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Tumor progression is independent of tumor associated macrophages in two lineage-based mouse models of GBM [TAMdepletedVsControl RNAseq]

ABSTRACT: Tumor progression is independent of tumor associated macrophages in two lineage-based mouse models of GBM [TAMdepletedVsControl RNAseq]

PROVIDER: PRJNA938430 | ENA |

REPOSITORIES: ENA

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Tumor progression is independent of tumor associated macrophages in two lineage-based mouse models of GBM

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Tumor progression is independent of tumor associated macrophages in two lineage-based mouse models of GBM [SortedTAM RNAseq]

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Tumor progression is independent of tumor associated macrophages in two lineage-based mouse models of GBM [TAMdepletedVsControl RNAseq]

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In vitro models of glioblastoma (GBM)

Project description:Characterization of gene expression for a panel of 50 in vitro and in vivo models of glioblastoma (GBM). Models include subcutaneously established xenograft lines, orthotopically grown subcutaneously established xenograft lines, serum derived cell lines and stem cell media derived cell lines. Multiple replicates of each line were run on different dates to determine the effect of batch and processing date on reproducibility of gene expression profiles 117 samples analyzed from 50 distinct GBM xenografts or cell lines. Biological replicates from the same passage number were included for many, but not all, of the lines.

2011-12-01 | E-GEOD-26344 | biostudies-arrayexpress

Single RNA-Seq on GBM cells from NPCTKO mouse models

Project description:Glioblastoma multiforme (GBM), a highly malignant and heterogeneous brain tumor, contains various types of tumor and non-tumor cells. Whether GBM cells can trans-differentiate into non-neural cell types, including mural cells or endothelial cells, to support tumor growth and invasion remains controversial. Here we generated two genetic GBM models de novo in immunocompetent mouse brains, mimicking essential pathological and molecular features of human GBMs. Single-cell RNA sequencing showed that patterns of copy-number variations (CNVs) of mural cells and endothelial cells were distinct from those of GBM cells, indicating discrete origins of GBM cells and vascular components. Furthermore, lineage tracing and transplantation studies demonstrated that, although blood vessels in GBM brains underwent drastic remodeling, GBM cells did not give rise to non-neural cell types in the brain. Intriguingly, GBM cells could randomly express mesenchymal markers, including those for mural cells, during gliomagenesis. Most importantly, single-cell CNV analysis of human GBM specimens also strongly suggested that GBM cells and vascular cells are separate lineages. Instead, non-neural cell types expanded by proliferation during tumorigenesis. Therefore, cross-lineage trans-differentiation of GBM cells is very unlikely to occur during gliomagenesis. Our findings advance understanding of cell lineage dynamics during gliomagenesis, and have implications for targeted treatment of GBMs.

2022-07-07 | GSE190154 | GEO

Tumor progression is independent of tumor associated macrophages in two lineage-based mouse models of GBM

Project description:This SuperSeries is composed of the SubSeries listed below.

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Construction of GBM patient-derived xenograft mouse models

Project description:Our adult GBM patient-derived xenograft mouse models keep the genomics characteristics of GBM patient tumors.

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Bulk RNA-Seq on GBM cells from NPCTKO and NSCHRas-shp53 mouse models

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Human GBM tumor vs Normal Human DNA

Project description:We have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18INK4C and p16INK4A codeletion. Functional reconstitution of p18INK4C in GBM cells null for both p16INK4A and p18INK4C resulted in impaired cell-cycle progression and tumorigenic potential. Conversely, RNAi-mediated depletion of p18INK4C in p16INK4A-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo. Furthermore, acute suppression of p16INK4A in primary astrocytes induced a concomitant increase in p18INK4C. Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18INK4C in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation. Keywords: comparative genomic hybridization DNA copy number abberation of human glioblastoma tumors were obtained by comparative genomic hybridization of GBM tumor vs. normal human DNA. 11 human GBM samples were analyzed on Agilent human 244A human cgh array (G4411B). Normal Human DNA was used as reference. Some samples were hybridized with dye-swap replica.

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