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Links from GEO DataSets

Items: 17

1.

The effect of MEK inhibition on transcription in melanoma

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL14550
76 Samples
Download data: TXT
Series
Accession:
GSE51115
ID:
200051115
2.

The effect of MEK inhibition, Interferon beta, and their combination on transcription in melanoma

(Submitter supplied) We examined the transcriptional effect of interferon beta, MEK inhibition or their combination on 6 melanoma cell lines 3 cell lines have high basal acitvity of the interferon pathway, and 3 have low basal activity
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL14550
24 Samples
Download data: TXT
Series
Accession:
GSE51114
ID:
200051114
3.

The effect of MEK inhibition on transcription in melanoma [Batch 2]

(Submitter supplied) In order to reveal the downstream targets of MAPK in melanoma, we measured the expression of 14 melanoma cell lines pre and post MEK inhibition
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL14550
28 Samples
Download data: TXT
Series
Accession:
GSE51113
ID:
200051113
4.

The effect of MEK inhibition on transcription in melanoma [Batch 1]

(Submitter supplied) In order to reveal the downstream targets of MAPK in melanoma, we measured the expression of 12 melanoma cell lines pre and post MEK inhibition
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL14550
24 Samples
Download data: TXT
Series
Accession:
GSE51051
ID:
200051051
5.

MEK Inhibition Overcomes Cisplatin Resistance Conferred by SOS/MAPK Pathway Activation in Squamous Cell Carcinoma (SCC)

(Submitter supplied) Genomic analyses of SCC have yet to yield significant strategies against pathway activation to improve treatment. Platinum-based chemotherapy remains the mainstay of treatment for SCC of different histotypes either as a single agent or alongside other chemotherapeutic drugs or radiotherapy; however, resistance inevitably emerges, which limits the duration of treatment response. To elucidate mechanisms that mediate resistance to cisplatin, we compared drug-induced perturbations to gene expression between cisplatin-sensitive and -resistant SCC cells.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
32 Samples
Download data: CEL
Series
Accession:
GSE66549
ID:
200066549
6.

Expression data from exponentially proliferating ovarian cancer cell lines

(Submitter supplied) We used microarrays to assess gene expression in proliferating ovarian cancer cell lines
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
98 Samples
Download data: CEL
Series
Accession:
GSE43765
ID:
200043765
7.

MX2 mediates establishment of interferon response profile, regulates XAF1 and can sensitize melanoma cells to targeted therapy  

(Submitter supplied) The goal of the study was to identify downstream genes affected by overexpresion on MX2 gene in a huma melanoma cell line WM983
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
9 Samples
Download data: CSV
8.

Gene expression profile of peripheral blood lymphocytes: comparison between melanoma patients and healthy controls

(Submitter supplied) We focused on the major peripheral blood lymphocyte populations that may be involved in anti-tumor responses and negatively impacted by cancer, specifically CD8 T cells, CD4 T cells, B cells and CD56dim natural killer cells. The pure cell subsets were stringently sorted by flow cytometry from PBMC samples. Gene expression profiles of these cell populations from melanoma patients were compared to healthy controls. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS2735
Platform:
GPL887
46 Samples
Download data
Series
Accession:
GSE6887
ID:
200006887
9.
Full record GDS2735

Metastatic melanoma: peripheral blood lymphocytes

Analysis of sorted peripheral blood lymphocytes (CD8 T cells, CD4 T cells, B cells, NK cells) from patients with melanoma. These subpopulations are involved in antitumor responses and negatively impacted by cancer. Results provide insight into molecular mechanisms of immune dysfunction in cancer.
Organism:
Homo sapiens
Type:
Expression profiling by array, log2 ratio, 4 cell type, 2 disease state sets
Platform:
GPL887
Series:
GSE6887
46 Samples
Download data
10.

Identification of direct transcriptional targets of V600EBRAF/MEK in melanoma

(Submitter supplied) A375P melanoma cells were treated with 1uM of the MEK inhibitor PD184352 or 0.4uM of the V600EBRAF inhibitor PLX4720 for 2hr, 6hr and 24hrs. DMSO treatment for 2hr, 6hr and 24hrs serves as the negative control
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL5175
9 Samples
Download data: CEL
Series
Accession:
GSE17089
ID:
200017089
11.

Adaptive resistance of melanoma cells to RAF inhibition via reversible induction of a slowly-dividing de-differentiated state

(Submitter supplied) Treatment of BRAF-mutant melanomas with MAP-kinase pathway inhibitors is paradigmatic of the promise of precision cancer therapy but also highlights problems with drug resistance that limit patient benefit. We use live-cell imaging, single-cell analysis and molecular profiling to show that exposure of tumor cells to RAF/MEK inhibitors elicits a heterogeneous response in which some cells die, some arrest and a remaining fraction adapts to drug. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
12 Samples
Download data: TXT
Series
Accession:
GSE87641
ID:
200087641
12.

Gene expression of the A375 melanoma cell line treated with RAF inhibitors Vemurafenib and time-course with EGF stimulation during Vemurafenib RAF inhibitor treatment alone or with the MEK inhibitor Cobimetinib

(Submitter supplied) We treated for 24 hours the BRAF-V600E melanoma cell line A375 with 7 doses of the RAF inhibitor Vemurafenib and, in a second experimental desing, we treated for 24 hours the BRAF-V600E melanoma cell line A375 with Vemurafenib (1 uM) alone or in combination with the MEK inhibitor Cobimetinib (1 uM) and subsequently stimulated with EGF in a time-course of 7 time points for up to 8 hours (0, 0.5, 1, 2, 3, 4, 8 hours).
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
96 Samples
Download data: CSV
13.

Somatic Loss of Wild-Type Kras Enhances Cancer Fitness and Promotes MEK Dependence

(Submitter supplied) Investigating therapeutic “outliers” that show exceptional responses to anti-cancer treatment can reveal unexpected synthetic lethal interactions and uncover biomarkers of drug sensitivity. Preclinical trials investigating primary murine acute myeloid leukemias (AMLs) generated by retroviral insertional mutagenesis in KrasG12D “knock-in” mice showed that the MEK inhibitor PD0325901 (PD901) extended survival while the pan-phosphoinositide 3-kinase (PI3K) inhibitor GDC-0941 was ineffective. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE92682
ID:
200092682
14.

Expression data from BRAF-mutant melanoma cell lines

(Submitter supplied) Melanoma cell lines were assessed for differences in gene expression patterns between the lines sensitive and resistant to BRAF and MEK inhibitor drugs.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
46 Samples
Download data: CEL
Series
Accession:
GSE45558
ID:
200045558
15.

HDAC inhibition enhances the in vivo efficacy of MEK inhibitor therapy in uveal melanoma

(Submitter supplied) Purpose: The clinical use of MEK inhibitors in uveal melanoma is limited by the rapid acquisition of resistance. The current study has used unbiased multi-omics and drug screens to identify the pan-HDAC inhibitor panobinostat as an effective strategy to limit MEK inhibitor resistance.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
8 Samples
Download data: TXT
16.

Comparative gene expression profiles of immune inhibitory and non-inhibitory melanoma cell lines

(Submitter supplied) Dysfunction in type I interferon (IFN) signaling occurs in patients with stage II or more advanced cancer. After screening the effects of a panel of 12 melanoma cell lines on PBMCs of healthy volunteers of IFNalpha signal pathway, two groups of melanoma cell lines could be identified one with stronger suppression (low pSTAT-1 group) than the other (high pSTAT-1 group). Comparative global gene expression between two groups identified 6771 differential expression genes. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
65 Samples
Download data: CEL
Series
Accession:
GSE44851
ID:
200044851
17.

CGH array profiles of melanoma cell lines

(Submitter supplied) Dysfunction in type I interferon (IFN) signaling occurs in patients with stage II or more advanced cancer. After screening the effects of a panel of 12 melanoma cell lines on PBMCs of healthy volunteers of IFNalpha signal pathway, two groups of melanoma cell lines could be identified one with stronger suppression (low pSTAT-1 group) than the other (high pSTAT-1 group). Comparative genomic hybridization (CGH) identified consistent amplification of 12q22-24 as a genomic marker for the immune suppressive melanoma cell lines. more...
Organism:
Homo sapiens
Type:
Genome variation profiling by array
Platform:
GPL4093
12 Samples
Download data: TXT
Series
Accession:
GSE44850
ID:
200044850
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