We analyzed transcriptional changes in 4 prostate cancer cell lines following treatment with the BET inhibitor I-BET762 using Affymetrix Human Genome U133 Plus 2.0 Arrays.
Inhibition of BET bromodomain proteins as a therapeutic approach in prostate cancer.
Cell line, Time
View SamplesTranscriptional changes were analyzed in two colorectal cancer, two pancreatic cancer, and one small cell lung cancer cell line following treatment with the BET inhibitor GSK525762 and/or the MEK inhibitor trametinib using Affymetrix Human Genome U133 Plus 2.0 Arrays.
MEK inhibitors overcome resistance to BET inhibition across a number of solid and hematologic cancers.
Cell line, Treatment, Time
View SamplesGene expression changes were analyzed in 2 acute lymphoblastic leukemia cell lines treated with the GSK126 EZH2 inhibitor using Affymetrix Human Genome U133 Plus 2.0 arrays.
A687V EZH2 is a driver of histone H3 lysine 27 (H3K27) hypertrimethylation.
Cell line, Treatment, Time
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EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations.
Specimen part, Cell line, Treatment
View SamplesWe studied transcriptional changes by Affymetrix human microarrays in DLBCL cell lines as a result of treatment with GSK126, a potent, highly-selective, SAM-competitive, small molecule inhibitor of EZH2
EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations.
Specimen part, Cell line, Treatment
View SamplesWe studied transcriptional changes by Affymetrix human microarrays in 2 DLBCL cell lines as a result of shRNA mediated knockdown of EZH2.
EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations.
Specimen part, Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A DNA Hypomethylation Signature Predicts Antitumor Activity of LSD1 Inhibitors in SCLC.
Specimen part, Cell line, Treatment
View SamplesEpigenetic dysregulation has emerged as an important mechanism in cancer. Alterations in epigenetic machinery have become a major focus for new targeted therapies. The current report describes the discovery and biological activity of a cyclopropylamine containing inhibitor of Lysine Demethylase 1 (LSD1), GSK2879552. This small molecule is a potent, selective, orally bioavailable, mechanism-based irreversible inhibitor of LSD1. A proliferation screen of cell lines representing a number of tumor types indicated that small cell lung carcinoma (SCLC) is sensitive to LSD1 inhibition. The subset of SCLC lines and primary samples that undergo growth inhibition in response to GSK2879552 exhibit DNA hypomethylation of a signature set of probes suggesting this may be used as a predictive biomarker of activity. The targeted mechanism coupled with a novel predictive biomarker make LSD1 inhibition an exciting potential therapy for SCLC, a highly prevalent, rarely cured, tumor type representing approximately 15% of all lung cancers.
A DNA Hypomethylation Signature Predicts Antitumor Activity of LSD1 Inhibitors in SCLC.
Cell line, Treatment
View SamplesTime-course and concentration-effect experiments with multiple time points and drug concentrations provide far more valuable information than experiments with just two design-points (treated vs. control), as commonly performed in most microarray studies. Analysis of the data from such complex experiments, however, remains a challenge. Here we present a semi-automated method for fitting time profiles and concentration-effect patterns, simultaneously, to gene expression data. The submodels for time-course included exponential increase and decrease models with parameters such as initial expression level, maximum effect, and rate-constant (or half-time). The submodel for concentration-effect was a 4-parameter Hill model.
Simultaneous modeling of concentration-effect and time-course patterns in gene expression data from microarrays.
No sample metadata fields
View SamplesProstate cancer C4-2B cells were cultured in docetaxel in a dose-escalation manner. After nine months selection, cells were able to divide freely in 5 nM docetaxel, with a specific sets of genes been deregulated.
Inhibition of ABCB1 expression overcomes acquired docetaxel resistance in prostate cancer.
Cell line
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