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  • Oxford University Press (OUP)  (9)
  • Iwabuchi, Satoshi  (9)
  • Sakurai, Takatoshi  (9)
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  • Oxford University Press (OUP)  (9)
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  • 1
    Online Resource
    Online Resource
    CBMT-04. MOLECULAR MECHANISM OF OLIG2-CDK2 INTERACTION IN GLIOMA CELLS
    Oxford University Press (OUP) ; 2019
    In:  Neuro-Oncology Vol. 21, No. Supplement_6 ( 2019-11-11), p. vi33-vi33
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 21, No. Supplement_6 ( 2019-11-11), p. vi33-vi33
    Abstract: Oligodendrocyte transcription factor 2 (OLIG2) promotes proliferation of normal neural stem/progenitor cells and glioma cells. However, the mechanisms underlying the regulation of OLIG2 remain largely unknown. Here we identified OLIG2 as a critical phosphorylation target for cyclin-dependent kinase 2 (CDK2). CDK2-mediated OLIG2 phosphorylation stabilizes OLIG2 protein from proteasomal degradation. Phosphorylated OLIG2 binds to the E-Box regions of p27 promoter and represses p27 transcription, which in turn activates CDK2 in positive feedback manner. CDK2-mediated OLIG2 phosphorylation promotes cell cycle progression, cell proliferation, and tumorigenesis. OLIG2 inhibition disrupted cell cycle control mechanism by decreasing CDK2 and elevating apoptosis-related molecules. Inhibition of CDK2 activity disrupted OLIG2-CDK2 interactions and attenuated OLIG2 protein stability. In addition, OLIG2-high glioma initiating cells are highly sensitive to CDK2 inhibitor treatment, indicating that OLIG2 can be a biomarker for personalized treatment for glioblastoma patients with CDK2 inhibitors. Further investigation on these mechanisms may lead to novel targeted therapy on GBMs with high OLIG2 expression.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noz175.126
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2094060-9
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  • 2
    Online Resource
    Online Resource
    CBIO-20. MOLECULAR MECHANISMS OF OLIG2 TRANSCRIPTION FACTOR IN GLIOBLASTOMA
    Oxford University Press (OUP) ; 2020
    In:  Neuro-Oncology Vol. 22, No. Supplement_2 ( 2020-11-09), p. ii19-ii20
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 22, No. Supplement_2 ( 2020-11-09), p. ii19-ii20
    Abstract: Oligodendrocyte lineage transcription factor 2 (OLIG2) promotes proliferation of normal neural stem/progenitor cells and glioma cells. However, the mechanisms underlying the regulation of OLIG2 remain largely unknown. Here, we show that a comprehensive analysis of the critical gene regulatory networks involving OLIG2 in glioma initiating cell (GIC) lines. In vitro differentiation studies showed that proneural GIC lines possess the potential to differentiate into astrocytic, neuronal, and oligodendrocytic lineages, whereas mesenchymal GICs exhibited limited potential for neural lineage differentiation following retinoic acid induction. We also showed that CDK2-mediated OLIG2 phosphorylation stabilizes OLIG2 protein from proteasomal degradation. Phosphorylated OLIG2 binds to the E-Box regions of p27 promoter and represses p27 transcription, which in turn activates CDK2 in positive feedback manner. CDK2-mediated OLIG2 phosphorylation promotes cell cycle progression, cell proliferation, and tumorigenesis. OLIG2 inhibition disrupted cell cycle control mechanism by decreasing CDK2 and elevating apoptosis-related molecules. Inhibition of CDK2 activity disrupted OLIG2-CDK2 interactions and attenuated OLIG2 protein stability.　In addition, OLIG2-high glioma initiating cells are highly sensitive to CDK2 inhibitor treatment, indicating that OLIG2 can be a biomarker for personalized treatment for glioblastoma patients with CDK2 inhibitors. In conclusion, we have identified OLIG2-CDK2 interactions in glioma stem cells that can be targeted by CDK2 inhibitors and this may allow the selection of patients with high likelihood of responding to this therapy.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noaa215.080
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
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  • 3
    Online Resource
    Online Resource
    ANGI-16. NOTCH SIGNALING IN BEVACIZUMAB-INDUCED VASCULAR NORMALIZATION IN GLIOBLASTOMA
    Oxford University Press (OUP) ; 2017
    In:  Neuro-Oncology Vol. 19, No. suppl_6 ( 2017-11-06), p. vi25-vi25
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 19, No. suppl_6 ( 2017-11-06), p. vi25-vi25
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/nox168.094
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2017
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  • 4
    Online Resource
    Online Resource
    COT-20 Clinical experience with tumor-treating fields therapy for newly diagnosed glioblastoma
    Oxford University Press (OUP) ; 2020
    In:  Neuro-Oncology Advances Vol. 2, No. Supplement_3 ( 2020-11-28), p. ii23-ii23
    Details
    In: Neuro-Oncology Advances, Oxford University Press (OUP), Vol. 2, No. Supplement_3 ( 2020-11-28), p. ii23-ii23
    Abstract: Introduction: Tumor-treating fields (TTF) is an established modality for glioblastoma (GBM) treatment administered through the portable Optune system. The efficacy of Optune for newly diagnosed GBM was demonstrated in the EF-14 phase 3 trial. Although TTF is now included as part of initial treatment in the Japan GBM guideline, it is not yet a standard therapy because the procedures are cumbersome and may impose unnecessary psychological burdens on patients with dire prognoses. In our institution, TTF therapy has been offered as a treatment option for GBM patients since January 2018. This report summarizes our initial experience with this novel treatment. Methods: The medical records of the first eight patients with newly diagnosed glioblastoma who underwent TTF were retrospectively reviewed. Results: The eight patients with newly diagnosed glioblastoma treated with TTF comprised five men and three women (median age, 68 years; range 34–83 years). Nine patients were offered TTF therapy, but one declined because of the need for a shaved head. The patients continued TTF for 1–7 months, without major complications. Skin reaction was the most prevalent adverse event (n = 5). One patient could not continue TTF treatment after femoral neck fracture due to the weight of the mobile battery. One patient who did not have a helper at home received TTF treatment from a nurse visiting his home. Conclusions: Patients should be provided with information on TTF, such as the timing of informed consent during and after chemoradiotherapy, to help them better understand this new modality and secure their consent.
    Type of Medium: Online Resource
    ISSN: 2632-2498
    URL: Article
    DOI: 10.1093/noajnl/vdaa143.102
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 3009682-0
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  • 5
    Online Resource
    Online Resource
    CBMS-03 PHOSPHORYLATION STATE OF OLIG2 REGULATES PROLIFERATION OF GLIOMA STEM CELLS
    Oxford University Press (OUP) ; 2019
    In:  Neuro-Oncology Advances Vol. 1, No. Supplement_2 ( 2019-12-16), p. ii5-ii5
    Details
    In: Neuro-Oncology Advances, Oxford University Press (OUP), Vol. 1, No. Supplement_2 ( 2019-12-16), p. ii5-ii5
    Abstract: The Cancer Genome Atlas project described a robust gene expression-based molecular classification of glioblastoma with the functional and biological significance of the subclasses yet to be determined. Here, we show that a comprehensive analysis of a panel of glioma initiating cell (GIC) lines can identify a group of stem cells with high OLIGg2 expression as in Proneural-like GBM subtype. In vitro differentiation studies showed that proneural GIC lines possess the potential to differentiate into astrocytic, neuronal, and oligodendrocytic lineages, whereas mesenchymal GICs exhibited limited potential for neural lineage differentiation following retinoic acid induction. A considerable decline of OLIG2 in proneural GIC lines was observed following retinoic acid treatment. We also showed that OLIG2 is a functional marker associated with cell proliferation in Olig2-high GIC lines. In addition, OLIG2 inhibition disrupted cell-cycle control mechanism by decreasing CDK2 and CDK4 and elevating apoptosis-related molecules. Mechanistic investigations revealed molecular interactions between CDK2/CDK4 and OLIG2. Inhibition of CDK2/CDK4 activity disrupted OLIG2-CDK2/CDK4 interactions and attenuated OLIG2 protein stability. Further investigation on these mechanisms may lead to novel targeted therapy on GBMs with high OLIG2 expression.
    Type of Medium: Online Resource
    ISSN: 2632-2498
    URL: Article
    DOI: 10.1093/noajnl/vdz039.023
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 3009682-0
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  • 6
    Online Resource
    Online Resource
    CSIG-41. ONCOGENE ADDICTION SWITCH FROM NOTCH TO PI3K REQUIRE SIMULTANEOUS TARGETING OF DUAL PATHWAY INHIBITION IN GLIOBLASTOMA
    Oxford University Press (OUP) ; 2018
    In:  Neuro-Oncology Vol. 20, No. suppl_6 ( 2018-11-05), p. vi52-vi52
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 20, No. suppl_6 ( 2018-11-05), p. vi52-vi52
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noy148.207
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2018
    detail.hit.zdb_id: 2094060-9
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  • 7
    Online Resource
    Online Resource
    NQPC-15 DEVELOPMENT OF BRAIN TUMOR SURVIVORSHIP PROGRAM
    Oxford University Press (OUP) ; 2022
    In:  Neuro-Oncology Advances Vol. 4, No. Supplement_3 ( 2022-12-03), p. iii20-iii20
    Details
    In: Neuro-Oncology Advances, Oxford University Press (OUP), Vol. 4, No. Supplement_3 ( 2022-12-03), p. iii20-iii20
    Abstract: Brain tumor patients suffer from psychological distress and various sequelae from the moment they are diagnosed with a brain tumor, during and after treatment. Although the number of brain tumor survivors is increasing as a result of improved treatment outcomes for brain tumors, the support system is not sufficient. We, in collaboration with the University of California San Francisco Brain Tumor Center, have established a multidisciplinary professional staff of physicians, nurses, pharmacists, rehabilitation therapists, nutritionists, and social workers to support brain tumor patients, their families, and care givers. The brain tumor survivorship program is designed to support brain tumor patients, their families, and caregivers. This report describes their efforts. Methods This program started in December 2021. We asked relevant departments in the hospital to cooperate with the program. In July 2022, the “Brain Tumor Survivorship Care Program 360” website was opened to the public. Results As of the end of August 2022, there were 9 participants, of which 7 were patients and 2 were care givers. Of these, two were patients being treated at other hospitals. Various information is provided on the website. Web meetings are also held to provide a place where participants can communicate directly with each other. When participants were asked about their requests for the program, many of them requested information on treatment, public services, and a place for communication among patients. Discussion Brain tumor patients face not only life-threatening but also painful symptoms associated with the impairment of their own physical motor and cognitive functions, which they had possessed until then. Through the survivorship program, we will continue to scientifically examine and develop a support system for the various survival-related issues that brain tumor patients and their families experience from diagnosis to the end of life.
    Type of Medium: Online Resource
    ISSN: 2632-2498
    URL: Article
    DOI: 10.1093/noajnl/vdac167.075
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
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  • 8
    Online Resource
    Online Resource
    MTR-15A PRONEURAL SIGNATURE PROFILE PREDICTS RESISTANCE TO BEVACIZUMAB THERAPY IN GLIOBLASTOMA
    Oxford University Press (OUP) ; 2015
    In:  Neuro-Oncology Vol. 17, No. suppl 5 ( 2015-11), p. v127.3-v127
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 17, No. suppl 5 ( 2015-11), p. v127.3-v127
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/nov219.15
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2015
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  • 9
    Online Resource
    Online Resource
    COT-15 PATHOLOGICAL ANALYSIS OF MALIGNANT GLIOMA IN THE END STAGE
    Oxford University Press (OUP) ; 2022
    In:  Neuro-Oncology Advances Vol. 4, No. Supplement_3 ( 2022-12-03), p. iii26-iii26
    Details
    In: Neuro-Oncology Advances, Oxford University Press (OUP), Vol. 4, No. Supplement_3 ( 2022-12-03), p. iii26-iii26
    Abstract: Malignant gliomas have an extremely high rate of recurrence and brain invasion despite standard treatment, ultimately leading to tumor death. Tumor death is generally thought to be caused by brain herniation due to mass effect, as confirmed by studies of malignant glioma brain autopsies performed in the 1960s and 1980s. However, there have been few studies of brain autopsies of malignant gliomas after the introduction of chemotherapy with temozolomide, and the pathological characteristics of the end stage of the disease have not been clarified in recent years. In this study, we report the clinical and pathological characteristics of the end stages of malignant glioma cases treated at our hospital from the initial treatment to the confirmation of death. Methods 10 cases of malignant glioma that were treated from initial treatment to pathological autopsy at our hospital from 2007 to 2018 were included in this study. We analyzed the pathology, neuroradiological changes, and clinical course of these cases at the end stage. Results The mean age of the 10 patients was 59 (15-77) years, and the median overall survival was 16.5 months. The primary tumor sites were 2 frontal lobes, 3 parietal lobes, 3 temporal lobes, 1 cerebellum, and 1 multiple lesions. The direct cause of death in all cases was neurological death due to tumor progression. Gross findings of pathological autopsy specimens showed that tumor excision sites were cavitated or recurrent, but mass effect was poor and there were few cases of brain herniation. On the other hand, microscopic findings showed infiltration of tumor cells into the brain stem through the brain parenchyma. Conclusion This study suggests that tumor invasion into the brainstem is involved as a cause of tumor death. It is possible that the new treatment may change the recurrence pattern or alter the morphology of glioma cells.
    Type of Medium: Online Resource
    ISSN: 2632-2498
    URL: Article
    DOI: 10.1093/noajnl/vdac167.102
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 3009682-0
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