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Gene profile of glioblastoma cells treated with y15 and temozolomide

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE43452 | GEO | 2013/01/12

SECONDARY ACCESSION(S): PRJNA186439

REPOSITORIES: GEO

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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

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.

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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

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

Plasma Mouse LC-MSMS - Bortezomib administered prior to temozolomide depletes MGMT, chemosensitizes glioblastoma with unmethylated MGMT promoter and prolongs animal survival

Project description:Patients diagnosed with glioblastoma (GBM) with sustained synthesis of the DNA repair enzyme, O6-methyl guanine DNA methytransferase (MGMT), are rendered resistant to Temozolomide (TMZ) chemotherapy. Here, we hypothesized that pretreatment with the proteasome inhibitor Bortezomib (BTZ, Velcade) might sensitize these GBM to TMZ by depleting MGMT.

2019-08-20 | PXD007193 | Pride

BET protein inhibition sensitizes glioblastoma cells to temozolomide treatment by attenuating MGMT expression

Project description:Two cell lines were used for methylation profiling to investigate how BET protein inhibition sensitizes glioblastoma cells to temozolomide treatment by attenuating MGMT expression

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Relevance of temozolomide for elderly patients with MGMT promoter-methylated malignant astrocytomas outside the RTK I methylation group

Project description:The data contains Illumina 450k/EPIC array methylation files from 104 patients of the NOA-08 study comparing temozolomide alone vs. radiotherapy in elderly patients with glioblastoma

2019-10-31 | GSE122920 | GEO

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.

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Characterization of a new small-molecule inhibitor of HDAC6 in glioblastoma

Project description:Histone deacetylase 6 (HDAC6) is an epigenetic modifier that is an attractive pharmacological target in cancer. In this work, we show that HDAC6 is elevated in glioblastoma, the most malignant and common brain tumor in adults, and in glioma stem cells. Moreover, we identified a new small-molecule inhibitor of HDAC6, called JOC1, which presents strong sensitivity for HDAC6 inhibition and exerts high cytotoxic activity, alone or in combination with temozolomide. Moreover, it is able to significantly reduce tumor growth in vivo. Transcriptomic analysis of patient derived glioma stem cells revealed an increase in cell differentiation and cell death as well as decrease in cell cycle activity and cell division as relevant cellular pathways whose activities are significantly altered by the treatment with JOC1. In conclusion, our data reveal the efficacy of a novel HDAC6 inhibitor in glioblastoma pre-clinical setting

2020-01-18 | GSE143887 | GEO

RNASeq analysis of NB1691 neuroblastoma cells treated with MDM2-p53 inhibitor RG7388 alone and in combination with temozolomide

Project description:RNASeq analysis of NB1691 neuroblastoma cells treated with MDM2-p53 inhibitor RG7388 alone and in combination with temozolomide

| PRJNA414128 | ENA

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