Gene expression profiling was performed in ccRCC cells, which either express both HIF1alpha and HIF2alpha (either naturally or by virtue of induced expression of HIF1alpha) or express HIF2alpha alone (either naturally or by virtue of a HIF1alpha shRNA), to identify genes regulated by HIF1alpha in ccRCC cells.
Genetic and functional studies implicate HIF1α as a 14q kidney cancer suppressor gene.
Specimen part, Cell line
View SamplesExpression data from treatment of actinomycin D (2.5uM) and triptolide (500 nM) on MCF7 cells for 2, 4 and 6 hours.
Chemical genomics identifies small-molecule MCL1 repressors and BCL-xL as a predictor of MCL1 dependency.
Cell line, Compound, Time
View SamplesIn this manuscript, we described male-biased mutations in chrX genes in cancer. In this RNA-seq experiment we tested the transcriptional consequences of shRNA knockdown of one of those genes, CNKSR2 Overall design: Murine NIH 3T3 cells were infected with and selected for expression of lentiviruses expressing shRNAs targeting Cnksr2 (2 independent shRNA sequences) or a control shRNA (targeting RFP, a gene not present in these cells). Each was performed in biological triplicate independent cultures for n=9 total samples
Tumor-suppressor genes that escape from X-inactivation contribute to cancer sex bias.
Cell line, Subject
View SamplesThe PARK2 gene was knocked down using 2 independent siRNAs in SNB19 and SF539 cell lines
Pan-cancer genetic analysis identifies PARK2 as a master regulator of G1/S cyclins.
Cell line
View SamplesMYC-amplified medulloblastomas are highly lethal tumors. BET bromodomain inhibition was recently described to downregulate MYC-associated transcriptional activity in various cancer subtypes. To investigate whether JQ1, a BET bromodomain inhibitor is downregulation MYC and MYC-associated transcriptional activity, we performed global gene expression profiling of five medulloblastomas MYC-amplified patient-derived cell lines treated by JQ1 and the inactive form of JQ1.
BET bromodomain inhibition of MYC-amplified medulloblastoma.
Specimen part, Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The histone methyltransferase SETDB1 is recurrently amplified in melanoma and accelerates its onset.
Specimen part, Cell line
View SamplesCombination therapy with Smo and PI3K inhibitors results in a synergistic effect in reducing tumor growth in PTEN-deficient Glioblastoma. To identify consequences of combination therapy with an Smo inhibitor and a PI3K inhibitor on a genome-wide scale, we performed Affymetrix microarrays with two different PTEN-deficient GBMs treated with single drugs or combination therapy. A small set of genes was significantly affected by combination therapy in hBT70 and/or hBT112, including several genes implicated in GBM prognosis, or identified as targets of Shh, PI3K or S6 pathways 29-33 .
Coordinate activation of Shh and PI3K signaling in PTEN-deficient glioblastoma: new therapeutic opportunities.
Treatment
View SamplesAndrogen receptor (AR) is a ligand-dependent transcription factor that plays a key role in the onset and progression of prostate cancer. We investigated AR-induced gene expression in prostate cancer cells LNCaP and abl by transfecting siAR / siControl or treating cells with androgen (DHT) over a time course.
Androgen receptor regulates a distinct transcription program in androgen-independent prostate cancer.
No sample metadata fields
View SamplesBreast cancer cell lines containing stable dox inducible shRNAs targeting SF3B1 were profiled by RNA sequencing. We determined the effect of gene expression and splicing changes before and after knocking down SF3B1 in cell lines with normal copy number (SF3B1neutral) or partial copy loss (SF3B1loss) cell lines Overall design: RNA profiles for SF3B1 suppression were generated from 8 breast cancer cell line pairs (-/+ dox) with no techincal replicates.
Copy-number and gene dependency analysis reveals partial copy loss of wild-type SF3B1 as a novel cancer vulnerability.
Subject
View SamplesTo identify the role of the SH3PXD2A-HTRA1 fusion on gene expression in Schwann cells
The genomic landscape of schwannoma.
Specimen part
View Samples