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Immune Checkpoint B7x Promotes Immune Evasion and Resistance to PD-1/PD-L1 Blockade in Bladder Cancer

GSE315244 Mus musculus (mouse) RNA-seq (gene expression) 15 samples Submitted 2025/12/30 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 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
Mus musculus (mouse)
Samples
15 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
Immune checkpoint B7x promotes immune evasion and resistance to PD-1/PD-L1 blockade in bladder cancerGenes & diseases · 2026
Summary (written by the submitters)
Cancer cells adopt multiple strategies to avoid detection and destruction by the immune system, including exploiting immune checkpoint pathways. B7x (B7-H4, B7S1, or VTCN1), a member of the B7/CD28 family, is frequently expressed in advanced bladder cancer (BC), yet its role in BC progression and resistance to therapy remains poorly understood.
Read the full summary ↓
Resistance to PD-1/PD-L1 immune checkpoint blockade immunotherapy significantly limits durable responses, with only 20%–25% of patients with muscle-invasive BC achieving long-term benefits. Here, we demonstrated that B7x mRNA and protein expression were associated with poor survival outcomes in muscle-invasive BC patients and mouse models of BC. Stable expression of B7x in immune-competent BC mouse models resulted in enhanced tumor growth and splenomegaly, driven by the exclusion and suppression of tumor-infiltrating anti-tumor immune cells and the enrichment of pro-tumor and immunosuppressive cells. Consistently, in the IMvigor210 clinical trial, high B7x mRNA expression was correlated with poorer survival in muscle-invasive BC patients treated with PD-L1 blockade. Notably, combination therapy targeting B7x alongside PD-1/PD-L1 or CTLA-4 blockade reduced tumor burden and overcame resistance to monotherapy. These findings establish B7x as a substantial driver of immune evasion in BC and highlight its potential as a therapeutic target to improve immune checkpoint blockade efficacy in muscle-invasive BC.
Published in
Immune checkpoint B7x promotes immune evasion and resistance to PD-1/PD-L1 blockade in bladder cancer
Pulanco MC, Zheng XY, Sankin A et al. · Genes & diseases 2026 · PMID 42004225 · doi:10.1016/j.gendis.2025.101950
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 GSE315244_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 PRJNA1395474 and SRA study SRP658836. Searching any of these in the dataset finder brings you back here.

Samples in this study

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