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Martinostat as a Novel HDAC Inhibitor to Overcome Tyrosine Kinase Inhibitor Resistance in Chronic Myeloid Leukemia

GSE292088 Homo sapiens (human) RNA-seq (gene expression) 15 samples Submitted 2025/07/23 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 15 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
Chronic myeloid leukemiaThis series is part of our curated briefing on it.
Samples
15 samples: 5 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.
Paper
Martinostat as a novel HDAC inhibitor to overcome tyrosine kinase inhibitor resistance in chronic myeloid leukemiaClinical epigenetics · 2025
Summary (written by the submitters)
Chronic Myeloid Leukemia (CML) remains a therapeutic challenge, particularly in patients who develop resistance to standard tyrosine kinase inhibitors (TKIs) such as imatinib. Here, we present the first demonstration of the potent anti-leukemic activity of the histone deacetylase (HDAC) inhibitor martinostat in both TKI-sensitive and TKI-resistant CML.
Read the full summary ↓
Structural and biochemical analyses confirmed the efficient and selective binding of martinostat to HDAC isoenzyme ligand-binding pockets, resulting in histone and tubulin hyperacetylation in both imatinib-sensitive and resistant CML cells, outperforming vorinostat, a clinically used HDAC inhibitor (HDACi). It selectively impaired CML cell proliferation and viability and induced apoptosis across various CML models, including resistant cell models and patient blasts, with minimal toxicity to healthy cells and low developmental toxicity in zebrafish. In addition to its single-agent efficacy, martinostat demonstrated enhanced anticancer effects when combined with imatinib, both in vitro and in vivo, significantly reducing tumor growth in resistant CML xenograft models. Mechanistically, mRNA-seq data showed that martinostat disrupted key survival signaling pathways and amplified apoptotic responses, thereby contributing to its anticancer activity. These findings highlight the potential of martinostat as a selective, low-toxicity HDACi that, when combined with TKIs, could provide an effective strategy to overcome drug resistance in CML and improve therapeutic outcomes.
Published in
Martinostat as a novel HDAC inhibitor to overcome tyrosine kinase inhibitor resistance in chronic myeloid leukemia
Yang H, Li V, Park SJ et al. · Clinical epigenetics 2025 · PMID 40671124 · doi:10.1186/s13148-025-01921-0
This dataset
Open GSE292088 in finder → Find more human RNA-seq datasets → Chronic myeloid leukemia 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 GSE292088_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: 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 PRJNA1236844 and SRA study SRP570764. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40671124) ↗
Study design
5 conditions, mostly in triplicate
K-562 cells, untreated, biol ×3 K-562 cells, Martinostat 24h, 0.15 μM. Biol ×3 K-562 cells, Martinostat 24h, 0.25 μM. Biol ×3 K-562 cells, Martinostat 24h, 0.5 μM. Biol ×3 K-562 cells, Martinostat 24h, 1 μM. Biol ×3

Supports a between-group comparison across 15 samples.

How we read this: 5 replicated groups read from 15 sample titles; they account for 15 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 Chronic myeloid leukemia datasets

Search all human RNA-seq datasets in GEO →

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