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KMT2D depletion promote KRAS-induced pancreatic carcinogenesis independent of TP53

GSE328371 Mus musculus (mouse) RNA-seq (gene expression) 24 samples Submitted 2026/07/08 Platform GPL34328
At a glance

RNA-seq (gene expression) · mouse · 24 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
24 samples: 8 conditions, mostly in triplicateGroups 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
KMT2D depletion promotes KRAS-induced pancreatic carcinogenesis independent of TP53The Journal of biological chemistry · 2026
Summary (written by the submitters)
We examined the role Kmt2d in PDAC development using two independent genetically engineered mouse models driven by mutant Kras in the presence and absence of the tumor suppressor Tp53. Loss Kmt2d reduces survival and promotes disease progression in both models even in absence of Tp53. Similarly, in human PDAC the loss of TP53 does not affect the prognosis value of KMT2D low cases.
Read the full summary ↓
Of note, the sole Kmt2d depletion did not affect normal pancreas development or mice survival. RNA-seq analysis demonstrates the enrichment of pathways controlling cell growth in Kmt2df/+ PDAC cells. Interestingly, inactivation of Kmt2d resulted in increased levels of Ki67 positive cells in vivo. Together, these findings define the role of this methyltransferase in Kras-driven PDAC biology as tumor suppressor candidate for this dismal condition.
Published in
KMT2D depletion promotes KRAS-induced pancreatic carcinogenesis independent of TP53
Tolosa EJ, Raja Arul GL, Sigafoos AN et al. · The Journal of biological chemistry 2026 · PMID 42208891 · doi:10.1016/j.jbc.2026.113203
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 GSE328371_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 PRJNA1454861 and SRA study SRP692728. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, mostly in triplicate
KPC Mouse 2974 ×3 KPC Mouse 12278 ×3 KPC Mouse 3622 ×3 KPC Kmt2df/+ Mouse 2500 ×3 KPC Kmt2df/+ Mouse 2940 ×3 KPC Kmt2df/+ Mouse 12145 ×3 KPC Kmt2df/+ Mouse 12352 ×3 KPC Kmt2df/+ Mouse 12349 ×3

Supports a between-group comparison across 24 samples.

How we read this: 8 replicated groups read from 24 sample titles; they account for 24 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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