← BioTransfer GEO Dataset Finder
GEO series

DMAP1 promotes lung cancer progression by maintaining replication fork stability and suppressing IFN signaling-mediated anti-tumor immunity [scRNA-seq]

GSE304429 Mus musculus (mouse) Single-cell RNA-seq 2 samples Submitted 2026/06/24 Platform GPL34290
At a glance

Single-cell RNA-seq · mouse · 2 samples

What it is
Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart.
Organism
Mus musculus (mouse)
Samples
2 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
DMAP1 Deficiency Suppresses Lung Cancer Progression by Destabilizing Replication Fork and Activating IFN Signaling-Mediated Anti-tumor ImmunityAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
Summary (written by the submitters)
Despite substantial progress in targeted and immune therapies, lung cancer remains the leading cause of cancer-related mortality, highlighting the urgent need for novel therapeutic strategies. Through a CRISPR-based knock-out screen, we identified the DNA methyltransferase 1-associated protein 1 (DMAP1) as a critical regulator of tumor progression.
Read the full summary ↓
Functional studies showed that loss of DMAP1 exerts its anti-tumor effects through attenuating tumor cell proliferation and activating T cell-mediated adaptive anti-tumor effects. Mechanistically, loss of DMAP1 causes replication fork retardance, disturbs genome stability, and induces endogenous DNA damage, thereby activating tumor-intrinsic immune signaling and enhancing anti-tumor immune response during cancer cell growth. Clinical data analyses revealed that high DMAP1 expression is associated with reduced immune infiltration, a “cold” tumor microenvironment, and poorer overall survival in lung cancer. These findings significantly advance our knowledge of DMAP1's function in lung cancer development and offer a scientific basis for designing novel treatment approaches.
Published in
DMAP1 Deficiency Suppresses Lung Cancer Progression by Destabilizing Replication Fork and Activating IFN Signaling-Mediated Anti-tumor Immunity
Huang K, Dai X, Li S et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2026 · PMID 41904944 · doi:10.1002/advs.202517634
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 GSE304429_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: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1301299 and SRA study SRP606274. Searching any of these in the dataset finder brings you back here.

Samples in this study

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

+ 2 more — browse all 2 samples with per-sample file links →

Datasets on a similar topic

Search all mouse RNA-seq datasets in GEO →

Share this dataset

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.