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Intestinal LKB1 loss drives a pre-malignant program along the serrated cancer pathway [bulkRNA-seq]

GSE302659 Mus musculus (mouse) Single-cell RNA-seq 36 samples Submitted 2026/04/20 Platform GPL30172Platform GPL19057
At a glance

Single-cell RNA-seq · mouse · 36 samples

What it is
Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart. Read from the summary: GEO's own type field only says 'expression profiling by sequencing', so confirm it in the paper.
Organism
Mus musculus (mouse)
Samples
36 samples: 12 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
Intestinal LKB1 Loss Drives a Premalignant Program Along the Serrated Cancer PathwayGastroenterology · 2026
Summary (written by the submitters)
Background & Aims Heterozygous inactivating mutations of Serine Threonine Kinase 11 (STK11)/Liver Kinase B1 (LKB1) are causative to the Peutz-Jeghers syndrome (PJS), a hereditary disease characterized by gastrointestinal hamartomatous polyposis and increased cancer susceptibility. While LKB1 loss-induced polyp formation has been ascribed to non-epithelial tissues, how LKB1 deficiency increases cancer risk of patients by altering the phenotypical landscape and hierarchical organization of epithelial tissues remains poorly understood.
Read the full summary ↓
Methods Using CRISPR/Cas9, we generated heterozygous and homozygous Lkb1-deficient mouse small intestinal and human colon organoids. These organoids were characterized by an integrated approach that combines imaging, bulk and single-cell RNA sequencing and growth factor dependency assays. Our findings were validated in human PJS-derived tissues using immunohistochemistry and linked to colorectal cancer profiles using the TCGA cancer database. Results Our results reveal that heterozygous Lkb1 loss is sufficient to push intestinal cells into a premalignant transcriptional program associated with serrated colorectal cancer, which is further amplified by loss-of-heterozygosity. This altered epithelial growth state associates with persistent features of regeneration and enhanced EGFR ligand and receptor expression, conferring niche-independent growth properties to Lkb1-deficient organoids. Moreover, our newly generated LKB1-mutant signature is enriched in sporadic serrated colorectal cancer, and synergistic cooperation of Lkb1-deficiency with mutant Kras was experimentally confirmed by assessing organoid growth properties and transcriptomes. Conclusions Heterozygous loss of LKB1 pushes intestinal cells into a chronic regenerative state which is amplified upon loss-of-heterozygosity. Lkb1-deficiency thereby generates fertile ground for serrated colorectal cancer formation in the intestine, potentially explaining the increased cancer risk observed in PJS.
Published in
Intestinal LKB1 Loss Drives a Premalignant Program Along the Serrated Cancer Pathway
Plugge SF, Ma H, van der Vaart JY et al. · Gastroenterology 2026 · PMID 41128695 · doi:10.1053/j.gastro.2025.07.041
This dataset
Open GSE302659 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 GSE302659_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: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1291689 and SRA study SRP601213. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41128695) ↗
Study design
12 conditions, mostly in triplicate
mSI_org_WT ×3 mSI_org_Lkb1Het ×3 mSI_org_Lkb1HomBud ×3 mSI_org_Lkb1HomCys ×3 mSI_org_WT_APCKO ×3 mSI_org_Lkb1Het_APCKO ×3 mSI_org_Lkb1HomBud_APCKO ×3 mSI_org_Lkb1HomCys_APCKO ×3 +4 more

Supports a between-group comparison across 36 samples.

How we read this: 12 replicated groups read from 36 sample titles; they account for 36 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
Datasets on a similar topic

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