration, side effects, apparent drug resistance, and rebound tumor progression after cessation. In these situations, the gene product of the
    MeSH term(s) High-Temperature Requirement A Serine Peptidase 1 ; Humans ; Neurilemmoma/genetics ; Neurilemmoma/therapy ; Neurofibromatosis 2 ; Phosphatidylinositol 3-Kinases/metabolism ; Signal Transduction ; Tumor Microenvironment ; Vascular Endothelial Growth Factor A
    Chemical Substances Vascular Endothelial Growth Factor A ; High-Temperature Requirement A Serine Peptidase 1 (EC 3.4.21.-) ; HTRA1 protein, human (EC 3.4.21.-)
    Language Japanese
    Publishing date 2022-02-15
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 197053-7
    ISSN 1882-1251 ; 0301-2603
    ISSN (online) 1882-1251
    ISSN 0301-2603
    DOI 10.11477/mf.1436204541
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 1834: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 268: Show issues

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  6. Article ; Online: A Critical Overview of Targeted Therapies for Vestibular Schwannoma.

    Tamura, Ryota / Toda, Masahiro

    International journal of molecular sciences

    2022  Volume 23, Issue 10

    Abstract: Vestibular schwannoma (VS) is a benign tumor that originates from Schwann cells in the vestibular component. Surgical treatment for VS has gradually declined over the past few decades, especially for small tumors. Gamma knife radiosurgery has become an ... ...

    Abstract Vestibular schwannoma (VS) is a benign tumor that originates from Schwann cells in the vestibular component. Surgical treatment for VS has gradually declined over the past few decades, especially for small tumors. Gamma knife radiosurgery has become an accepted treatment for VS, with a high rate of tumor control. For neurofibromatosis type 2 (NF2)-associated VS resistant to radiotherapy, vascular endothelial growth factor (VEGF)-A/VEGF receptor (VEGFR)-targeted therapy (e.g., bevacizumab) may become the first-line therapy. Recently, a clinical trial using a VEGFR1/2 peptide vaccine was also conducted in patients with progressive NF2-associated schwannomas, which was the first immunotherapeutic approach for NF2 patients. Targeted therapies for the gene product of SH3PXD2A-HTRA1 fusion may be effective for sporadic VS. Several protein kinase inhibitors could be supportive to prevent tumor progression because merlin inhibits signaling by tyrosine receptor kinases and the activation of downstream pathways, including the Ras/Raf/MEK/ERK and PI3K/Akt/mTORC1 pathways. Tumor-microenvironment-targeted therapy may be supportive for the mainstays of management. The tumor-associated macrophage is the major component of immunosuppressive cells in schwannomas. Here, we present a critical overview of targeted therapies for VS. Multimodal therapy is required to manage patients with refractory VS.
    MeSH term(s) High-Temperature Requirement A Serine Peptidase 1 ; Humans ; Neurilemmoma/metabolism ; Neurofibromatosis 2 ; Neuroma, Acoustic/genetics ; Neuroma, Acoustic/therapy ; Phosphatidylinositol 3-Kinases ; Tumor Microenvironment ; Vascular Endothelial Growth Factor A
    Chemical Substances Vascular Endothelial Growth Factor A ; High-Temperature Requirement A Serine Peptidase 1 (EC 3.4.21.-) ; HTRA1 protein, human (EC 3.4.21.-)
    Language English
    Publishing date 2022-05-13
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23105462
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  7. Article: Meningioma Cell Invasion into DuraGen-Derived Dura Mater: A Case Report.

    Tamura, Ryota / Kuranari, Yuki / Orikasa, Hideki / Katayama, Makoto

    Medicines (Basel, Switzerland)

    2022  Volume 9, Issue 4

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2022-04-11
    Publishing country Switzerland
    Document type Case Reports
    ZDB-ID 2777965-8
    ISSN 2305-6320
    ISSN 2305-6320
    DOI 10.3390/medicines9040030
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  8. Article ; Online: A Critical Overview of Targeted Therapies for Vestibular Schwannoma

    Ryota Tamura / Masahiro Toda

    International Journal of Molecular Sciences, Vol 23, Iss 5462, p

    2022  Volume 5462

    Abstract: Vestibular schwannoma (VS) is a benign tumor that originates from Schwann cells in the vestibular component. Surgical treatment for VS has gradually declined over the past few decades, especially for small tumors. Gamma knife radiosurgery has become an ... ...

    Abstract Vestibular schwannoma (VS) is a benign tumor that originates from Schwann cells in the vestibular component. Surgical treatment for VS has gradually declined over the past few decades, especially for small tumors. Gamma knife radiosurgery has become an accepted treatment for VS, with a high rate of tumor control. For neurofibromatosis type 2 (NF2)-associated VS resistant to radiotherapy, vascular endothelial growth factor (VEGF)-A/VEGF receptor (VEGFR)-targeted therapy (e.g., bevacizumab) may become the first-line therapy. Recently, a clinical trial using a VEGFR1/2 peptide vaccine was also conducted in patients with progressive NF2-associated schwannomas, which was the first immunotherapeutic approach for NF2 patients. Targeted therapies for the gene product of SH3PXD2A-HTRA1 fusion may be effective for sporadic VS. Several protein kinase inhibitors could be supportive to prevent tumor progression because merlin inhibits signaling by tyrosine receptor kinases and the activation of downstream pathways, including the Ras/Raf/MEK/ERK and PI3K/Akt/mTORC1 pathways. Tumor-microenvironment-targeted therapy may be supportive for the mainstays of management. The tumor-associated macrophage is the major component of immunosuppressive cells in schwannomas. Here, we present a critical overview of targeted therapies for VS. Multimodal therapy is required to manage patients with refractory VS.
    Keywords schwannoma ; NF2 ; bevacizumab ; VEGF ; SH3PXD2A-HTRA1 fusion ; molecular targeted therapy ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 616
    Language English
    Publishing date 2022-05-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Complete Genome Sequence of

    Yamamoto-Tamura, Kimiko / Moriuchi, Ryota / Ogawa, Naoto

    Microbiology resource announcements

    2021  Volume 10, Issue 31, Page(s) e0041621

    Abstract: ... ...

    Abstract Caballeronia
    Language English
    Publishing date 2021-08-05
    Publishing country United States
    Document type Journal Article
    ISSN 2576-098X
    ISSN (online) 2576-098X
    DOI 10.1128/MRA.00416-21
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Study on the Extrapolability of Current Tumorgenicity Test With Mice by Comparing the Syngeneic or Allogeneic Mouse Transplantation Model.

    Tamura, Takashi / Tahara, Tsuyoshi / Inoue, Michiko / Nanjo, Ryota / Onoe, Hirotaka / Yamamoto, Takako / Kawamata, Shin

    Stem cells translational medicine

    2024  

    Abstract: The extrapolability of the current tumorigenicity test performed by transplanting human cell product into immunodeficient (NOG) mice was investigated. For this purpose, the susceptibility to form teratomas of NOG mice was assessed by transplanting ... ...

    Abstract The extrapolability of the current tumorigenicity test performed by transplanting human cell product into immunodeficient (NOG) mice was investigated. For this purpose, the susceptibility to form teratomas of NOG mice was assessed by transplanting undifferentiated human-induced pluripotent stem cells (hiPSCs) as positive control cells via the liver, striatum, or tail vein and evaluating the TPD50 value (dose required to form teratomas in half of the transplanted mice). This was then compared to the TPD50 of syngeneic or allogeneic mouse models. The TPD50 of C57/BL/6(B6)-iPSC or 129/Ola(129)-embryonic stem cell (ESC) transplanted into the liver of syngeneic mice was 4.08 × 105 and 4.64 × 104 cells, respectively, while the TPD50 of hiPSC administered into the liver of NOG mice was 4.64 × 104 cells. The TPD50 of B6-miPSC-synergic, 129-mESC-synergic, or 129-cell/B6 allogeneic transplantation into the striatum was 5.09 × 102, 1.0 × 104, and 3.73 × 104 cells, respectively, while that of hiPSC/NOG mice was 1.0 × 103 cells. The TPD50 for B6-miPSC or 129-mESC syngeneic tail vein infusion was 3.16 × 106 or 5.62 × 106 cells, respectively, while no incidence was observed from 1 × 107 B6-miPSCs in 129 mice or hiPSCs in NOG mice infusion study. Although the number of data sets was limited, these data indicate that the teratoma formation from transplanted undifferentiated hiPSCs via the liver or striatum in NOG mice is comparable to that in syngeneic or allogeneic mouse transplantation model, suggesting that the result of the current tumorigenicity test in NOG mice would provide useful information to infer the incidence of teratoma from residual undifferentiated hPSCs in hPSC-derived products after transplantation.
    Language English
    Publishing date 2024-03-30
    Publishing country England
    Document type Journal Article
    ZDB-ID 2642270-0
    ISSN 2157-6580 ; 2157-6580
    ISSN (online) 2157-6580
    ISSN 2157-6580
    DOI 10.1093/stcltm/szae019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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