Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA279410 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Establishment of tractable human iPSC-based models for the study and targeting of glioma initiation (Expression)
| PRJNA279409 | ENA
Project description:Establishment of tractable human iPSC-based models for the study and targeting of glioma initiation (ChIP-Seq)
| PRJNA279411 | ENA
Project description:Establishment of human iPSC-based models for the study and targeting of glioma initiating cells
| PRJNA279406 | ENA
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 | GSE67282 | GEO
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
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 | GSE67283 | GEO
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.
2022-09-16 | GSE150470 | GEO
Project description:Gene expression profiling by RNA-seq of human iPSC and iPSC-derived cardiomyocytes from an Yoruban individual (NA19101)
2025-01-23 | E-MTAB-6013 | ExpressionAtlas
Project description:RNA sequencing of human iPSC-derived brain microvascular endothelial cells.
2025-01-16 | E-MTAB-8802 | ExpressionAtlas
Project description:RNA-seq of human midbrain organoid models of Parkinson's Disease
2025-01-23 | E-MTAB-7302 | ExpressionAtlas