Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MAPK-related gene signature predicting MAPKi sensitivity in pLGG - Charite cohort

ABSTRACT: MAPK-related gene signature predicting MAPKi sensitivity in pLGG - Charite cohort

PROVIDER: PRJNA921878 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23018162_1.fastq.gz	Fastqsanger.gz
	SRR23018162_2.fastq.gz	Fastqsanger.gz
	SRR23018163_1.fastq.gz	Fastqsanger.gz
	SRR23018163_2.fastq.gz	Fastqsanger.gz
	SRR23018164_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Project description:MAPK-related gene signature predicting MAPKi sensitivity in pLGG - McGill cohort

| PRJNA921881 | ENA

Project description:MAPK-related gene signature predicting MAPKi sensitivity in pLGG

| PRJNA921876 | ENA

Project description:MAPK inhibitor sensitivity scores (MSS) were developed to predict sensitivity to MAPK inhibitors in pediatric low-grade gliomas (pLGG). The scores were validated in pLGG cell lines in vitro and in the publicly available Open Pediatric Brain Tumor Atlas dataset. Validation in independent datasets is warranted.

2023-06-28 | GSE222405 | GEO

2023-06-28 | GSE222404 | GEO

Drug-class specific gene-based MAPK sensitivity scores predict sensitivity to MAPK inhibitors in pediatric low-grade gliomas

Project description:Pediatric low-grade gliomas (pLGG) have shown heterogeneous responses to MAPK inhibitors (MAPKi) in clinical trials. A predictive feature for stratification is needed to identify patients likely to benefit from MAPKi therapy. MAPK-related genes differentially regulated between MAPKi sensitive and non-sensitive cell lines from the Genomics of Drug Sensitivity in Cancer dataset identified class-specific MAPKi sensitivity gene signatures used to calculate the MAPKi sensitivity score (MSS) via single sample gene set enrichment analysis. The MSS discerned gliomas with varying MAPK alterations from those without, and was higher in pLGG compared to other pediatric CNS tumors. As in clinical trials, the MSS was heterogeneous within pLGGs with a common MAPK alteration. A positive correlation between the MSS and the predicted immune infiltration determined by the ESTIMATE signature was observed. The MSS therefore represents a potential tool for the stratification of pLGG patients, worth of further investigation in upcoming clinical trials. Our data could support a role of microglia in the response to MAPKi, warranting further validation.

2023-06-27 | GSE222850 | GEO

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

2023-06-27 | GSE222406 | GEO

RNAseq changes in pre MAPKi treatment and post MAPKi resistance Melanomas

Project description:Melanoma resistance to MAPK- or T cell checkpoint-targeted therapies represents a major clinical challenge, and treatment failures of MAPK-targeted therapies due to acquired resistance often require salvage immunotherapies. We show that genomic analysis of acquired resistance to MAPK inhibitors revealed key driver genes but failedto adequately account for clinical resistance. From a large-scale comparative analysis of temporal transcriptomes from patient-matched tumor biopsies, we discovered highly recurrent differential expression and signature outputs of c-MET, LEF1 and YAP1 as drivers of acquired MAPK inhibitor resistance. Moreover, integration of gene- and signature-based transcriptomic analysis revealed profound CD8 T cell deficiency detected in half of resistant melanomas in association with downregulation of dendritic cells and antigen presentation. We also propose a major methylomic basis to transcriptomic evolution under MAPK inhibitor selection. Thus, this database provides a rich informational resource, and the current landscape represents a benchmark to understanding melanoma therapeutic resistance. Melanoma biopsies pre and post MAPKi treatment were sent for RNAseq analysis

2015-09-15 | E-GEOD-65185 | biostudies-arrayexpress

Expression changes in pre MAPKi treatment and post MAPKi resistance Melanomas

2015-09-15 | E-GEOD-65184 | biostudies-arrayexpress

Methylation changes in pre MAPKi treatment and post MAPKi resistance Melanomas

2015-09-15 | E-GEOD-65183 | biostudies-arrayexpress

Expression changes in Melanomas pre MAPKi treatment vs. on MAPKi treatment (Affymetrix)

Project description:Treatment of advanced V600BRAF mutant melanoma using a BRAF inhibitor (BRAFi) or its combination with a MEKi typically elicits partial responses. We compared the transcriptomes of patient-derived tumors regressing on MAPKi therapy against MAPKi-induced temporal transcriptomic states in human melanoma cell lines or murine melanoma in immune-competent mice. Despite heterogeneous dynamics of clinical tumor regression, residual tumors displayed highly recurrent transcriptomic alterations and enriched processes, which were also observed in MAPKi-selected cell lines (implying tumor cell-intrinsic reprogramming) or in bulk mouse tumors (and the CD45-negative or -positive fractions,, implying tumor cell-intrinsic or stromal/immune alterations, respectively). Tumor cell-intrinsic reprogramming attenuated MAPK-dependency, while enhancing mesenchymal, angiogenic and IFN-inflammatory features and growth/survival dependence on multi-RTKs and PD-L2. In the immune compartment, PD-L2 upregulation in CD11c+ immunocytes drove the loss of T-cell inflammation and promoted BRAFi resistance. Thus, residual melanoma early on MAPKi therapy already displays potentially exploitable adaptive transcriptomic, epigenomic, immune-regulomic alterations.

2017-09-05 | GSE75311 | GEO