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Homo sapiens

ABSTRACT: Establishment of tractable human iPSC-based models for the study and targeting of glioma initiation (ChIP-Seq)

PROVIDER: PRJNA279411 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1929990.fastq.gz	Fastqsanger.gz
	SRR1929991.fastq.gz	Fastqsanger.gz
	SRR1929992.fastq.gz	Fastqsanger.gz
	SRR1929993.fastq.gz	Fastqsanger.gz
	SRR1929984.fastq.gz	Fastqsanger.gz

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Homo sapiens

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Establishment of human iPSC-based models for the study and targeting of glioma initiating cells

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Establishment of tractable human iPSC-based models for the study and targeting of glioma initiation (Expression)

Project description:Gliomas can originate upon transformation of adult Neural Progenitor Cells (NPCs) to Tumor Initiating Cells (TICs). Studies on human Glioma TICs (GTICs) have focused on the use of primary tumors from which GTICs could be isolated. Therefore investigations on the driver events underlying NPC transformation and human glioma initiation remain limited to the use of human embryonic material. Here we report on the development of strategies for the modeling of human gliomagenesis based on the use of human induced Pluripotent Stem Cells (hiPSCs). Transformation of hiPSC-derived NPCs (iNPCs) by defined genetic alterations led to the establishment of tractable human GTIC models suitable for studying the early steps of gliomagenesis as well as for screening studies. Dysregulation of PI3K, MAPK and p53 signaling in iNPCs led to the acquisition of functional GTIC properties. In vivo transplantation led to the formation of highly aggressive, infiltrative and heterogeneous tumors upon limited dilutions and secondary transplantation, faithfully recapitulating gliomagenesis. Metabolic modulation by chemical approaches compromised GTIC viability. Pilot screening of 101 anti-cancer compounds identified 3 molecules specifically targeting transformed iNPCs and primary GTICs. Together, our results demonstrate the potential of hiPSCs for the functional testing of putative driver mutations underlying human tumorigenesis and pave new avenues for the development of personalized cancer therapeutics.

2015-12-01 | GSE67284 | GEO

Establishment of tractable human iPSC-based models for the study and targeting of glioma initiation (Methlyation)

2015-12-01 | GSE67283 | GEO

Establishment of tractable human iPSC-based models for the study and targeting of glioma initiation (ChIP-Seq)

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Gene therapy using genome-edited human iPS cell-derived neural stem cells overcomes refractory course of invasive glioma stem cells

Project description:Spatiotemporal analyses using brain slice culture and brain clearing demonstrated that human induced pluripotent stem cell-derived neural stem cells (iPSC-NSCs) possess higher tumor-trophic migratory capacity than fetal NSCs, adipose tissue and bone marrow derived mesenchymal stem cells (MSCs). NSCs expressing prodrug converting enzyme fusion gene exhibited strong anti-tumor effect for glioma stem cell in vivo models. The present research concepts may become a platform of cell-based gene therapy for glioma.

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Cooperativity between H3-K27M and PDGFRA poses multiple therapeutic vulnerabilities in human iPSC-derived diffuse midline glioma avatars (CUT&RUN)

Project description:PDGFRA and H3.3 mutations cooperate in an iPSC-based model of diffuse midline glioma to alter tumor biology.

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Transcriptome-wide analysis of CRISPR-edited iPSC-derived glioma models

Project description:Transcriptome-wide analysis of CRISPR-edited iPSC-derived glioma models

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Ets factors regulate neural stem cell depletion and gliogenesis in Ras pathway-driven glioma

Project description:As the list of putative driver mutations in glioma grows, we are just beginning toAs the list of putative driver mutations in glioma grows, we are just beginning to elucidate the effects of dysregulated developmental signaling pathways on the transformation of neural cells. We have employed a postnatal, mosaic, autochthonous, glioma model that captures the first hours and days of gliomagenesis in more resolution than conventional genetically engineered mouse models of cancer. We provide evidence that disruption of the Nf1-Ras pathway in the ventricular zone at multiple signaling nodes uniformly results in rapid neural stem cell depletion, progenitor hyperproliferation, and gliogenic lineage restriction. Abolishing Ets subfamily activity, which is upregulated downstream of Ras, rescues these phenotypes and blocks glioma initiation. Thus, the Nf1-Ras-Ets axis might be one of the select molecular pathways that are perturbed for initiation and maintenance in glioma. Mouse Gene 1.0 ST Microarrays from Affimetryx were used for microarray analysis. For each experiment, total RNA was fluorescently labeled and hybridized. 3 cell lines derived from in vivo electroporated neural stem and progenitors were compared.

2015-05-28 | E-GEOD-69254 | biostudies-arrayexpress

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