Gene expression signature-based prognostic risk score in patients with glioblastoma.
Atsushi Kawaguchi,Naoki Yajima,Naoto Tsuchiya,Jumpei Homma,Masakazu Sano,Manabu Natsumeda,Hitoshi Takahashi,Yukihiko Fujii,Tatsuyuki Kakuma,Ryuya Yamanaka +9 more
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TLDR
The method was effective for objectively classifying grade 4 gliomas and was a more accurate prognosis predictor than histological grading.Abstract:
The present study aimed to identify genes associated with patient survival to improve our understanding of the underlying biology of gliomas. We investigated whether the expression of genes selected using random survival forests models could be used to define glioma subgroups more objectively than standard pathology. The RNA from 32 non-treated grade 4 gliomas were analyzed using the GeneChip Human Genome U133 Plus 2.0 Expression array (which contains approximately 47 000 genes). Twenty-five genes whose expressions were strongly and consistently related to patient survival were identified. The prognosis prediction score of these genes was most significant among several variables and survival analyses. The prognosis prediction score of three genes and age classifiers also revealed a strong prognostic value among grade 4 gliomas. These results were validated in an independent samples set (n = 488). Our method was effective for objectively classifying grade 4 gliomas and was a more accurate prognosis predictor than histological grading.read more
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N6-methyladenosine Modulates Nonsense-mediated mRNA Decay in Human Glioblastoma
Fuxi Li,Yang Yi,Yanyan Miao,Wenyong Long,Teng Long,Siyun Chen,Weisheng Cheng,Changye Zou,Yueyuan Zheng,Xingui Wu,Junjun Ding,Kaiyu Zhu,Delin Chen,Qiong-Cong Xu,Jinkai Wang,Qing Liu,Feng Zhi,Jian Ren,Qi Cao,Wei Zhao +19 more
TL;DR: It is shown that the m6A methyltransferase METTL3 sustained its oncogenic role by modulating NMD of splicing factors and alternative splicing isoform switches in glioblastoma (GBM) and uncovered the mechanism by whichMETTL3 promotes GBM tumor growth and progression.
Journal ArticleDOI
EGFR/SRC/ERK-stabilized YTHDF2 promotes cholesterol dysregulation and invasive growth of glioblastoma.
Runping Fang,Xin Chen,Sicong Zhang,Hui Shi,Youqiong Ye,Hailing Shi,Hailing Shi,Zhongyu Zou,Zhongyu Zou,Peng Li,Qing Guo,Li Ma,Chuan He,Suyun Huang,Suyun Huang +14 more
TL;DR: In this paper, the authors show that YTHDF2 overexpression correlates with poor glioma patient prognosis and highlight the essential role of RNA m6A methylation in cholesterol homeostasis.
Journal ArticleDOI
Identification of potential biomarkers related to glioma survival by gene expression profile analysis
TL;DR: This study identified 104 key genes shared between glioblastoma multiforme (GBM) and lower-grade glioma (LGG) which could have the potential capability to classify patients into high- and low- risk groups, which differ significantly in the overall survival.
Journal ArticleDOI
P4HB and PDIA3 are associated with tumor progression and therapeutic outcome of diffuse gliomas.
TL;DR: The data suggest that high expression of P4HB and PDIA3 plays an important role in gliomas progression, and could predict the survival outcome and therapeutic response of glioma patients.
Journal ArticleDOI
lncRNAs PVT1 and HAR1A are prognosis biomarkers and indicate therapy outcome for diffuse glioma patients
Hecun Zou,Lan-Xiang Wu,Yong-Long Yang,Shuang Li,Ying Mei,Yong-Bin Liu,Lihua Zhang,Yu Cheng,Hong-Hao Zhou,Hong-Hao Zhou +9 more
TL;DR: Analysis of TCGA and GEO data revealed that the expressions of PVT1 and CYTOR were up-regulated, while HAR1A and MIAT expressions were down-regulated in gliomas, implying that these four lncRNAs might play important role in diffuse glioma progression.
References
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TL;DR: The interim integrative analysis of DNA copy number, gene expression and DNA methylation aberrations in 206 glioblastomas reveals a link between MGMT promoter methylation and a hypermutator phenotype consequent to mismatch repair deficiency in treated gliobeasts, demonstrating that it can rapidly expand knowledge of the molecular basis of cancer.
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