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Targeting transcriptional dependencies in cancer using a covalent CDK7 inhibitor (expression)

GSE50624 Homo sapiens (human) Expression microarray 79 samples Submitted 2014/06/22 Platform GPL16043
At a glance

Expression microarray · human · 79 samples

What it is
Expression microarrayGene activity read on a chip (the older technology that RNA-seq replaced).
Organism
Homo sapiens (human)
Topic
Acute lymphoblastic leukemiaThis series is part of our curated briefing on it.
Samples
79 samples: 36 conditions, mostly in duplicateGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed expression table (series matrix) and the array files, from NCBI.
Summary (written by the submitters)
Cyclin-dependent kinase 7 (CDK7) plays a critical role in the general regulation of RNA polymerase II-mediated transcription. However, the absence of selective CDK7 inhibitors has hindered the ability to investigate the consequences of acute and prolonged inhibition of CDK7 under normal and pathological conditions.
Read the full summary ↓
Here we present the discovery and characterization of the first covalent CDK7 inhibitor, CDK7-IN-1, that has the unprecedented ability to target a unique cysteine residue located outside of the canonical kinase domain, providing an unanticipated means of achieving selectivity for CDK7 amongst the 20 known CDKs. Cancer cell line profiling indicates that a subset of cancer cell lines, including T-cell acute lymphoblastic leukemia (T-ALL), exhibit 100-fold greater sensitivity to CDK7-IN-1 over other tumor and normal cell lines. Genome-wide expression analysis in Jurkat T-ALL indicates that CDK7-IN-1 disproportionally affects RUNX1 as well as other components of the TAL1 transcriptional network and its targets, downregulating key regulators of transcription and apoptosis critical for the T-ALL state. These oncogenes are encoded by short-lived mRNA transcripts, are associated with super-enhancers, and exhibit a strong dependency on continuous transcription for sustained expression. Therefore, pharmacological modulation of CDK7 kinase activity may define a method for the identification and treatment of tumor types exhibiting extreme dependencies on transcription for maintenance of the oncogenic state.
This dataset
Download · which file do I need?

Direct links to NCBI, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need.

All supplementary files ↗
3 · The original raw files

Whole study · RAW.tar

Everything the authors deposited as one archive (GSE50624_RAW.tar), including the raw array or instrument files. Can be large; the picker in step 2 takes just the samples you need.

What the files usually look like: For arrays the series matrix is normally the normalised expression table you want; the raw array files (CEL and similar) are in the RAW.tar.

Also filed as BioProject PRJNA218105. Searching any of these in the dataset finder brings you back here.

Study design
36 conditions, mostly in duplicate
B5_Jurkat_DMSO_2h ×3 B5_Jurkat_CDK7i_250nM_2h ×3 B1_Jurkat_DMSO_6h ×2 B1_Jurkat_CDK7i_6h_250nM ×2 BI_Jurkat_CDK7i-R_6h_250nM ×2 B1_Jurkat_DMSO_12h ×2 B1_Jurkat_CDK7i_12h ×2 B2_Jurkat_DMSO_4h ×2 +33 more

Supports a between-group comparison across 74 samples.

How we read this: 36 replicated groups read from 79 sample titles; they account for 74 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

+ 39 more — browse all 79 samples with per-sample file links →

More Acute lymphoblastic leukemia datasets

Search all human microarray datasets in GEO →

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.