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Phenotypical states modulate sensitivity and transcriptional reprogramming in patient-derived glioblastoma cells in response to temozolomide and radiation therapy. [RNA-Seq]

ABSTRACT: Differential molecular response involving epigenetic, transcriptomic and proteomic adaptstions of glioblastoma cancer stem-like cells and serum differentiaed cells in response to temozolomide and ionizing radiation

ORGANISM(S): Homo sapiens

PROVIDER: GSE249544 | GEO | 2024/03/25

REPOSITORIES: GEO

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Phenotypical states modulate sensitivity and transcriptional reprogramming in patient-derived glioblastoma cells in response to temozolomide and radiation therapy. [array]

Project description:Genome wide DNA methylation profiling of patient-derived glioblastoma cells cultured as neurospheres or FBS differentited cells. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 450,000 CpGs in glioblastoma CSCs and serum differentiated cells treated with 4 Gy ionizing radiation or IC30 concentration of temozolomide as well as vehicle control samples. Samples included 3 technical replicates in each treatment group for 2 primary glioblastoma cell lines.

2024-03-25 | GSE249636 | GEO

Phenotypical states modulate sensitivity and transcriptional reprogramming in patient-derived glioblastoma cells in response to temozolomide and radiation therapy.

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

2024-03-25 | GSE249637 | GEO

Gene profile of glioblastoma cells treated with y15 and temozolomide

Project description:The gene expression profiles were identified in glioblastoma cells treated with FAK inhibitor Y15, temozolomide alone or with combination of Y15 and Temozolomide DBTRG and U87 were treated with FAK inhibitor Y15 at 10 microM for 24 h; U87 cells were treated with Temozolomide 100 microM for 24 h and Y15+temozolomide at the same dose as each agent alone

2013-01-12 | E-GEOD-43452 | biostudies-arrayexpress

Genomic Exploration of Distinct Molecular Phenotypes Steering Temozolomide Resistance Development in Patient-Derived Glioblastoma Cells

Project description:Temozolomide resistance is a major obstacle in the therapy of glioblastoma. This is also due to the insufficient understanding of glioma heterogeneity in relation to temozolomide resistance. More in depth biological knowledge would benefit the development of different approaches to tackle the problem from its root. We explored the different outcomes derived from the long-term exposure to temozolomide and identified two different behavioral phenotypes associated to specific categories of pathways. In addition, we investigated the intra-tumoral heterogeneity of these phenotypes revealing the complexity of the temozolomide resistance phenomenon.

2023-10-24 | GSE226202 | GEO

Proteomics of Temozolomide for Glioblastoma

Project description:Using the human glioblastoma cell line LN229, temozolomide was used to detect proteome changes and identify critical components regulating chemotherapy sensitivity.

2023-05-17 | PXD042080 | Pride

Ex vivo drug sensitivity screening predicts response to temozolomide in glioblastoma patients and identifies candidate biomarkers

Project description:To investigate in situ-in vitro molecular correspondence and the relationship between in vitro and patient response to temozolomide (TMZ)

2023-08-23 | GSE232173 | GEO

Gene profile of glioblastoma cells treated with y15 and temozolomide

Project description:The gene expression profiles were identified in glioblastoma cells treated with FAK inhibitor Y15, temozolomide alone or with combination of Y15 and Temozolomide

2013-01-12 | GSE43452 | GEO

ATR inhibition using gartisertib enhances cell death and synergises with temozolomide and radiation in patient-derived glioblastoma cell lines

Project description:Glioblastoma is an aggressive and highly invasive disease that often resists treatment. Tumour cells can restrict the DNA-damaging effects of temozolomide (TMZ) and radiation therapy (RT) using the DNA damage response (DDR) mechanism which activates cell cycle arrest and DNA repair pathways. Ataxia-telangiectasia and Rad3-Related protein (ATR) plays a pivotal role in the recognition of DNA damage induced by chemotherapy and radiation and downstream activation of DDR pathways. Furthermore, a growing body of evidence indicates DNA damage and inhibition of ATR can stimulate a proinflammatory response that activates innate immunity against tumour cells. Here, we investigated the change of gene expression of treated glioblastoma cell lines from TMZ+RT and ATR inhibition (using gartisertib (M4344)) combined with TMZ+RT.

2024-01-18 | GSE211272 | GEO

Transcriptomic profiling associated with temozolomide (TMZ) response of glioblastoma mouse model

Project description:The gene expression of an orthotopic mouse model developed from human glioblastoma neurospheres was compared between temozolomide treated and untreated mice.

2015-06-03 | GSE47809 | GEO

Study on the effects of CD44 knockdown in glioblastoma multiforme cells in combination with Temozolomide

Project description:Our goal is to investigate the effects of CD44 knockdown alone and in combination with Temozolomide on glioblastoma multiforme cells. To achieve this, we treated U251 cells that had been transfected with either shCtrl lentivirus or shCD44 lentivirus with either DMSO or Temozolomide.

2023-08-31 | GSE225869 | GEO

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