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Targeting PKMYT1 enhances antitumor immune responses in castration-resistant prostate cancer.

GSE317406 Mus musculus (mouse) RNA-seq (gene expression) 2 samples Submitted 2026/02/11 Platform GPL19057
At a glance

RNA-seq (gene expression) · mouse · 2 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
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
Targeting PKMYT1 enhances antitumor immune responses to PD-L1 blockade in castration-resistant prostate cancerJournal for immunotherapy of cancer · 2026
Summary (written by the submitters)
Although immunotherapy has been successful in various tumors, its efficacy in castration resistant prostate cancer (CRPC) is minimal, due to reduced presence of intratumoral immune effector cells in CRPC. How CRPC cells escape immune surveillance is not fully defined. Here we demonstrate that PKMYT1 expression is elevated in CRPC cases, which related to low immune infiltration in these patients.
Read the full summary ↓
Patients with high PKMYT1 expression exhibit low CD8+ T cells signature and resistance to ICB therapy. Targeting PKMYT1 can suppress CRPC progression, accompanied with increased intratumoral CD8+ T cells. Selective PKMYT1 inhibitor, RP-6306, augmented ICB in a manner dependent on CD8+ T cells. PKMYT1 inhibitors alone or in combination with PD-L1 blockade causes CD8+ T cell infiltration and remarkable tumor suppression, which suggests a promising immunotherapeutic approach in CRPC. Mechanically, targeting PKMYT1 activated the cGAS-STING pathway, which increases expression of type I and II interferon response genes and led to upregulation of key immune regulators. These findings highlight a key role of PKMYT1 in CRPC progression and rationalize PKMYT1 as a potential therapeutic target.
Published in
Targeting PKMYT1 enhances antitumor immune responses to PD-L1 blockade in castration-resistant prostate cancer
Gao L, Wang B, Liu H et al. · Journal for immunotherapy of cancer 2026 · PMID 41617394 · doi:10.1136/jitc-2025-013247
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 GSE317406_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 PRJNA1412541 and SRA study SRP665846. Searching any of these in the dataset finder brings you back here.

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