A5042727441- Glioma Diagnosis and Treatment
- Cancer Research and Treatments
- Cancer Immunotherapy and Biomarkers
- Advanced Breast Cancer Therapies
- Radiomics and Machine Learning in Medical Imaging
- Advanced biosensing and bioanalysis techniques
- Nanoplatforms for cancer theranostics
- RNA Interference and Gene Delivery
- Immune cells in cancer
- Ferroptosis and cancer prognosis
- Immunotherapy and Immune Responses
- Cancer, Hypoxia, and Metabolism
- Epigenetics and DNA Methylation
- Ubiquitin and proteasome pathways
- Brain Tumor Detection and Classification
- Meningioma and schwannoma management
- Retinoids in leukemia and cellular processes
- PARP inhibition in cancer therapy
- Circular RNAs in diseases
- Cancer-related molecular mechanisms research
- Advanced Proteomics Techniques and Applications
- Neuroblastoma Research and Treatments
- Supramolecular Self-Assembly in Materials
- Medical Imaging and Analysis
- Intracerebral and Subarachnoid Hemorrhage Research
The University of Tokyo
2017-2024
Harvard University
2021-2024
Massachusetts General Hospital
2021-2024
University of Tokyo Hospital
2024
Tokai University
2018
Tokyo University of Science
2017
University hospital Medical Information Network
2017
Microsoft (United States)
2017
SAS Institute (United States)
2017
Central Brain Tumor Registry of the United States
2017
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Immune-based therapies have shown limited efficacy in glioma thus far. This might be at least part due to insufficient numbers of neoantigens, thought targets immune attack. In addition, we hypothesized that dynamic genetic and epigenetic tumor evolution gliomas also affect the mutation/neoantigen landscape contribute treatment resistance through evasion. Here, investigated changes neoantigen immunologic features during progression using exome RNA-seq paired primary recurrent samples...
Treatment paradigms for isocitrate dehydrogenase (IDH)-mutant gliomas are rapidly evolving. Although typically indolent and responsive to initial treatment, these tumors invariably recur at a higher grade require salvage treatment. Homozygous deletion of the tumor suppressor gene CDKN2A/B frequently emerges recurrence in tumors, driving poor patient outcomes. We investigated effect CDK-Rb pathway blockade on IDH-mutant glioma growth vitro vivo using CDK4/6 inhibitors (CDKi).
Abstract To elucidate the mechanisms of malignant progression lower-grade glioma, molecular profiling using methylation array, whole-exome sequencing, and RNA sequencing was performed for 122, 36 31 gliomas, respectively. This cohort included 24 matched pairs initial gliomas recurrent tumors, most which showed progression. Nearly half IDH-mutant glioblastomas that had progressed from exhibited characteristic partial DNA demethylation in previously methylated genomic regions their...
Five-aminolevulinic acid (5-ALA) is widely used as an intraoperative fluorescent probe for radical resection of high-grade glioma, and thus aids in extending progression-free survival patients. However, there exist some cases where 5-ALA fails to fluoresce. In other cases, it may undergo fluorescence quenching but cannot be orally readministered during surgery. This study aimed develop a novel hydroxymethyl rhodamine green (HMRG)-based labeling system that can repeatedly administered topical...
Immunotherapy has emerged as a promising approach for treating aggressive solid tumors, even within the CNS. Mutation in metabolic gene isocitrate dehydrogenase 1 (IDH1) represents not only major glioma defining biomarker but also an attractive therapeutic neoantigen. As patients with IDH-mutant enter early-phase vaccine and immune checkpoint inhibitor clinical trials, there is emerging evidence that implicates oncometabolite, 2-hydroxyglutarate (2HG), generated by neomorphic activity of...
Abstract The majority of low‐grade isocitrate dehydrogenase‐mutant (IDH mt ) gliomas undergo malignant progression (MP), but their underlying mechanism remains unclear. IDH exhibit global DNA methylation, and our previous report suggested that MP could be partly attributed to passive demethylation caused by accelerated cell cycles. However, during MP, there is also active mediated ten‐eleven translocation, such as hydroxymethylation. Hydroxymethylation reported potentially contribute gene...
Surgical resection is considered for most brain tumors to obtain tissue diagnosis and eradicate or debulk the tumor. Glioma, common primary malignant tumor, generally has a poor prognosis despite multidisciplinary treatments with radical chemoradiotherapy. of glioma often complicated by obscure border between tumor adjacent tissues tumor's infiltration into eloquent brain. 5-aminolevulinic acid frequently used visualization, as it exhibits high fluorescence in high-grade glioma. Here, we...
OPINION article Front. Oncol., 06 August 2019Sec. Cancer Imaging and Image-directed Interventions Volume 9 - 2019 | https://doi.org/10.3389/fonc.2019.00727
In conducting medical research, a system which can objectively predict the future trends of given research field is awaited. This study aims to establish novel and versatile algorithm that predicts latest in neuro-oncology. Seventy-nine neuro-oncological fields were selected with computational sorting methods such as text-mining analyses. Thirty journals represent recent neuro-oncology also selected. As concept, annual impact (AI) each year was calculated for journal (number articles...
2041 Background: IDH-mutant astrocytomas represent the most prevalent primary tumors in younger adults (<45yo). A substantial minority of these exhibit deletion CDKN2A (Cyclin-Dependent Kinase Inhibitor Gene 2A). Homozygous this gene– which encodes tumor suppressor protein p16 – is associated with a malignant phenotype and poorer prognosis astrocytoma. deletions are primarily observed that have received radiation therapy (RT), suggesting potential mechanistic relationship between RT...
<p>Supplemental Figure 1: Representative raw flow cytometry profiles for each cell line used creating summary data in 3A.</p>
<p>Supplemental Figure 2: Combination treatment with lomustine does not lead to an added benefit.</p>
<p>Supplemental Figure 3: Continuous abemaciclib treatment is tolerated appropriately.</p>
<div>AbstractPurpose:<p>Treatment paradigms for isocitrate dehydrogenase (IDH)–mutant gliomas are rapidly evolving. Although typically indolent and responsive to initial treatment, these tumors invariably recur at a higher grade require salvage treatment. Homozygous deletion of the tumor suppressor gene <i>CDKN2A/B</i> frequently emerges recurrence in tumors, driving poor patient outcomes. We investigated effect CDK-Rb pathway blockade on IDH-mutant glioma growth...
<p>Supplemental Figure 3: Continuous abemaciclib treatment is tolerated appropriately.</p>
<p>Supplemental Figure 2: Combination treatment with lomustine does not lead to an added benefit.</p>
<div>AbstractPurpose:<p>Treatment paradigms for isocitrate dehydrogenase (IDH)–mutant gliomas are rapidly evolving. Although typically indolent and responsive to initial treatment, these tumors invariably recur at a higher grade require salvage treatment. Homozygous deletion of the tumor suppressor gene <i>CDKN2A/B</i> frequently emerges recurrence in tumors, driving poor patient outcomes. We investigated effect CDK-Rb pathway blockade on IDH-mutant glioma growth...
<p>Supplemental Figure 1: Representative raw flow cytometry profiles for each cell line used creating summary data in 3A.</p>
Gliomas vary in prognosis with World Health Organization (WHO) grade. Low-grade gliomas can undergo malignant progression (MP), becoming aggressive high-grade tumors, worsening prognosis. This is prevalent isocitrate dehydrogenase-mutant (IDH-mt) like astrocytoma and oligodendroglioma, but the mechanism of MP still not fully understood. High-grade IDH-mt have been reported to exhibit TET-mediated DNA hydroxymethylation, which suggested potentially influence gene expression. We hypothesized...