GEO DataSets

(Submitter supplied) Targeting components of the mitogen-activated protein kinase (MAPK) pathway prolongs survival of patients with advanced BRAFV600E melanomas but such an approach is not curative because of the rapid acquisition of numerous resistance mechanisms. Here we analyze melanoma cells that evade MAPK inhibitors by undergoing a senescence-like, slow-growth, phenotype, which leads to acquired resistance. The initial therapeutic response is characterized by an integrated stress response program, including stimulation of autophagic flux, activation of the endoplasmic reticulum machinery, and an enhanced ability of detoxifying reactive oxygen species. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

14 Samples

Download data: TXT

(Submitter supplied) Melanoma resistant to MAPK inhibitors (MAPKi) displays loss of fitness upon experimental MAPKi withdrawal and, clinically, may be resensitized to MAPKi therapy after a drug holiday. Here, we uncovered and therapeutically exploited the mechanisms of MAPKi addiction in MAPKi-resistant BRAF MUT or NRAS MUT melanoma. MAPKi-addiction phenotypes evident upon drug withdrawal spanned transient cell-cycle slowdown to cell-death responses, the latter of which required a robust phosphorylated ERK (pERK) rebound. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

6 Samples

Download data: XLSX

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing

Platform:

GPL24676

29 Samples

Download data: CSV, TXT

(Submitter supplied) To analyse the RNA expression differences between melanoma tumour samples treated with BRAF and MEK-inhibitors at different time points

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24676

17 Samples

Download data: TXT

(Submitter supplied) To analyse smallRNA expression differences between A375 and A375-BIR during the treatment with dabrafenib (DAB)

Organism:

Homo sapiens

Type:

Non-coding RNA profiling by high throughput sequencing

Platform:

GPL24676

12 Samples

Download data: CSV

(Submitter supplied) Therapeutic targeting of BRAFV600E has shown a significant impact on progression-free and overall survival in advanced melanoma, but only a fraction of patients benefit from these treatments, suggesting that additional signaling pathways involved in melanoma growth/survival need to be identified. In fact MAPK and PI3K/mTOR signaling pathways are constituively activated in most cancers, including melanoma, to sustain the melanoma growth/survival. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

24 Samples

Download data: TXT

(Submitter supplied) Metastatic melanoma is either intrinsically resistant or rapidly acquires resistance to targeted therapy treatments, such as MAPK inhibitors. A leading cause of resistance to targeted therapy is a dynamic transition of melanoma cells from a proliferative to a highly invasive state, a phenomenon called phenotype switching. Mechanisms regulating phenotype switching represent potential targets for improving treatment of melanoma patients. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL16791

4 Samples

Download data: BED, BIGWIG

(Submitter supplied) The prognosis for most patients with advanced malignant melanoma is traditionally very poor, as the disease is either intrinsically resistant or rapidly acquires resistance to targeted therapy treatments. Here, using a drug screen targeting chromatin regulators in patient-derived 3D melanoma cell cultures, we discovered that PARP inhibitors are capable of restoring MAPKi sensitivity. This synergy was found to be independent of DNA damage repair pathways and was effective both in vitro and in vivo in patients-derived xenografts. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

24 Samples

Download data: TXT

(Submitter supplied) ETV1 is an oncogene in GIST and melanoma and a downstream transcriptional effector of MAP kinase signaling. Here, mapped the ETV1 binding sites in GIST and melanoma cell lines using ChIP-seq.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL9115 GPL11154

8 Samples

Download data: NARROWPEAK

(Submitter supplied) ETV1 is amplified in a subset of melanomas. Here, we performed RNA-seq on two BRAF V600E mutant melonoma cell lines transduced with a scrambed shRNA and two individual ETV1 shRNA

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

6 Samples

Download data: TXT

(Submitter supplied) COP1 regulates MAP kinase dependent stability Pea3 transcription factors. We determined the role of COP1 in the regulation of MAP kianse transciptional output. We generated A375 melanoma cells with CRISPR/Cas9 mediated COP1 (gene symbol RFWD) knockout. We treated control sgEGFP and COP1 loss sgCOP1 cells with vehicle, 1 µM vemurafinib, or 5 nM trametinib for 8 hours and isolated RNA for sequencing.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

6 Samples

Download data: TXT

(Submitter supplied) COP1 regulates MAP kinase dependent stability Pea3 transcription factors. We determined the role of COP1 in the regulation of MAP kianse transciptional output. We transfected GIST882 cells with siRNA against a scrambled sequence and two sequences against COP1. We treated cells for 8 hours with vehicle or 100 nM PD0325901 in duplicate and isolated RNA for sequencing.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

12 Samples

Download data: TXT

(Submitter supplied) Combined proteomic and RNAseq analysis on 6 melanoma cell cultures reveals a signature for resistance to MAPKi resistance.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

6 Samples

Download data: TXT

(Submitter supplied) Our aim is to compare whole-genome expression profiles of partially reprogrammed C790 melanoma murine cells after induction of stem cell related genes (+ dox vs -dox)

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL25831

6 Samples

Download data: TXT

(Submitter supplied) Our aim is to compare whole-genome expression profiles of partially reprogrammed 4434 melanoma murine cells after induction of stem cell related genes (+ dox vs -dox)

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

6 Samples

Download data: CEL

(Submitter supplied) Our aim is to compare whole-genome expression profiles of partially reprogrammed C790 melanoma murine cells ( - dox vs + dox) after treatment with trametinib, in order to identify potential candidates related with drug resistance.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

12 Samples

Download data: CEL

(Submitter supplied) We report the changes in translatome of a commercially available melanoma line upon acquisition of therapy resistance

Organism:

Homo sapiens

Type:

Other

Platform:

GPL18573

26 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array; Expression profiling by high throughput sequencing; Methylation profiling by genome tiling array

Platforms:

GPL17692 GPL11154 GPL13534

218 Samples

Download data: CEL, IDAT

(Submitter supplied) 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. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

70 Samples

Download data: TXT

(Submitter supplied) 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. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17692

4 Samples

Download data: CEL