E-MTAB-6681
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-6681 | ExpressionAtlas | 2019-05-14
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:RNA-seq of Glioma Neural Stem (GNS) cell line G144 after MEK inhibition in wild type (WT) and CIC (Capicua) depleted cells.
| PRJEB26384 | ENA
Project description:Recent preclinical studies suggest that combining MEK and MDM2 inhibition synergize to induce apoptosis in RAS/BRAF-mutant and TP53 wild-type CRC models. In vitro, in RKO cell lines (poorly differentiated colon carcinoma cell line resistant to single agent targeting MDM2 and MEK and BRAF inhibition), the MDM2 plus MEK inhibitor combination generated a synergistic increase in apoptotic index. In vivo, in mice harboring human RKO colon tumor xenografts the combination of MDM2 plus MEK inhibition elicited 93% decreases in tumor volume.
This trial is to conduct a single-center, Phase 1 dose escalation study of trametinib combined with HDM201 (a HDM2 inhibitor) in patients with advanced/metastatic RAS/RAF mutant and TP53 wt CRC.
| 2287507 | ecrin-mdr-crc
Project description:A human microarray comprising 1658 human genome probes was used to evaluate the specific expression of miRNA between brian glioma stem cells (GSC) and normal neural stem cells(NSC). 2 total RNA samples are analyzed, brian glioma stem cells (GSC) and normal neural stem cells(NSC). cell type: brain glioma stem cells:GSC_1, GSC_2, GSC_3 ; cell line: normal neural stem cells: NSC_1, NSC_2, NSC_3 biological replicate: NSC_1, NSC_2, NSC_3; biological replicate: GSC_1, GSC_2, GSC_3
2014-07-30 | E-GEOD-41032 | biostudies-arrayexpress
Project description:A human cDNA microarray comprising 29,187 human genome probes was used to evaluate the transcriptional changes between brian glioma stem cells (GSC) and normal neural stem cells(NSC). There were 6 samples that were analyzed, 3 samples were from glioma stem cells and the other 3 samples form normal neural stem cells were controls. cell type: brain glioma stem cells:GSC_H004, GSC_H005, GSC_H006 ; cell line: normal neural stem cells: NSC_H001, NSC_H002, NSC_H003 biological replicate: NSC_H001, NSC_H002, NSC_H003; biological replicate: GSC_H004, GSC_H005, GSC_H006
2014-07-30 | E-GEOD-41031 | biostudies-arrayexpress
Project description:In this study, we combined a genome-wide analysis of the Polycomb protein Bmi1 and an in vivo RNAi screening to identify critical targets whose repression in neural progenitor and Malignant Glioma cells enables normal and aberrant self-renewal. Bmi1 ChIP-sequencing generated in 2 primary adult mouse Neural Progenitor cell lines, 1 mouse astrocytic cell line, 1 mouse Glioma initiating cell line, and 1 mouse Glioma cell line. In human cell lines, Bmi1 ChIP-seq was performed for foetal Neural Progenitor Cells, and 2 Glioblastoma Stem-like cells. ChIP-seq for AP-1 in one Glioblastoma stem-like cell line. ChIP-sequencing were generated using either Illumina GxII or HiSeq. We have further performed RNA-seq of adult Ink4a/Arf -/-;BMI1or GFP dox-inducible shRNA mNPC with a doxycycline inducible shRNA targeting BMI1 or GFP (as control). These cells were either treated with doxyclyine for 48h to ablate BMI1 and GFP expression or further subjected to short-term differentiation using either BMP4 (10ng/ml or 50ng/ml for 3 or 6hrs), or FBS (1 or 10% for 3 or 6hrs). Additional mouse RNA-seq were performed in two biological replica of adult mouse brains (littermate) with either wild-type FVB background or BMI1 -/-. Finally, we performed RNA-seq in human Glioblastoma stem-like cells (most likely belonging to the mesenchymal GBM subtype) treated with BMP7, Arvanil and doxycycline or EtOH treated as ctrl.
2013-05-21 | E-GEOD-33912 | biostudies-arrayexpress
Project description:Primary objectives: The primary objective of first line treatment is:- Evaluation of efficacy (in terms of PFS) of ongoing FOLFIRI + Cetuximab as first line treatment in wild type (WT) K-ras metastatic colorectal cancer patients.
the primary objective of second line treatment is:- evaluation of efficacy (in terms of PFS) of ongoing cetuximab as second line tretment in combination with chemotherapy after progerssion of first line treatment with FOLFIRI plus cetuximab in wild type (WT) K-ras metastatic colorectal cancer patients.
Primary endpoints: The primary objective of first line treatment is:- Evaluation of efficacy (in terms of PFS) of ongoing FOLFIRI + Cetuximab as first line treatment in wild type (WT) K-ras metastatic colorectal cancer patients.
the primary objective of second line treatment is:- evaluation of efficacy (in terms of PFS) of ongoing cetuximab as second line tretment in combination with chemotherapy after progerssion of first line treatment with FOLFIRI plus cetuximab in wild type (WT) K-ras metastatic colorectal cancer patients
| 2526788 | ecrin-mdr-crc
Project description:B7H3 (also known as CD276) is a co-stimulator checkpoint protein of the cell surface B7 superfamily. Recently, the function beyond immune regulation of B7H3 has been widely studied. However, the expression preference and the regulation mechanism underlying B7H3 in different subtypes of gliomas is rarely understood. We show here that B7H3 expression is significantly decreased in IDH-mutated gliomas and in cultured IDH1-R132H glioma cells. Accumulation of 2-HG leads to a remarkable downregulation of B7H3 protein and the activity of IDH1-R132H mutant is responsible for B7H3 reduction in glioma cells. Inhibition of autophagy by inhibitors like leupeptin, chloroquine (CQ), and Bafilomycin A1 (Baf-A1) blocks the degradation of B7H3 in glioma cells. In the meantime, the autophagy flux is more active with higher LC3B-II and lower p62 in IDH1-R132H glioma cells than in IDH1-WT cells. Furthermore, sequence alignment analysis reveals potential LC3-interacting region (LIR) motifs 'F-V-S/N-I/V' in B7H3. Moreover, B7H3 interacts with p62 and CQ treatment significantly enhances this interaction. Additionally, we find that <i>B7H3</i> is positively correlated with <i>VEGFA</i> and <i>MMP2</i> by bioinformatics analysis in gliomas. B7H3 and VEGFA are decreased in IDH-mutated gliomas and further reduced in 2-HG<sup>high</sup> gliomas compared to 2-HG<sup>low</sup> glioma sections by IHC staining. Our study demonstrates that B7H3 is preferentially overexpressed in IDH wild-type gliomas and could serve as a potential theranostic target for the precise treatment of glioma patients with wild-type IDH.
2021-05-26 | MTBLS2692 | MetaboLights
Project description:Gioma stem cells from Nf1-associated optic gliomas and NSCs from third ventricle zone show differencies in gene expression patterns and physiological functions. We used microarrays to identify differential gene expression between glioma stem cells and the control counterparts including the wild type and Nf1-/- neural stem cells from the third ventricle.
2014-12-01 | GSE58260 | GEO
Project description:Resistance to Ras pathway inhibition is a major challenge in the treatment of colorectal cancer (CRC), but the underlying mechanisms are incompletely understood. Here we performed large-scale small molecule screens in CRC and identified inhibitors of MEK1/2 as potent activators of Wnt/beta-catenin signalling. Targeting MEK increased Wnt activity in different CRC cell lines and in the murine intestine in vivo. The MEK-induced Wnt response was strongly enhanced by truncating mutations in APC and proteomic experiments identified that AXIN1 levels are depleted upon MEK inhibition. We generated patient-derived colon cancer organoids and showed that a clinically approved MEK inhibitor leads to increased Wnt activity, elevated LGR5 levels and enrichment of gene signatures associated with stem cells and cancer relapse. This reprogramming was reverted by co-treatment with Wnt inhibitors. Our study demonstrates that MEK inhibition affects cellular plasticity and induces an intestinal stem cell program which constitutes a novel mechanism of drug resistance.
2018-05-08 | GSE114060 | GEO
Project description:Resistance to Ras pathway inhibition is a major challenge in the treatment of colorectal cancer (CRC), but the underlying mechanisms are incompletely understood. Here we performed large-scale small molecule screens in CRC and identified inhibitors of MEK1/2 as potent activators of Wnt/beta-catenin signalling. Targeting MEK increased Wnt activity in different CRC cell lines and in the murine intestine in vivo. The MEK-induced Wnt response was strongly enhanced by truncating mutations in APC and proteomic experiments identified that AXIN1 levels are depleted upon MEK inhibition. We generated patient-derived colon cancer organoids and showed that a clinically approved MEK inhibitor leads to increased Wnt activity, elevated LGR5 levels and enrichment of gene signatures associated with stem cells and cancer relapse. This reprogramming was reverted by co-treatment with Wnt inhibitors. Our study demonstrates that MEK inhibition affects cellular plasticity and induces an intestinal stem cell program which constitutes a novel mechanism of drug resistance.
2018-05-08 | GSE114059 | GEO