Expression profiling of MRC5, IFN gamma treated MRC5 and PGF cells.
Reconfiguration of genomic anchors upon transcriptional activation of the human major histocompatibility complex.
No sample metadata fields
View SamplesActivating mutations in either KIT or PDGFRA are present in approximately 90% of gastrointestinal stromal tumors (GISTs). Although treatment with the KIT and PDGFR inhibitor imatinib can control advanced disease in about 80% of GIST patients, the beneficial effect is not durable. Here, we report that ligands from the FGF family reduced the effectiveness of imatinib in GIST cells, and FGF2 and FGFR1 are highly expressed in all primary GIST samples examined. The combination of KIT and FGFR inhibition showed increased growth inhibition in imatinib-sensitive GIST cell lines in the presence or absence of added FGF2 in vitro, and delayed tumor regrowth in vivo. In addition, inhibition of mitogen-activated protein kinase (MAPK) signaling by imatinib was not sustained in GIST cells. An extracellular signal-regulated kinase (ERK) rebound occurred through activation of FGF signaling, and was repressed by FGFR1 inhibition. Downregultation of Sprouty proteins played a role in the imatinib-induced feedback activation of FGF signaling in GIST cells.
FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors.
Cell line
View SamplesThis experiment is designed to detect genes differentially expressed in 2uM erlotinib treatment versus DMSO treatment and to identify differential gene set enrichments.
Inhibition of Casein Kinase 1 Alpha Prevents Acquired Drug Resistance to Erlotinib in EGFR-Mutant Non-Small Cell Lung Cancer.
Specimen part, Cell line
View SamplesKnockdown of mutant and/or wild-type SF3B1 in MEL202 cell line by Degron knock-in, followed by RNA-seq, to identify splicing events governed by mutant SF3B1. Overall design: Control: parental MEL202 cell line. Experiments: mutant-SF3B1 knockdown; wildtype-SF3B1 knockdown; mutant SF3B1 knockout. Treatments: each of these four conditions plus and minus shld.
A chemical genetics approach for the functional assessment of novel cancer genes.
No sample metadata fields
View SamplesAdult neural tissue was treated with an HDAC inhibitor, TSA to assess changes in gene expression, which was then correlated with control adult tissue as well as early postnatal controls to determine effects of increased histone acetylation on gene expression in various neural cell populations
Transcriptomics of critical period of visual cortical plasticity in mice.
No sample metadata fields
View SamplesA dataset for coordinated transcriptome analysis of the effect of ethanol on human embryonic cerebral slices in vitro and on the mouse embryonic cerebral cortex in a in vivo model.
Combined transcriptome analysis of fetal human and mouse cerebral cortex exposed to alcohol.
Time
View SamplesLNCaP-derived MDV3100-resistant clones were treated with MDV3100 for 24h prior to collection
An F876L mutation in androgen receptor confers genetic and phenotypic resistance to MDV3100 (enzalutamide).
Cell line
View SamplesGenetically engineered LNCaPs overexpressing various AR alleles were treated with 0.1% DMSO or 10uM MDV3100 for 24h prior to collection
An F876L mutation in androgen receptor confers genetic and phenotypic resistance to MDV3100 (enzalutamide).
Cell line
View SamplesWe aimed to find gene signatures associated with different subgroups of alveolar rhabdomyosarcoma cell lines defined by differences in detection of pro-apoptotic stress
FGFR4 signaling couples to Bim and not Bmf to discriminate subsets of alveolar rhabdomyosarcoma cells.
Specimen part, Cell line
View SamplesHere, we apply differential transcriptome analysis on microscopically isolated cell populations, to define five transcriptional programs that represent each transient embryonic zone and the progression between these zones. The five transcriptional programs contain largely uncharacterized genes in addition to transcripts necessary for stem cell maintenance, neurogenesis, migration, and differentiation. Additionally, we found intergenic transcriptionally active regions that possibly encode novel zone-specific transcripts. Finally, we present a high-resolution transcriptome map of transient zones in the embryonic mouse forebrain. Overall design: mRNAseq performed after laser microdissection of cells from transient embryonic zones in the mouse cortex
Transcriptional programs in transient embryonic zones of the cerebral cortex defined by high-resolution mRNA sequencing.
Specimen part, Cell line, Subject
View Samples