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Evaluation of an Anti-thyroid Mode of Action for Thyroid Follicular Cell Adenomas in Female Mice Exposed to Tertiary Butyl Alcohol

GSE301052 Mus musculus (mouse) RNA-seq (gene expression) 72 samples Submitted 2025/10/21 Platform GPL34328
At a glance

RNA-seq (gene expression) · mouse · 72 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
72 samples: 72 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.
Paper
Evaluation of an anti-thyroid mode of action for thyroid follicular cell adenomas in female mice exposed to tertiary butyl alcoholRegulatory toxicology and pharmacology : RTP · 2025
Summary (written by the submitters)
Chronic exposure to high concentrations of tertiary butyl alcohol (TBA) in drinking water is associated with, low, but increased (15% vs 3% in controls) thyroid follicular cell (TFC) adenomas in female mice. The U. S. Environmental Protection Agency (EPA) developed linear cancer toxicity criteria on this endpoint. This study evaluates whether TBA, a nongenotoxic alcohol, induces TFC adenomas in female B6C3F1 mice through a nonlinear anti-thyroid mode of action (MOA).
Read the full summary ↓
Female mice were exposed to TBA either by oral gavage (500 and 1000 mg/kg) for 5 days or via drinking water (5, 10, 20, or 40 mg/mL) for 14 or 28 days. Key events (KEs) within an anti-thyroid MOA framework—including activation of CAR/PXR, induction of phase I and II liver enzymes, changes in serum thyroxine (T4) and thyroid-stimulating hormone (TSH), and histopathological and proliferative alterations in the thyroid—were evaluated. TBA exposure was found to activate CAR/PXR and induce hepatic phase I and II enzymes; however, it did not produce consistent alterations in T4 or changes in TSH levels, nor did it cause histological changes in the thyroid or increased TFC proliferation in these short-term exposure studies. Considered together with the TBA chronic study demonstrating TFC hyperplasia, there is some evidence to support an anti-thyroid MOA. The data, herein demonstrate TBA activates upstream KEs (CAR/PXR signaling, with upregulation of UGT and SULT transcripts, enzymes that can influence T4 serum levels) in the MOA while downstream events (serum TSH changes nor histopathological changes in the thyroid) were not demonstrated in these short-term studies. The inability to unequivocally demonstrate downstream KEs is likely a consequence of the overall weak tumor response following chronic exposure to high-dose levels (~2110 mg/kg-bw/day) of TBA. Notably, the EPA considered the evidence for thyroid adenomas as “suggestive”, a level that would typically not support a dose-response assessment. The MOA analyses herein highlight an important consequence of conducting risk assessments on weak, suggestive tumor data.
Published in
Evaluation of an anti-thyroid mode of action for thyroid follicular cell adenomas in female mice exposed to tertiary butyl alcohol
Borghoff SJ, Heintz MM, Rivera BN et al. · Regulatory toxicology and pharmacology : RTP 2025 · PMID 40914479 · doi:10.1016/j.yrtph.2025.105936
This dataset
Open GSE301052 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 GSE301052_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 PRJNA1283147 and SRA study SRP595626. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40914479) ↗
Study design
72 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 72 sample titles: 72 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

+ 32 more — browse all 72 samples with per-sample file links →

Datasets on a similar topic

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.