Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA273361 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression changes in pre MAPKi treatment and post MAPKi resistance Melanomas
| PRJNA273360 | ENA
Project description:RNAseq changes in pre MAPKi treatment and post MAPKi resistance Melanomas
| PRJNA273359 | ENA
Project description:Expression changes in Melanomas pre MAPKi treatment vs. on MAPKi treatment (Affymetrix)
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Project description:Expression changes in Melanomas pre MAPKi treatment vs. on MAPKi treatment (RNA-seq_Patient.batch3)
| PRJNA403850 | ENA
Project description:Expression changes in Melanomas pre MAPKi treatment vs. on MAPKi treatment (RNA-seq)
| PRJNA303170 | ENA
Project description:Expression changes in melanoma cell lines pre MAPKi treatment vs. post-MAPKi resistance (RNA-seq_CellLine.batch2)
| PRJNA403816 | ENA
Project description:Expression changes in Melanomas pre MAPKi treatment vs. on MAPKi treatment
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Project description:Expression changes in Melanomas pre MAPKi treatment vs. on MAPKi treatment [Y1.7.FPKM.batch1.2]
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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 DNA methylation analysis using Illumina Human Methylation 450K bead chips
2015-09-15 | E-GEOD-65183 | biostudies-arrayexpress
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