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Metabolic Reprogramming Associated with Aggressiveness Occurs in the G-CIMP-High Molecular Subtypes of IDH1mut Lower Grade Gliomas

ABSTRACT: Metabolic Reprogramming Associated with Aggressiveness Occurs in the G-CIMP-High Molecular Subtypes of IDH1mut Lower Grade Gliomas

PROVIDER: PRJNA577647 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10278840_1.fastq.gz	Fastqsanger.gz
	SRR10278840_2.fastq.gz	Fastqsanger.gz
	SRR10278841_1.fastq.gz	Fastqsanger.gz
	SRR10278841_2.fastq.gz	Fastqsanger.gz
	SRR10278842_1.fastq.gz	Fastqsanger.gz

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Metabolic reprogramming associated with aggressiveness occurs in the G-CIMP-high molecular subtypes of IDH1mut lower grade gliomas.

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Metabolic Reprogramming Associated with Aggressiveness Occurs in the G-CIMP-High Molecular Subtypes of IDH1mut Lower Grade Gliomas

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2019-10-16 | GSE138873 | GEO

Isocitrate dehydrogenase 1 (IDH1) mutant gliomas demonstrate a distinct global CpG island methylation profile compared to IDH1 wildtype gliomas using MRSE

Project description:In order to identify other molecular aberrations that may cooperate with IDH1R132MUT in gliomagenesis, we performed CpG-island methylation profiling analysis using MSRE (Tran et al. Front. Neurosci. 3:57. Doi: 10.3389/neuro.15.005.2009) on a subset of IDH1R132MUT and IDH1R132WT GBMs and found a distinct pattern of CpG island hypermethylation that was detected in all GBMs and lower grade gliomas with IDH1R132MUT. While absent from nearly all IDH1R132WT glioma, the methylation pattern in IDH1R132MUT GBMs shows similarity to the recently reported CpG island methylator phenotype (CIMP) found to be tightly associated with IDH1R132MUT gliomas(Noushmehr et al. Cancer Cell, Volume 17, Issue 5, 18 May 2010, Pages 510-522, ISSN 1535-6108, DOI: 10.1016/j.ccr.2010.03.017). Methylation profiling performed on 40 distinct brain tumor samples: 7 Anaplastic Astrocytomas, including 3 IDH1MUT and 4 IDH1WT; 5 Lowgrade Astrocytomas, including 4 IDH1MUT and 1 IDH1WT; 28 Glioblastoma, including 8 IDH1MUT and 20 IDH1WT.

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CImP: Cellular Imprinting Proteomics applied to ocular disorders

Project description:A method (termed Cellular Imprinting Proteomics, CImP) for the identification and quantification of the ocular surface proteome using a minimally invasive membrane filter device is described. Moreover, The CImP method was applied to profile the molecular alterations in the eyes of infants exposed to Zika virus (ZIKV) infection during gestation.

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Expression analysis of 52 glioma clinical samples (36 CIMP+ and 16 CIMP-) and 6 cell line samples

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Methylation analysis of 81 glioma clinical samples (49 CIMP+ and 32 CIMP-) and 53 cell line samples

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Transcription profiling of human colorectal cancer samples with CpG island methylator phenotype (CIMP)

Project description:The CpG island methylator phenotype (CIMP) in colorectal tumors can be recognized by an increased frequency of aberrant methylation in a specific set of genomic loci. Because of the strong association of CIMP with high microsatellite instability (MSI-H), the identification of CIMP+ tumors within microsatellite stable (MSS) colorectal cancers may not be straightforward. To overcome this potential limitation, we have built an improved 7-loci set of methylation markers that includes CACNA1G, IGF2, RUNX3, HTR6, RIZ1, MINT31 and MAP1B. This new set of CIMP markers revealed a bimodal distribution of methylation frequencies in a group of 95 MSS colorectal cancers, which allowed a clearer separation between CIMP classes. Correlation of CIMP+ tumors with bio-pathological traits revealed significant associations with location to the proximal colon, mucinous histology and chromosomal stability. Although not statistically significant, a trend toward an adverse prognosis for CIMP+ cases was observed. Microarray analysis revealed that CIMP+ tumors are characterized by a unique expression profile, a result that confirms that CIMP+ tumors represent a distinct molecular class within MSS colorectal cancers. Moreover, our results suggest that this expression pattern may represent the molecular background for the development of CIMP+ tumors that, in turn, develop MSI when aberrant methylation occurs at the MLH1 gene promoter.

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Methylation analysis of 81 glioma clinical samples (49 CIMP+ and 32 CIMP-) and 53 cell line samples

Project description:Glioma CIMP (G-CIMP) is a powerful determinant of tumor pathogenicity but the molecular cause of G-CIMP is a fundamental question that is unresolved. Here, we show that mutation of a single gene, isocitrate dehydrogenase 1 (IDH1), directly causes the G-CIMP in gliomas by remodeling the methylome. In this study 81 glioma clinic samples (49 CIMP+ and 32 CIMP-) were analyzed. Parental IDH1 wild-type and IDH1 mutant cells were passaged until passage 50.

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Project description:Glioma CIMP (G-CIMP) is a powerful determinant of tumor pathogenicity but the molecular cause of G-CIMP is a fundamental question that is unresolved. Here, we show that mutation of a single gene, isocitrate dehydrogenase 1 (IDH1), directly causes the G-CIMP in gliomas by remodeling the methylome. In this study 52 glioma clinic samples (36 CIMP+ and 16 CIMP-) were analyzed. Parental IDH1 wild-type and IDH1 mutant cells were passaged 40 and passage 40 were cell line was sent for expression array.

2012-02-16 | E-GEOD-30336 | biostudies-arrayexpress

Cellular senescence escape and antiviral response discriminate glioblastoma from lower grade gliomas

Project description:Cellular senescence is a negative prognostic indicator in glioblastoma (GB). However, the specific cell types exhibiting senescence and the molecular mechanisms by which senescent cells (SCs) contribute to GB pathogenesis remain unknown. We performed multi-omics integration of publicly available GB patient-derived datasets to identify SCs and their functional impact on GB pathogenesis. We created a transcriptomic definition of SCs to verify their presence in GB datasets. Next, we analyzed transcriptomic profiles of GB and low-grade gliomas to reveal key features of GB aggressiveness. The GB patients’ phosphoproteome was analyzed with a focus on key regulators of senescence. To assess chemotherapy-evoked secondary senescence, we performed a proteomic analysis of temozolomide-induced senescence in human GB spheroids. We identified GB-associated SCs in clusters radial glia, endothelial cells, and immature astrocytes localized primarily in the hypoxic zones. Notably, we identified senescence-escape features and tumor antiviral responses as processes distinguishing GB from low-grade gliomas. In GB samples, we detected inhibitory phosphorylation of p21 and p27 proteins and active PI3K signaling, which can lead to senescence escape and belong to the typical manipulation arsenal of herpesviruses. Our proteomic analysis of temozolomide-induced senescent GB cells reveals that primary (pre-radiochemotherapy) and secondary senescence in GB share similar phenotypic features. Pathways associated with GB aggressiveness are upregulated after therapy, which can promote more aggressive behavior of recurrent tumors. Our data indicate that senescence and viral reactivation may fuel GB progression, including recurrence, suggesting that senolytics and antiviral drugs are potential therapeutic avenues.

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