GEO series

Pan-Cancer MLL3 Mutational Landscape and Its Association with Immunotherapy

GSE307073 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2025/09/07 Platform GPL24247Platform GPL23479

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 12 samples

What it is: ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism: Mus musculus (mouse)
Samples: 12 samples: 3 × CT26 cell, Mll3 wild-type, RNA-seq vs 3 × CT26 cell, Mll3 knock-out, RNA-seqGroups 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.
Paper: The pan-cancer mutational landscape of MLL3 and its impact on prognosis and immunochemotherapyCell reports · 2025

Summary (written by the submitters)

Translocation-linked Mixed Lineage Leukemia (MLL) genes were discovered ~ 30 years ago and are homologs of Trithorax in Drosophila. MLL3 is a histone methyltransferase catalyzing the monomethylation of histone H3 lysine 4 (H3K4me1), a hallmark for gene enhancers. Although recurrent mutations of MLL3 are reported across a broad spectrum of cancers and MLL3 represents one of the most commonly mutated cancer genes, a pan-cancer-wide portrait of this high-frequency mutational event is still lacking.

Read the full summary ↓

We report here a comprehensive analysis of MLL3 mutation and its association with molecular, cellular, and clinical features in 33 cancer types. The genetic alterations of MLL3 are primarily driven by point mutations or small INDELs rather than large-scale chromosomal perturbations and exhibit lineage-specific variations, which spontaneously yet heterogeneously impinge on the clinical behaviors of cancers and are intrinsically linked to hot tumor microenvironments, especially in uterine corpus endometrial carcinoma (UCEC) and colon adenocarcinoma (COAD), where MLL3 aberrances surprisingly predict better overall survivals and favorable responses to immunochemotherapy. Concurrent mutation of MLL3 and POLE in UCEC is associated with high immune cell infiltration and immune checkpoint gene expression, endowing the applicability of immune checkpoint inhibitors in these patients. Mouse models with Mll3-ablated colon cancer validate the immunostimulatory trait of Mll3 aberration. Our study provides a pan-cancer spectrum of the MLL3 mutational event and will contribute to the understanding of the genetic evolution and disease management of cancers, especially COAD and UCEC.

Published in

The pan-cancer mutational landscape of MLL3 and its impact on prognosis and immunochemotherapy

Liu X, Xu Y, Wang Y et al. · Cell reports 2025 · PMID 41205171 · doi:10.1016/j.celrep.2025.116548

This dataset

Open GSE307073 in finder → Find more mouse ChIP / ATAC / CUT&Tag 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 GSE307073_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1314211 and SRA study SRP616594. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41205171) ↗

Study design

3 × CT26 cell, Mll3 wild-type, RNA-seq vs 3 × CT26 cell, Mll3 knock-out, RNA-seq

Supports a case/control comparison: 1 samples read as cases, 5 as controls.

How we read this: 2 replicated groups read from 12 sample titles; they account for 6 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

GSM9215378 CT26 cell, Mll3 wild-type, RNA-seq rep1 CT26 cell, Mll3 wild-ty…
GSM9215379 CT26 cell, Mll3 wild-type, RNA-seq rep2 CT26 cell, Mll3 wild-ty…
GSM9215380 CT26 cell, Mll3 wild-type, RNA-seq rep3 CT26 cell, Mll3 wild-ty…
GSM9215381 CT26 cell, Mll3 knock-out, RNA-seq rep1 CT26 cell, Mll3 knock-o…
GSM9215382 CT26 cell, Mll3 knock-out, RNA-seq rep2 CT26 cell, Mll3 knock-o…
GSM9215383 CT26 cell, Mll3 knock-out, RNA-seq rep3 CT26 cell, Mll3 knock-o…
GSM9215384 CT26 cell, Mll3 wild-type, H3K27ac CUT&Tag
GSM9215385 CT26 cell, Mll3 knock-out, H3K27ac CUT&Tag
GSM9215386 CT26 cell, Mll3 wild-type, H3K4me1 CUT&Tag
GSM9215387 CT26 cell, Mll3 knock-out, H3K4me1 CUT&Tag
GSM9215388 Tumor tissue, Mll3 wild-type, scRNA-seq
GSM9215389 Tumor tissue, Mll3 kncok-out, scRNA-seq

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