Nagoya University · Medicine
Professor Fumiharu Ohka's research lab focuses on understanding the molecular mechanisms underlying gliomas, particularly glioblastoma multiforme (GBM) and meningioma, with an emphasis on identifying therapeutic resistance mechanisms and novel treatment targets. The lab investigates key factors such as MGMT promoter methylation, glioma stem-like cells, the blood-brain barrier, and the role of IDH status in gliomagenesis. Utilizing advanced models including patient-derived organoids and genetically engineered mouse models, the lab aims to uncover molecular drivers of aggressive glioma subtypes and develop targeted therapies. Their work bridges translational neuroscience and precision oncology to improve outcomes for brain tumor patients.
Figures are computed from collected data and may differ slightly.
Glioblastoma multiforme (GBM) is one of the most frequently occurring tumors in the central nervous system and the most malignant tumor among gliomas. Despite aggressive treatment including surgery, adjuvant TMZ-based chemotherapy, and radiotherapy, GBM still has a dismal prognosis: the median survival is 14.6 months from diagnosis. To date, many studies report several determinants of resistance to this aggressive therapy: (1) O(6)-methylguanine-DNA methyltransferase (MGMT), (2) the complexity o
Gliomas are the most frequently occurring primary brain tumor in the central nervous system of adults. Glioblastoma multiformes (GBMs, WHO grade 4) have a dismal prognosis despite the use of the alkylating agent, temozolomide (TMZ), and even low grade gliomas (LGGs, WHO grade 2) eventually transform to malignant secondary GBMs. Although GBM patients benefit from promoter hypermethylation of the O(6)-methylguanine-DNA methyltransferase (MGMT) that is the main determinant of resistance to TMZ, rec
An organoid model for meningioma enabled us to elucidate the tumor biology of meningioma along with potent treatment targets for meningioma.
Gliomas are classified by combining histopathologic and molecular features, including isocitrate dehydrogenase (<i>IDH</i>) status. Although <i>IDH</i>-wild-type diffuse astrocytic glioma (DAG) shows a more aggressive phenotype than <i>IDH</i>-mutant type, lack of knowledge regarding relevant molecular drivers for this type of tumor has hindered the development of therapeutic agents. Here, we examined human <i>IDH</i>-wild-type DAGs and a glioma mouse model with a mosaic analysis with double mar
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