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Expression data (A2058) after treatment with MAPKi, HDACi or both

ABSTRACT: Expression data (A2058) after treatment with MAPKi, HDACi or both

PROVIDER: PRJNA516830 | ENA |

REPOSITORIES: ENA

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Expression data (A2058) after treatment with MAPKi, HDACi or both

Project description:Transcriptional profiles were examined in A2058 melanoma cells treated with vehicle (DMSO), dabrafenib+trametinib (DT, MAPKi), entinostat (E, HDACi) or all 3 agents (DTE) at 24 hours, prior to the commencement of cell death, to investigate the molecular mechamism by which these drugs and their combinations are functioning.

2019-01-25 | GSE125560 | GEO

Expression data (Hs695T) after treatment with MAPKi, HDACi or both

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Expression data (SKMEL2) after treatment with MAPKi, HDACi or both

Project description:Transcriptional profiles were examined in SKMEL2 melanoma cells treated with vehicle (DMSO), dabrafenib+trametinib (DT, MAPKi), entinostat (E, HDACi) or all 3 agents (DTE) at 24 hours, prior to the commencement of cell death, to investigate the molecular mechamism by which these drugs and their combinations are functioning.

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Expression data of 3 melanoma cell lines after treatment with MAPKi, HDACi or both

Project description:Expression data of 3 melanoma cell lines after treatment with MAPKi, HDACi or both

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TGFβ1 treatment of A2058 melanoma cells

Project description:4 replicates were prepared from A2058 melanoma cells [transfected with 10ng of empty vector (pcDNA3.1+)] and treated with 5ng/ml TGFβ1 or vehicle control for 24hrs This is the control arm of a larger experiment where cells transfected with a particular expression plasmid were treated with TGFβ1 or control vehicle. The transfection with the expresion plasmid was unsucessful so this empty vector data has been used alone to simply examine the effect of TGFβ1 treatment on A2058 cells.

2015-02-20 | E-GEOD-66114 | biostudies-arrayexpress

TGFβ1 treatment of A2058 melanoma cells

Project description:4 replicates were prepared from A2058 melanoma cells [transfected with 10ng of empty vector (pcDNA3.1+)] and treated with 5ng/ml TGFβ1 or vehicle control for 24hrs

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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.

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Expression changes in Melanomas pre MAPKi treatment vs. on MAPKi treatment (RNA-seq)

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