MGMT Expression Contributes to Temozolomide Resistance in H3K27M-Mutant Diffuse Midline Gliomas and MGMT Silencing to Temozolomide Sensitivity in IDH-Mutant Gliomas
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- ABE Hideaki
- Department of Neurosurgery, Brain Research Institute, Niigata University
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- NATSUMEDA Manabu
- Department of Neurosurgery, Brain Research Institute, Niigata University
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- KANEMARU Yu
- Department of Neurosurgery, Brain Research Institute, Niigata University
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- WATANABE Jun
- Department of Neurosurgery, Brain Research Institute, Niigata University
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- TSUKAMOTO Yoshihiro
- Department of Neurosurgery, Brain Research Institute, Niigata University
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- OKADA Masayasu
- Department of Neurosurgery, Brain Research Institute, Niigata University
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- YOSHIMURA Junichi
- Department of Neurosurgery, Brain Research Institute, Niigata University
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- OISHI Makoto
- Department of Neurosurgery, Brain Research Institute, Niigata University
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- FUJII Yukihiko
- Department of Neurosurgery, Brain Research Institute, Niigata University
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抄録
<p>Histone H3 mutations are frequently found in diffuse midline gliomas (DMGs), which include diffuse intrinsic pontine gliomas and thalamic gliomas. These tumors have dismal prognoses. Recent evidence suggests that one reason for the poor prognoses is that O6-methylguanine-DNA methyltransferase (MGMT) promoter frequently lacks methylation in DMGs. This review compares the epigenetic changes brought about by histone mutations to those by isocitrate dehydrogenase-mutant gliomas, which frequently have methylated MGMT promoters and are known to be sensitive to temozolomide.</p>
収録刊行物
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- Neurologia medico-chirurgica
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Neurologia medico-chirurgica 58 (7), 290-295, 2018
一般社団法人 日本脳神経外科学会