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Disruption of the Wnt-antagonist APC in the pituitary stem cells drives adamantinomatous craniopharyngioma

GSE282683 Mus musculus (mouse) RNA-seq (gene expression) 11 samples Submitted 2025/01/01 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 11 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
11 samples: 11 samples, each with a distinct title — no replicated groupsGroups 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)
Adamantinomatous craniopharyngioma (aPCs) are complex intracranial neoplasms that arise in the sellar or parasellar region affecting the endocrine system and leading to severe comorbidities. Activating mutations resulting in degradation resistant from of b-Catenin (CTNNB1 gene) have been shown to be the main driver for a large proportion of these neoplasms.
Read the full summary ↓
However, the underlying genetic driver for a proportion of these tumours is still unknown. Using murine transgenic models, we show that genetic deletion of the Wnt-antagonist and tumour suppressor, Adenomatous Polyposis Coli (Apc) within the pituitary progenitors/stem cells leads to pituitary tumours that closely resemble human aCPs. These tumours present classical histopathological hallmarks of aCPs such as clusters of accumulating nuclear b-catenin that are slow dividing and undergo secretory phenotype. These tumours present wet keratin, stellar-reticular-like structures and cystic components. We show that a hypomorphic allele of Apc is sufficient for tumour development indicating that disruption of Apc function can lead to aCP formation independent of b-Catenin mutations. Moreover, we identify that bi-allelic loss of Apc in the Sox2+ve pituitary stem cells is sufficient to initiate tumour formation, indicating that Sox2+ve stem cells are the cell origin of these Apc-driven tumours. Transcriptomic analyses of early tumour-initiating cells reveal that clusters of accumulating b-Catenin, undergo p21-mediated cellular senescence and that the secretory phenotype is composed of inflammasome, angiosome and developmental growth factors which are different from the b-Catenin-driven aCP tumours. Our data, unequivocally shows, that disruption of the tumour suppressor Apc in the pituitary progenitors/stem cells is a main driver of aCPs independent of mutations in b-Catenin. We provide two novel murine models that represents a genetic subtype of aCPs which helps to further understand aCP pathogenesis.
This dataset
Open GSE282683 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 GSE282683_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 PRJNA1189788 and SRA study SRP547143. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
11 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 11 sample titles: 11 distinct titles with little repetition. 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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