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RNA-seq of CT26 cells and tumors treated with or without Midostaurin

GSE319170 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2026/02/14 Platform GPL34290
At a glance

RNA-seq (gene expression) · mouse · 12 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
12 samples: 3 × CT26 cell_con vs 3 × CT26 cell_midos vs 3 × CT26 tumor_con vs 3 × CT26 tumor_midosGroups 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)
Immune checkpoint inhibitor therapy has demonstrated efficacy in a variety of tumors. However, due to the high heterogeneity of colorectal cancer, the clinical efficacy of ICB in the treatment of this disease remains quite limited. Activating mutations of KRAS are detected in 35%–50% of colorectal cancer tissues in clinical. Colorectal cancers with these activating mutations are characterized by an immune desert phenotype and aberrant immune-inflammatory microenvironment.
Read the full summary ↓
Studies have indicated that oncogene addiction in tumorigenesis (such as KRAS mutation) and non-genetic mechanisms, particularly epigenetic regulation, can synergistically modulate multiple types of plasticity of the tumor microenvironment and tumor cells, but how epigenetic regulators function in the immunosuppressive microenvironment specific to KRAS-mutant colorectal cancer is barely known. In this study, we identify that PHF8 functions as a MHC-I suppressor that limits anti-tumor immunity in KRAS-mutant colorectal cancer. We also find a FDA-approved drug, Midostaurin, which can mimic the phenotype of PHF8 depletion and add to the efficacy of ICB treatment and KRAS inhibition.
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 GSE319170_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 PRJNA1422245 and SRA study SRP676329. Searching any of these in the dataset finder brings you back here.

Study design
3 × CT26 cell_con vs 3 × CT26 cell_midos vs 3 × CT26 tumor_con vs 3 × CT26 tumor_midos

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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