EGAS00001000815-sc-20170327 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001003260 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:A panel of 17 human melanoma cell lines with known BRAF and NRAS mutation status was stimulated with TNF-alpha for 72 hours. The goal of the study was to correlate the transcriptional response in BRAF versus NRAS mutated melanoma cell lines.
2014-02-10 | GSE51221 | GEO
Project description:Among children with multiple congenital melanocytic naevi (CMN), 25% have no established genetic cause. Here, we study 169 CMN patients, 38 of whom were double wild-type for NRAS/BRAF mutations. Nineteen of these 38 patients had sufficient tissue to undergo RNAseq, which revealed mosaic BRAF fusions in 11/19 patients and mosaic RAF1 fusions in 1/19. These findings offer a genetic diagnosis to an additional group of patients opening the possibility for treatment options.
2023-09-30 | E-MTAB-13182 | biostudies-arrayexpress
Project description:Recent technological advances in single-cell genomics make it possible to analyze cellular heterogeneity of tumor samples. Here, we applied single-cell RNA-seq to measure the transcriptomes of 307 single cells cultured from three biopsies of three different patients with a BRAF/NRAS wild type, BRAF mutant/NRAS wild type and BRAF wild type/NRAS mutant melanoma metastasis, respectively. Analysis based on self-organizing maps identified sub-populations defined by multiple gene expression modules involved in proliferation, oxidative phosphorylation, pigmentation and cellular stroma. Gene expression modules had prognostic relevance when compared with gene expression data from published melanoma samples and patient survival data. We surveyed kinome expression patterns across sub-populations of the BRAF/NRAS wild type sample and found that CDK4 and CDK2 were consistently highly expressed in the majority of cells, suggesting that these kinases might be involved in melanoma progression. Treatment of cells with the CDK4 inhibitor palbociclib restricted cell proliferation to a similar, and in some cases greater, extent than MAPK inhibitors. Finally, we identified a low abundant sub-population in this sample that highly expressed a module containing ABC transporter ABCB5, surface markers CD271 and CD133, and multiple aldehyde dehydrogenases (ALDHs), as markers for melanoma stem or initiating cells. Patient-derived cultures of the BRAF mutant/NRAS wild type and BRAF wild type/NRAS mutant metastases showed more homogeneous single-cell gene expression patterns with gene expression modules for proliferation and ABC transporters. Taken together, our results describe an intertumor and intratumor heterogeneity in melanoma short-term cultures which might be relevant for patient survival, and suggest promising targets for new treatment approaches in melanoma therapy.
2017-01-12 | GSE81383 | GEO
Project description:A panel of 17 human melanoma cell lines with known BRAF and NRAS mutation status was stimulated with TNF-alpha for 72 hours. The goal of the study was to correlate the transcriptional response in BRAF versus NRAS mutated melanoma cell lines. Total RNA was obtained from a panel of 17 human melanoma cell lines treated for 72 hours with TNF-alpha or left untreated. Gene expression profiling was done using the Illumina Human HT12 v4 platform.
2014-02-10 | E-GEOD-51221 | biostudies-arrayexpress
Project description:Despite recent therapeutic advances in the management of BRAFV600-mutant melanoma, there is still a compelling need for more effective treatments for patients who developed BRAF/NRAS wild type disease. Since the activity of single targeted agents is limited by innate and acquired resistance, we performed a high-throughput drug screen using 180 drug combinations to generate over 17,000 viability curves, with the aim of identifying agents that synergise to kill BRAF/NRAS wild type melanoma cells. From this screen we identified a promising drug combination that efficiency kills 30% of melanoma cell lines. We validated in vivo the synergy of the drug combination and found a potential marker to identify sensitive tumors. We applied a genome-wide CRISPR screening which revealed that resistance mechanisms to the drug combination. In order to investigate the mechanism of drug synergy, we treated sensitive and resistance melanoma cell lines with the single drugs and the drug combination and performed proteome analyses to investigate the changes in total proteins and protein phosphorylation. These analysis highlighted specific pathway deregulations associated to the drug synergy that allowed to get a better understanding of the drug interaction and their efficacy in killing melanoma cell lines.
2022-03-23 | PXD007649 | Pride
Project description:Study of global gene expression differences in malignant melanoma cell lines with or without specific abberations in BRAF NRAS or CDKN2A.
2014-10-25 | GSE62682 | GEO
Project description:Cyclin dependent kinase 11 (CDK11) is a protein kinase that regulates RNA transcription, pre-mRNA splicing, mitosis, and cell death. Targeting of CDK11 expression levels is effective in the experimental treatment of breast and other cancers, but these data are lacking in melanoma. To understand CDK11 function in melanoma, we evaluated protein and RNA levels of CDK11, Cyclin L1 and Cyclin L2 in benign melanocytes and BRAF- as well as NRAS-mutant melanoma cell lines. We investigated the effectiveness of reducing expression of this survival kinase using RNA interference on viability, clonal survival, and tumorsphere formation in melanoma cell lines. We examined the impact of CDK11 loss in BRAF-mutant melanoma on more than 700 genes important in cancer signaling pathways. Follow-up analysis evaluated how CDK11 loss alters cell cycle function in BRAF- and NRAS-mutant melanoma cells. We present data on CDK11, CCNL1 and CCNL2 mRNA expression in melanoma patients, including prognosis for survival. In sum, we found that CDK11 is necessary for melanoma cell survival, and a major impact of CDK11 loss in melanoma is to cause disruption of the cell cycle distribution with accumulation of G1- and loss of G2/M-phase cancer cells.
2019-05-08 | GSE128693 | GEO
Project description:Among the myriad tumors analyzed to date, cutaneous malignant melanomas bear some of the highest mutational burdens. Thus, it is somewhat surprising that oncogene exclusion between is so pronounced in melanomas where there is only a single melanoma out of 366 sequenced specimens which harbors concurrent BRAF(V600E/M) and NRAS(G13R) mutations (TCGA-ES-A2NC Sample; WWW.bioportal.org), In this senario some NRAS and BRAF mutations co-expressing cells show slow growth phenotypes by under study mechanism. We used Affymetrix GeneChip Expression Arrays to detail the global programme of gene expression underlying oncogenic exclusion and identified distinct classes of up and down-regulated genes during this process.
2018-11-22 | GSE122835 | GEO
Project description:siRNA mediated DUSP4 silencing in a cell line derived from a) AKT/NRAS double injected hepatocellular carcinoma in a mouse by hydrodynamic injection => AKT/NRAS and b) these cell lines with Cre knockout for AKT => AKT/NRAS Cre
2022-11-06 | GSE217233 | GEO
Project description:Study of global gene expression differences in malignant melanoma cell lines with or without specific abberations in BRAF NRAS or CDKN2A. Expression .CEL files from Affymetrix HG-U133A 2.0 arrays using total RNA from 5 human cell lines derived from metastasized melanoma
2014-10-25 | E-GEOD-62682 | biostudies-arrayexpress