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HDAC inhibition unlocks tumor plasticity and enhances immunotherapy response in Myc- Driven Small Cell Lung Cancer [ATAC-Seq]

GSE309213 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2026/04/02 Platform GPL17021
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 12 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
Mus musculus (mouse)
Samples
12 samples: 3 × ATACseq_RPM_tumor_Ctrl vs 3 × ATACseq_RPM_tumor_aPD1 vs 3 × ATACseq_RPM_tumor_ent vs 3 × ATACseq_RPM_tumor_aPD1_entGroups 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
HDAC inhibition unlocks tumor plasticity and enhances immunotherapy response in Myc-driven small cell lung cancerMolecular cancer therapeutics · 2026
Summary (written by the submitters)
Small Cell Lung Cancer (SCLC) is a highly aggressive malignancy, accounting for approximately 15% of all lung cancer cases. Characterized by low immunogenicity, SCLC may utilize epigenetic mechanisms to evade immune detection. Here, we demonstrate that entinostat, a class I histone deacetylase inhibitor (HDACi) upregulates immune-related genes in human SCLC cells.
Read the full summary ↓
In vivo, we confirmed entinostat treatment increased expression of immunecheckpoint ligands and antigen presentation machinery in Myc-driven tumors in a Rb1/Trp53/MycT58A (RPM) SCLC mouse model, while shifting tumors from a neuroendocrine(NE)-high to a NE-low phenotype. Notably, combining entinostat with anti-PD-1 immunotherapy significantly enhances T-cell infiltration, suppresses tumor growth, and prolongs survival in RPM allograft models. These findings underscore the potential of entinostat to reprogram the immunological landscape and NE status of SCLC, enhance immune checkpoint blockade efficacy, and improve therapeutic outcomes.
Published in
HDAC inhibition unlocks tumor plasticity and enhances immunotherapy response in Myc-driven small cell lung cancer
Ghafoor A, Zhu L, Weaver Ohler Z et al. · Molecular cancer therapeutics 2026 · PMID 42068133 · doi:10.1158/1535-7163.MCT-25-1077
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 GSE309213_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1334351 and SRA study SRP627210. Searching any of these in the dataset finder brings you back here.

Study design
3 × ATACseq_RPM_tumor_Ctrl vs 3 × ATACseq_RPM_tumor_aPD1 vs 3 × ATACseq_RPM_tumor_ent vs 3 × ATACseq_RPM_tumor_aPD1_ent

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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
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