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Glioblastoma is a highly malignant form of brain cancer, and although many active treatment options for the disease, including surgical excision and antimony-related chemotherapy, are currently in place, the prognosis of patients is particularly poor.
recent large-scale genomics study identified four mRNA expression/DNA methylation subtypes of glioblastoma and their signature genetic lesions: IDH, MES, RTK I, RTK II.
, meS, RTK I, and RTK II subsypes correspond to interstuming, primary neurons, and classical RNA expression subsypes, respectively.
these subsypes have been observed in patients' treatment, and this effect may also lead to worse patient prognosis.
, however, it is not clear whether these changes are due to the plasticity of tumor cells or to the amplification of pre-existing resistant subsumes.
comprehensive data analysis of the metagenome of the glioblastoma subtype In this study, the researchers conducted multi-histological analysis of 60 glioblastoma primary tumor tissue and orthosis using chromatin and RNA-derived gene regulatory networks.
researchers identified 38 subtypes of primary regulatory factors through analysis and further mapped the cell population specific activity of these factors to published single-cell RNA sequencing data.
analysis results of SOX10 deficiency induced interstuming esogen esophysiques show that the less protrusive glial cytocytosome markers and chromatin modification factor SOX10 are one of the main regulatory factors of RTK I subsopen tumors.
in-body functional experiments showed that the absence of SOX10 led to the transformation of tumor subsypes, and the transformation of primary neuro-intersocharging was observed at the patient's transcriptional hetology, oscientical genetics, and esogenic levels.
in mouse models of transplanted glioblastomas, inhibiting the expression of SOX10 can lead to increased tumor invasion, increased immune cell immersion, and significantly reduced survival.
, these findings reveal that SOX10 is a major regulatory factor in the RTK I subsype, which can affect tumor cells and related tumor micro-environments.
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