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Links from GEO DataSets

Items: 20

1.

Expression profiling of BRAFV600E melanoma cell lines upon RAF inhibition

(Submitter supplied) Microarray expression analysis to identify global changes in transcription in response to RAF inhibition. Genes under RAF control were identified in a panel of BRAFV600E tumor cells, following the short-term inhibition of RAF using a pan-RAF kinase inhibitor, PLX4032 (Plexxikon). For comparison with changes in gene expression in response to MEK inhibition using PD0325901 (Pfizer), the following array data was referenced: (http://www.ncbi.nlm.nih.gov/geo/ (accession no. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL571
12 Samples
Download data: CEL
Series
Accession:
GSE20051
ID:
200020051
2.

Genome-wide copy number variation in human metastatic melanoma cell lines

(Submitter supplied) Illumina HumanExon510S-DUO bead arrays (Illumina Inc) were performed according to the manufacturer's protocol.
Organism:
Homo sapiens
Type:
Genome variation profiling by SNP array; SNP genotyping by SNP array
Platform:
GPL6988
4 Samples
Download data: TXT
Series
Accession:
GSE24890
ID:
200024890
3.

Expression data from melanoma cell lines

(Submitter supplied) Differential gene expression analysis of parental and resistant sub-lines of melanoma cell lines treated or untreated with PLX4032 Using microarray we sought to obtain a genome-wide profile of differentially expressed genes in parental melanoma cell lines and resistant sub-lines in response to PLX4032 vs DMSO control treatment.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
24 Samples
Download data: CEL, TXT
Series
Accession:
GSE24862
ID:
200024862
4.

RNA-seq melanoma

(Submitter supplied) Using a chromatin regulator-focused shRNA library, we found that suppression of sex determining region Y-box 10 (SOX10) in melanoma causes resistance to BRAF and MEK inhibitors. To investigate how SOX10 loss leads to drug resistance, we performed transcriptome sequencing (RNAseq) of both parental A375 (Ctrl. PLKO) and A375-SOX10KD (shSOX10-1, shSOX10-2) cells. To ask directly whether SOX10 is involved indrug resistance in BRAF(V600E) melanoma patients, we isolated RNA from paired biopsies from melanoma patients (pre- and post- treatment) , that had gained BRAF or MEK inhibitor resistance . more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
9 Samples
Download data: TXT
Series
Accession:
GSE50535
ID:
200050535
5.

Identification of super-enhancers in colorectal cancer cell lines

(Submitter supplied) H3K27 acetylation statuses were analyzed in four colon cancer cell lines (RKO, Caco2, SW48, and SW620), and colorectal cancer-specific super-enhancers were identified.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
8 Samples
Download data: WIG
Series
Accession:
GSE96069
ID:
200096069
6.

Time course of MEK inhibition

(Submitter supplied) This study used microarray expression analysis to identify global changes in transcript alteration in response to MEK inhibition. Genes under ERK control were identified in a representative V600E BRAF cell line as a function of time following exposure to a small molecule inhibitor of MEK. Keywords: Time course
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL571
4 Samples
Download data: CEL
Series
Accession:
GSE10088
ID:
200010088
7.

Paired MEK inhibited and control

(Submitter supplied) This study used microarray expression analysis to identify global changes in transcript alteration in response to MEK inhibition. Genes under ERK control were identified in a panel of V600E BRAF and RTK-activated tumor cells and xenografts, using short-term inhibition of ERK activity using the MEK inhibitor PD0325901 (Pfizer). Keywords: paired treatment and control
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL571
32 Samples
Download data: CEL
Series
Accession:
GSE10087
ID:
200010087
8.

Expression profiling of V600E BRAF and RTK-activated cells upon MEK inhibition

(Submitter supplied) This study used microarray expression analysis to identify global changes in transcript alteration in response to MEK inhibition. Genes under ERK control were identified in a panel of V600E BRAF and RTK-activated tumor cells and xenografts, using short-term inhibition of ERK activity using the MEK inhibitor PD0325901 (Pfizer). This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL571
36 Samples
Download data: CEL
Series
Accession:
GSE10086
ID:
200010086
9.

Antitumor efficacy of RAF inhibitor GDC-0879 involving BRAFV600E mutational status and ERK/MAPK pathway suppression

(Submitter supplied) Unsupervised hierarchical clustering revealed a strong similarity in gene modulation resulting from either compound treatment or BRAF ablation mediated by RNA interference relative to DMSO-treated control samples . Keywords: Expression Array
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
30 Samples
Download data: CEL
Series
Accession:
GSE13487
ID:
200013487
10.

An NKX2-1/ERK/WNT feedback loop modulates gastric identity and response to targeted therapy in lung adenocarcinoma.

(Submitter supplied) Cancer cells often undergo lineage switching during their natural progression and in response to therapy. Lung adenocarcinomas (LUADs) exhibit a variety of differentiation states accompanied by dysregulation of lineage-specific transcription factors such as NKX2-1. Loss of NKX2-1 in human and murine LUAD leads to invasive mucinous adenocarcinoma (IMA), a subtype of lung cancer that exhibits pulmonary to gastric transdifferentiation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL17021 GPL24247
21 Samples
Download data: MTX, TSV, TXT
Series
Accession:
GSE145152
ID:
200145152
11.

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
12.

Analysis of A375 and A375 clones that acquired resistance to GSK2118436 after treatment with GSK2118436 (GSK436), GSK1120212 (GSK212), or the combination of GSK2118436 and GSK1120212 for 24 hour

(Submitter supplied) In an effort to understand the mechanisms of acquired resistance to BRAF inhibitors, we isolated clones that acquired resistance to the BRAF inhibitor GSK2118436 derived from the A375 BRAF V600E mutant melanoma cell line. This resistance clones acquired mutations in NRAS and MEK1. One clones, 16R6-4, acquired two mutations in NRAS – Q61K and A146T. Proliferation and western blot analyses demonstrated that these clones were insensitive to single agent GSK2118436 or GSK1120212 (an allosteric MEK inhibitor) but were sensitive to the combination of GSK2118436 and GSK1120212. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
38 Samples
Download data: CEL
Series
Accession:
GSE35230
ID:
200035230
13.

Braf inhibitors reverse the unique molecular signature and phenotype of hairy cell leukemia, and exert anti-leukemic activity

(Submitter supplied) Hairy cell leukemia (HCL) shows unique clinico-pathological and biological features. HCL responds well to purine analogues but relapses are frequent and novel therapies are required. BRAF-V600E is the key driver mutation in HCL and distinguishes it from other B-cell lymphomas, including HCL-like leukemias/lymphomas (HCL-variant and splenic marginal zone lymphoma). The kinase-activating BRAF-V600E mutation also represents an ideal therapeutic target in HCL. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
24 Samples
Download data: CEL
Series
Accession:
GSE63790
ID:
200063790
14.

Functional characterization of a PROTAC directed against BRAFV600E

(Submitter supplied) The RAF family kinases function in the RAS-ERK pathway to transmit signals from activated RAS to the downstream kinases MEK and ERK. This pathway regulates cell proliferation, differentiation, and survival enabling mutations in RAS and RAF to act as potent drivers of human cancers. Drugs targeting the prevalent oncogenic mutant BRAFV600E have shown great efficacy in the clinic but long-term effectiveness is limited by resistance mechanisms that often exploit the dimerization-dependent process by which RAF kinases are activated. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
21 Samples
Download data: TXT
15.

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
16.

Gene expression data from human metastatic melanoma tumors that may predict response to RAF265

(Submitter supplied) To determine how mutation of BRAF affected the response to RAF265, we utilized a tumor orthotopic implant model of early passage melanoma tumors in nude mice from a series of 17 patients with advanced metastatic Tumor growth was compared between RAF265 treatment (40 mg/kg, QD) and diluent control groups. The melanoma associated gene mutation profile and global gene expression profile were determined on these human melanoma samples by SNaPshot and Affymetrix Human Gene ST 1.0 Array, respectively. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
42 Samples
Download data: CEL
Series
Accession:
GSE30812
ID:
200030812
17.

Gene Signature for Aggression of Melanoma Metastases - Melanoma Metastasis

(Submitter supplied) Metastasis is the deadliest phase of cancer progression. Experimental models using immunodeficient mice have been used to gain insights into the mechanisms of metastasis. We report here the identification of a “metastasis aggressiveness gene expression signature” derived using human melanoma cells selected based on their metastatic potentials in a xenotransplant metastasis model. Comparison with expression data from human melanoma patients shows that this metastasis gene signature correlates with the aggressiveness of melanoma metastases in human patients. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS3966
Platform:
GPL96
83 Samples
Download data: CEL
Series
Accession:
GSE8401
ID:
200008401
18.
Full record GDS3966

Melanoma metastasis

Analysis of melanoma clinical samples representing 31 primary melanomas and 52 melanoma metastases. These results, together with results from tumor samples from highly-metastatic derivatives of an A375 (ATCC) melanoma cell line, provide insight into the molecular basis of metastasis.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 disease state sets
Platform:
GPL96
Series:
GSE8401
83 Samples
Download data: CEL
19.

Expression of BRAF inhibitor resistant colon cancer lines

(Submitter supplied) Colon cancer cell lines with partial sensitivity to the BRAF inhibitor PLX4720 were grown in increasing concentration of the drug to develop acquired resistance. Gene expression was performed for comparison of the resistant clones to the parental lines.
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4700
Platform:
GPL570
4 Samples
Download data: CEL
Series
Accession:
GSE34299
ID:
200034299
20.
Full record GDS4700

Colon cancer cell lines with acquired resistance to BRAF inhibitor

Analysis of HT29 and Colo205 parental colorectal cancer (CRC) cell lines and HT29 and Colo205 clones with acquired resistance to BRAF inhibitor PLX4720. BRAF is a protein kinase in the RAS/RAF/MEK/ERK pathway. Results provide insight into mechanisms of acquired resistance to BRAF inhibitors in CRC.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 4 cell line sets
Platform:
GPL570
Series:
GSE34299
4 Samples
Download data: CEL
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