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Links from GEO DataSets

Items: 20

1.

Combinatorial treatments targeting MAPK and PI3K/mTOR pathways in metastatic melanoma

(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
Series
Accession:
GSE59882
ID:
200059882
2.

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
3.

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
4.

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
5.

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
6.

Molecular changes induced in melanoma cells by stromal cells and anti-BRAF therapy.

(Submitter supplied) Tumor-associated stromal cells can enable cancer cells to become insensitive to therapy. They can promote aggressive phenotype in cancer cells, which become less responsive to drugs such as BRAF inhibitors (BRAFi) used to treat melanomas. To clarify potential mechanism behind stromal influence on melanoma, we analyzed gene expression in Melmet 5 melanoma cells grown as mono-cultures or co-cultures with lung fibroblasts with/without BRAFi. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
12 Samples
Download data: TXT
Series
Accession:
GSE67637
ID:
200067637
7.

PI3K/AKT/mTOR and Sonic hedgehog pathways cooperate together to inhibit human pancreatic cancer stem cell characteristics and tumor growth

(Submitter supplied) Cancer stem cells (CSCs) play major roles in cancer initiation, progression, and metastasis. It is evident from growing reports that PI3K/Akt/mTOR and Sonic Hedgehog (Shh) signaling pathway are aberrantly reactivated in pancreatic CSCs. Here, we examined the efficacy of combining NVP-LDE-225 (PI3K/mTOR inhibitor) and NVP-BEZ-235 (Smoothened inhibitor) on pancreatic CSCs characteristics, microRNA regulatory network, and tumor growth. more...
Organism:
synthetic construct; Homo sapiens
Type:
Non-coding RNA profiling by array
Platform:
GPL16384
8 Samples
Download data: CEL
Series
Accession:
GSE70087
ID:
200070087
8.

Human BRAF-V600E melanoma cell lines drug sensitive vs drug resistant

(Submitter supplied) aCGH of human melanoma cell lines comparing parental (drug sensitve) vs isogenic drug resistant-derived subline
Organism:
Homo sapiens
Type:
Genome variation profiling by genome tiling array
Platform:
GPL9777
4 Samples
Download data: TXT
Series
Accession:
GSE49430
ID:
200049430
9.

Acquired resistance to MEK-CDK4/6 inhibitor combinations in cutaneous melanoma

(Submitter supplied) Continuous MEK and CDK4/6 inhibition is effective in pre-clinical models, nevertheless, some tumors acquire resistance that was associated with enhanced phospho S6. To characterize the mechanism mediating the upregulation of mTOR-S6 pathway in these tumors, we performed RNA sequencing and targeted panel sequencing on xenograft tumors that progressed on either MEK plus CDK4/6 inhibitors (ComboR) or control diet. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
12 Samples
Download data: TXT
10.

Pan-Raf co-operates with PI3K-dependent signaling and critically contributes to myeloma cell survival independently of mutated RAS

(Submitter supplied) The most common oncogenic mutations in multiple myeloma (MM) affect N- and K-RAS leading to constitutive activation of RAS-dependent signaling. Signal transduction via RAS, Raf and MAPK has been well described as a canonical pathway. In accordance with this assumption, we showed that the activity of the MEK/ERK module is strictly dependent on pan-Raf activity. However, inhibition of MEK/ERK has no or only minor effects on MM cell survival, whereas oncogenic Ras and pan-Raf critically contribute to survival of multiple myeloma cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
12 Samples
Download data: CEL
Series
Accession:
GSE75078
ID:
200075078
11.

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
12.
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
13.

protein levels in BRAF/MEK inhibitor resistance melanoma cells treated with PF3758309 [CR]

(Submitter supplied) 3 BRAF/MEK inhibitor resistance melanoma cells were treated with PAK inhibitor PF3758309 for 48 hr, the cell lysis were analyzed by RPPA profiling by protein array (RPPA)
Organism:
Homo sapiens
Type:
Protein profiling by protein array
Platform:
GPL23213
6 Samples
Download data: XLSX
Series
Accession:
GSE96902
ID:
200096902
14.

protein levels in BRAF inhibitor resistance melanoma cells treated with PF3758309

(Submitter supplied) 11 BRAF inhibitor resistance melanoma cells were treated with PAK inhibitor PF3758309 for 48 hr, the cell lysis were analyzed by RPPA profiling by protein array (RPPA)
Organism:
Homo sapiens
Type:
Protein profiling by protein array
Platform:
GPL23192
22 Samples
Download data: XLS
Series
Accession:
GSE96753
ID:
200096753
15.

Targeting the MTOR-AKT pathway in DLBCL

(Submitter supplied) The mTOR (mammalian Target of Rapamycin) pathway is constitutively activated in Diffuse Large B-Cell Lymphoma (DLBCL). mTOR inhibition has been shown to have clinical activity in patients with DLBCL, although overall response rates remain low. We therefore evaluated differences in the transcriptome between DLBCL cell lines with differential sensitivity to the mTOR inhibitor Rapamycin, to (A) identify gene-expression patterns(GEP) capable of identifying sensitivity to Rapamycin, (B) understand the underlying mechanisms of resistance to Rapamycin in DLBCL and (C) identify bioactive molecules likely to synergize with mTOR inhibitors. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4236
Platform:
GPL6244
14 Samples
Download data: CEL, CHP
Series
Accession:
GSE27255
ID:
200027255
16.
Full record GDS4236

Rapamycin-resistant diffuse large B-cell lymphoma cell lines

Analysis of diffuse large B-cell lymphoma (DLBCL) cell lines resistant to rapamycin, the prototypical mTOR (mammalian Target Of Rapamycin) inhibitor. The mTOR pathway is constitutively activated in DLBCL. Results provide insight into mechanisms of resistance to mTOR inhibition in DLBCL.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 14 cell line, 2 other sets
Platform:
GPL6244
Series:
GSE27255
14 Samples
Download data: CEL, CHP
17.

Predominance of MAPK reactivation in early resistance to debrafenib/trametinib combination therapy of BRAF mutant metastatic melanoma.

(Submitter supplied) One third of BRAF-mutant metastatic melanoma patients treated with combined BRAF and MEK inhibition progress within six months. Treatment options for these patients remain limited. Here we analyse twenty BRAFV600 mutant melanoma metastases derived from 10 patients treated with the combination of debrafenib and trametinib for resistance mechanisms and genetic correlates of response. Resistance mechanisms are identified in 9/11 progressing tumors and MAPK reactivation occurred in 9/10 tumors, commonly via BRAF amplification and mutations activating NRAS and MEK2. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
26 Samples
Download data: TXT
Series
Accession:
GSE61992
ID:
200061992
18.

Role of Apollon in human melanoma resistance to anti-tumor agents that activate the intrinsic or the extrinsic apoptosis pathways

(Submitter supplied) PURPOSE: To assess the role of Apollon in melanoma resistance to intrinsic and extrinsic pathways of apoptosis and to identify strategies to reduce its expression. EXPERIMENTAL DESIGN: Expression of Apollon was assessed in melanoma cell lines and in surgical specimens.Gene expression profiling, mitochondrial depolarization, caspases activation and apoptosis assays were used to test the effect of Apollon silencing, by siRNA, on melanoma response to different anti-tumor agents. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
24 Samples
Download data: TXT
Series
Accession:
GSE34686
ID:
200034686
19.

Systems analysis of adaptive responses to MAP Kinase pathway blockade in BRAF mutant melanoma.

(Submitter supplied) Fifty percent of cutaneous melanomas are driven by activated BRAFV600E, but tumors treated with RAF inhibitors, even when they respond dramatically, rapidly adapt and develop resistance. Thus, there is a pressing need to identify the major mechanisms of intrinsic and adaptive resistance and develop drug combinations that target these resistance mechanisms. In a combinatorial drug screen on a panel of 12 treatment-naïve BRAFV600E mutant melanoma cell lines of varying levels of resistance to MAPK pathway inhibition we identified the combination PLX4720, a targeted inhibitor of mutated BRaf, and lapatinib, an inhibitor of the ERBB family of receptor tyrosine kinases, as synergistically cytotoxic in the subset of cell lines that displayed the most resistance to PLX4720. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
180 Samples
Download data
Series
Accession:
GSE68453
ID:
200068453
20.

Exosome-mediated interaction in the tumor microenvironment modulates MIR211 response via the DUSP6-ERK5 axis and contributes to BRAFV600E inhibitor resistance in melanoma

(Submitter supplied) It is uncertain whether the microRNA MIR211 is a tumor suppressor or an oncogene. To resolve this, we ectopically expressed MIR211 in BRAFV600E-mutant A375 melanoma cells and examined its effect in mouse xenografts. Ectopic MIR211 expression promoted aggressive tumor growth accompanied by increased cellular proliferation and angiogenesis. We provide evidence that MIR211 transfers to adjacent mouse endothelial cells via exosomes and alter the cellular properties. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
9 Samples
Download data: TXT
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