GEO series

Targeting AURKA to induce synthetic lethality in CREBBP-deficient DLBCL via attenuation of MYC expression

GSE232330 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 3 samples Submitted 2025/05/13 Platform GPL24676

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 3 samples

What it is: ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism: Homo sapiens (human)
Topic: Diffuse large B-cell lymphomaThis series is part of our curated briefing on it.
Samples: 3 samples
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper: Targeting AURKA to induce synthetic lethality in CREBBP-deficient B-cell malignancies via attenuation of MYC expressionOncogene · 2024

Summary (written by the submitters)

Loss-of-function mutations in CREBBP, which encodes for a histone acetyltransferase, occur frequently in diffuse large B-cell lymphoma (DLBCL), highlighting CREBBP deficiency as an attractive therapeutic target. Using established isogenic DLBCL cell models, we demonstrated that CREBBP-deficient cells are selectively vulnerable to AURKA inhibition.

Read the full summary ↓

Mechanistically, we found that co-targeting CREBBP and AURKA suppressed MYC transcriptionally and post-translationally to induce replication stress and apoptosis. Inhibition of AURKA dramatically decreased MYC protein level in CREBBP-deficient cells, implying a dependency on AURKA to sustain MYC stability. Furthermore, in vivo studies showed that pharmacological inhibition of AURKA was efficacious in delaying tumor progression in CREBBP-deficient cells and was synergistic with CREBBP inhibitors in CREBBP-proficient cells. Our study sheds light on a novel synthetic lethal interaction between CREBBP and AURKA, indicating that targeting AURKA represents a potential therapeutic strategy for high-risk DLBCL harboring CREBBP inactivating mutations. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for CREBBP and H3K27ac in SC1 cells.

Published in

Targeting AURKA to induce synthetic lethality in CREBBP-deficient B-cell malignancies via attenuation of MYC expression

Sun Y, Chen J, Hong JH et al. · Oncogene 2024 · PMID 38783101 · doi:10.1038/s41388-024-03065-6

This dataset

Open GSE232330 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Diffuse large B-cell lymphoma landscape →

Download · which file do I need?

Direct links to NCBI and ENA, 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.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE232330_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA971620 and SRA study SRP437290. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 38783101) ↗

Samples in this study

The sample list for this study is not cached yet. Press Load samples and it will be fetched from NCBI.

+ 3 more — browse all 3 samples with per-sample file links →

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GSE252690 Increased CCL2/CCR2 axis in MYC/BCL2 double-expressor DLBCL promotes tumor progression by increasing M2 macrophages 28 samples same disease briefing · shares dlbcl, myc
GSE231623 Effect of DLBCL-associated NOTCH2 mutants on genomic RBP-J localization and H3K27 acetylation 7 samples same disease briefing · shares dlbcl
GSE262641 Discovery of golcadomide (CC-99282) as a promising drug candidate for diffuse large B-cell lymphoma (DLBCL) 6 samples same disease briefing · shares dlbcl
GSE11318 Molecular subtypes of DLBCL have distinct chromosomal aberrations 406 samples same disease briefing · shares dlbcl
GSE230396 Selective Enhancer Dependencies in MYC-Intact and MYC-Rearranged Germinal Center B-cell Diffuse Large B-cell Lymphoma 132 samples same disease briefing · shares myc
GSE289194 6K-plex RNA CosMx data from DLBCL sections. 83 samples same disease briefing · shares dlbcl
GSE231624 (1) Effect of KLHL6 loss on the transcriptome in DLBCL upon NOTCH ligand stimulation. (2) Effect of KLHL6 and NOTCH2 loss on the transcriptome in DLBCL. (3) Effect of DLBCL-associated NOTCH2 mutants on the transcriptome in DLBCL. 48 samples same disease briefing · shares dlbcl

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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.