Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1188731 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31418976.fastq.gz | Fastqsanger.gz | |||
| SRR31418977.fastq.gz | Fastqsanger.gz | |||
| SRR31418978.fastq.gz | Fastqsanger.gz | |||
| SRR31418979.fastq.gz | Fastqsanger.gz | |||
| SRR31418980.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 10 |
Similar Datasets
Project description:Expression profiling of normal and glioblastoma-derived neural stem cells
2025-01-23 | E-MTAB-3864 | ExpressionAtlas
Project description:Transcriptional effect of an off-target shRNA targeting nucleostemin in human glioblastoma-derived cancer stem cells
2025-01-24 | E-GEOD-30448 | ExpressionAtlas
Project description:RNAseq of proneural glioblastoma stem-like cells 72 hours after infection with human cytomegalovirus (CMV) Towne strain
2025-01-23 | E-MTAB-7613 | ExpressionAtlas
Project description:Tumors are composed of cellular subpopulations with varying degree of proliferative and tumorigenic potential. Here, we identify inter- and intra-tumor heterogeneous expression of histone variant H2AFV in numerous cancer types, with high H2AFV expression correlating with cancer stem cells, poorly differentiated tumors and inferior patient survival. Depletion of H2AFV impairs proliferation, invasiveness, tumorigenicity and tumor initiating cell frequency of glioblastoma. Mechanistically, H2AFV regulates chromatin accessibility of both active and repressive complexes at the promoters and enhancers of genes: the former activates genes involved in cell proliferation/self-renewal and invasiveness while the latter suppresses cellular differentiation in cancer stem cells. Our studies uncover H2AFV as an important epigenetic determinant in cancer stem cell fate and a significant contributor of intratumor heterogeneity.
2022-01-15 | GSE152858 | GEO
Project description:Tumors are composed of cellular subpopulations with varying degree of proliferative and tumorigenic potential. Here, we identify inter- and intra-tumor heterogeneous expression of histone variant H2AFV in numerous cancer types, with high H2AFV expression correlating with cancer stem cells, poorly differentiated tumors and inferior patient survival. Depletion of H2AFV impairs proliferation, invasiveness, tumorigenicity and tumor initiating cell frequency of glioblastoma. Mechanistically, H2AFV regulates chromatin accessibility of both active and repressive complexes at the promoters and enhancers of genes: the former activates genes involved in cell proliferation/self-renewal and invasiveness while the latter suppresses cellular differentiation in cancer stem cells. Our studies uncover H2AFV as an important epigenetic determinant in cancer stem cell fate and a significant contributor of intratumor heterogeneity.
2022-01-15 | GSE152861 | GEO
Project description:Transcription profiling by array of mouse FLA2 cells (high frequency of leukemia stem cells) and FLB1 cells (low frequency of leukemia stem cells)
2015-10-22 | E-MEXP-1597 | ExpressionAtlas
Project description:Gene expression in intestinal stem cells
2014-07-30 | E-GEOD-58351 | ExpressionAtlas
Project description:RNA-sequencing analysis of glucose and acetate regulated transcripts in glioblastoma cells
2025-01-24 | E-GEOD-57488 | ExpressionAtlas
Project description:Kruppel-like factor-9 (KLF9), a member of the large KLF transcription factor family, has emerged as a regulator of oncogenesis, cell differentiation and neural development; however, the molecular basis for KLF9M-bM-^@M-^Ys diverse contextual functions remains unclear. This study focuses on the functions of KLF9 in human glioblastoma stem-like cells. We establish for the first time a genome-wide map of KLF9-regulated targets in human glioblastoma stem-like cells, and show that KLF9 functions as a transcriptional repressor and thereby regulates multiple signaling pathways involved in oncogenesis and stem cell regulation. A detailed analysis of one such pathway, integrin signaling, shows that the capacity of KLF9 to inhibit glioblastoma cell stemness and tumorigenicity requires ITGA6 repression. These findings enhance our understanding of the transcriptional networks underlying cancer cell stemness and differentiation, and identify KLF9-regulated molecular targets applicable to cancer therapeutics. Two cell lines were used as biological replicates. Each cell line have one KLF9 ChIP-enriched DNA sample and one input genomic DNA sample.
2014-10-10 | E-GEOD-62211 | biostudies-arrayexpress
Project description:The paper describes a model of glioblastoma.
Created by COPASI 4.25 (Build 207)
This model is described in the article:
Modeling the Treatment of Glioblastoma Multiforme and Cancer Stem Cells with Ordinary Differential Equations
Kristen Abernathy and Jeremy Burke BMC
Computational and Mathematical Methods in Medicine Volume 2016, Article ID 1239861, 11 pages
Abstract:
Despite improvements in cancer therapy and treatments, tumor recurrence is a common event in cancer patients. One explanation of recurrence is that cancer therapy focuses on treatment of tumor cells and does not eradicate cancer stem cells (CSCs). CSCs are postulated to behave similar to normal stem cells in that their role is to maintain homeostasis. That is, when the population of tumor cells is reduced or depleted by treatment, CSCs will repopulate the tumor, causing recurrence. In this paper, we study the application of the CSC Hypothesis to the treatment of glioblastoma multiforme by immunotherapy. We extend the work of Kogan et al. (2008) to incorporate the dynamics of CSCs, prove the existence of a recurrence state, and provide an analysis of possible cancerous states and their dependence on treatment levels.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models .
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide.
Please refer to CC0 Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000757 | BioModels