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Pharmacological inhibition of PRKDC-mediated DNA damage response by 3-hydroxyflavone selectively alleviates MLL-rearranged acute myeloid leukemia

GSE338690 Homo sapiens (human) RNA-seq (gene expression) 18 samples Submitted 2026/07/21 Platform GPL16791
At a glance

RNA-seq (gene expression) · human · 18 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Topic
Acute myeloid leukemiaThis series is part of our curated briefing on it.
Samples
18 samples: 6 conditions, mostly in triplicateGroups are read from the sample names, not from the paper. Check the list below.
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.
Summary (written by the submitters)
Genetic rearrangements involving mixed lineage leukemia (MLL-r) in acute myeloid leukemia (AML) have been associated with resistance to chemotherapy, and there is currently a clinical unmet need for effective targeted therapies. In this study, we performed high-throughput drug screening and identified 3-Hydroxyflavone (3-HF) as a selective inhibitor of the survival and growth of MLL-r AML cells, while having minimal effects on leukemia cells with wildtype MLL.
Read the full summary ↓
Mechanistically, 3-HF suppresses the transcription of MLL-targeted genes and exerts antileukemic activity by disrupting PRKDC-mediated DNA damage repair. Additionally, 3-HF enhances chemosensitivity in MLL-r AML cells and demonstrates synergistic antileukemic effects when combined with cytarabine, a standard chemotherapy agent, both in vitro and in vivo using two distinct mouse models of murine MLL-AF9 and human MLL-AF4 leukemia. Our findings provide a novel strategy and targeted therapeutic drug disrupting PRKDC-mediated DNA damage repair pathways for MLL-r leukemia.
This dataset
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.

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 GSE338690_RAW.tar (it can run to tens of gigabytes).

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.

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1495519 and SRA study SRP739431. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in triplicate
MOLM13, DMSO ×3 MOLM13, 3-HF ×3 MV411, DMSO ×3 MV411, 3-HF ×3 U937, DMSO ×3 U937, 3-HF ×3

Supports a between-group comparison across 18 samples.

How we read this: 6 replicated groups read from 18 sample titles; they account for 18 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
More Acute myeloid leukemia datasets

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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.