GEO series

Distinct neuroinflammatory effects of individual chemotherapeutics shape chemotherapy-induced peripheral neuropathy in a novel mouse model of CVAD combination regimen.

GSE333360 Mus musculus (mouse) RNA-seq (gene expression) 30 samples Submitted 2026/05/31 Platform GPL24247

At a glance

RNA-seq (gene expression) · mouse · 30 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: 30 samples: 18 × 2 vs 12 × 1Groups 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.

Summary (written by the submitters)

Chemotherapy-induced peripheral neuropathy (CIPN) is a common, dose-limiting toxicity of cancer treatment for which no disease-modifying therapies exist. Vincristine-induced neuropathy has been linked to neuroimmune activation and interleukin-1 (IL-1) signaling; however, vincristine is almost exclusively administered as part of combination chemotherapy regimens, where the relevance of IL-1–dependent mechanisms remains poorly defined.

Read the full summary ↓

Here we investigate the role of IL-1 receptor (IL-1R) signaling in neuropathy induced by vincristine alone and by the standard CVAD regimen (cyclophosphamide, vincristine, doxorubicin and dexamethasone) in male C57BL6/J mice. IL-1R blockade with the clinically approved antagonist anakinra prevented vincristine-induced mechanical hypersensitivity and attenuated established vincristine-induced peripheral neuropathy, without adverse effects on motor function, hematological parameters or body weight. Additionally, we established a novel CVAD-induced neuropathy model and demonstrate that anakinra partially attenuated CVAD-induced mechanical hypersensitivity and preserved motor function without exacerbating systemic toxicity. Dissection of individual CVAD components identified vincristine as the dominant driver of grip strength decline and IL-1–dependent neuroinflammatory signaling, whereas cyclophosphamide and doxorubicin contributed to sensory hypersensitivity through largely IL-1R–independent mechanisms, and dexamethasone did not induce sensory neuropathy. Immunohistochemistry and transcriptome profiling of peripheral nervous tissue revealed distinct, time-dependent and agent-specific neuroimmune responses with distinct inflammatory and immunosuppressive effects shaping the net CVAD neuroinflammatory phenotype. Together, these findings redefine CIPN as an emergent property of combination chemotherapy and establish IL-1R signaling as a context-dependent therapeutic target with translational relevance.

This dataset

Open GSE333360 in finder → Find more mouse RNA-seq datasets →

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 GSE333360_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 PRJNA1470746 and SRA study SRP703906. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

18 × 2 vs 12 × 1

Supports a between-group comparison across 30 samples.

How we read this: 2 replicated groups read from 30 sample titles; they account for 30 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

GSM9761483 1.1 1
GSM9761484 1.2 1
GSM9761485 1.3 1
GSM9761486 1.4 1
GSM9761487 1.5 1
GSM9761488 1.6 1
GSM9761489 1.7 1
GSM9761490 1.8 1
GSM9761491 1.9 1
GSM9761492 1.101 1
GSM9761493 1.11 1
GSM9761494 1.12 1
GSM9761495 2.101 2
GSM9761496 2.2 2
GSM9761497 2.3 2
GSM9761498 2.4 2
GSM9761499 2.5 2
GSM9761500 2.6 2
GSM9761501 2.7 2
GSM9761502 2.8 2
GSM9761503 2.9 2
GSM9761504 2.1 2
GSM9761505 2.11 2
GSM9761506 2.12 2
GSM9761507 2.13 2
GSM9761508 2.14 2
GSM9761509 2.15 2
GSM9761510 2.16 2
GSM9761511 2.17 2
GSM9761512 2.18 2

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GSE294832 Modular neuroinflammatory network discovery from large-scale phenotypic screening in genetically heterogeneous mice [part10] 1000 samples shares neuroinflammatory
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GSE294535 Modular neuroinflammatory network discovery from large-scale phenotypic screening in genetically heterogeneous mice[part5] 1000 samples shares neuroinflammatory
GSE294849 Modular neuroinflammatory network discovery from large-scale phenotypic screening in genetically heterogeneous mice [part13] 1000 samples shares neuroinflammatory

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