Similar studies for GEO DataSets (Select 200051113) - GEO DataSets

Select item 2000511131.

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

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000511152.

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

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000511143.

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

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000510514.

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

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000665495.

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

Select item 2000437656.

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

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Select item 2001681027.

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

Series

Accession:: GSE168102

ID:: 200168102

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 2000170898.

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

Select item 2000876419.

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

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20012798810.

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

Series

Accession:: GSE127988

ID:: 200127988

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 20009268211.

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

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20004555812.

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

Select item 20012794813.

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

Series

Accession:: GSE127948

ID:: 200127948

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 20004485114.

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

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20004485015.

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

PubMed Full text in PMC Similar studies Analyze with GEO2R

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