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Links from GEO DataSets

Items: 6

1.
Full record GDS5419

MEK inhibitor PD-0325901 and rapamycin combined treatment effect on malignant peripheral nerve sheath tumor model

Analysis of malignant peripheral nerve sheath tumors (MPNST) from NPcis animals (carrying Nf1 and p53 mutations) treated with rapamycin, MEK inhibitor PD-0325901, or the combination of rapamycin and PD-0325901. Results provide insight into the molecular mechanisms underlying MPNST pathogenesis.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 4 protocol sets
Platform:
GPL6246
Series:
GSE57141
8 Samples
Download data: CEL
2.

Defining key signaling nodes and therapeutic biomarkers in NF1-mutant cancers

(Submitter supplied) The NF1 tumor suppressor encodes a RAS GTPase-Activating Protein (RasGAP). Accordingly, deregulated RAS signaling underlies the pathogenesis of NF1-mutant cancers. However, while various RAS effector pathways have been shown to function in these tumors, it is currently unclear which specific proteins within these broad signaling pathways represent optimal therapeutic targets. Here we identify mTORC1 as the key PI3K pathway component in NF1-mutant nervous system malignancies and conversely show that mTORC2 and AKT are dispensable. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS5419
Platform:
GPL6246
8 Samples
Download data: CEL
Series
Accession:
GSE57141
ID:
200057141
3.

Gene profiles of pathway interference downstream neurofibromin signaling

(Submitter supplied) Malignant peripheral nerve sheath tumor (MPNST) is a type of soft tissue sarcoma that occurs in carriers of mutations in the neurofibromatosis type I gene (Nf1) as well as sporadically. Plexiform neurofibromas in NF1 patients have a significant risk of developing into MPNSTs leading to increased morbidity and mortality from this syndrome. Surgery is the primary intervention but it is not always effective due to the tendency of MPNSTs to infiltrate the surrounding tissue or grow in an inoperable location. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4133
24 Samples
Download data: TXT
Series
Accession:
GSE39764
ID:
200039764
4.

Intrinsic Resistance to MEK Inhibition Through BET Protein Mediated Kinome

(Submitter supplied) Mutation or deletion of Neurofibromin (NF1), an inhibitor of RAS signaling, frequently occurs in epithelial ovarian cancer (EOC), supporting therapies that target downstream RAS effectors, such as the RAF-MEK-ERK pathway. However, no comprehensive studies have been carried out testing the efficacy of MEK inhibition in NF1-deficient EOC. Here, we performed a detailed characterization of MEK inhibition in NF1-deficient EOC cell lines using kinome profiling and RNA sequencing. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
4 Samples
Download data: TXT
5.

Gene expression profiling of melanoma cell lines (carrying NF1 loss-of-function) treated with DMSO (vehicle), MTX-216, MTX-211, trametinib, the combination of MTX-216 and trametinib, or pictilisib

(Submitter supplied) In this study, we identified a multi-kinase inhibitor MTX-216 to be efficacious in blocking NF1 loss-of-function melanoma cells. To identify the mechansisms of action of MTX-216, we treated NF1 loss-of-function melanoma cell lines with MTX-216, MTX-211 (the structural analogue of MTX-216 that has no effect on melanoma cells) as well as commericial kinase inhibitors, trametinib and pictilisib, and compared their gene expression profiles.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
42 Samples
Download data: CSV
Series
Accession:
GSE213588
ID:
200213588
6.

mTOR and HDAC inhibitors converge on the TXNIP/thioredoxin pathway to cause catastrophic oxidative stress and regression of RAS-driven tumors

(Submitter supplied) mTOR and HDAC inhibitors induce cell death of malignant peripheral nerve sheath tumors (MPNSTs) in vitro, and in vivo We performed microarray analysis of mTOR and HDAC inhibition alone and in combination 24 hours after treatment, prior to induction of cell death, to identify transcriptional changes that might be mechanistic drivers of the therapeutic efficacy
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
12 Samples
Download data: CEL
Series
Accession:
GSE84205
ID:
200084205
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Supplemental Content

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