GEO series

Loss of aryl hydrocarbon receptor reduces pancreatic tumor growth by increasing immune cell infiltration

GSE279893 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2025/01/03 Platform GPL13112

At a glance

RNA-seq (gene expression) · mouse · 12 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: 12 samples: 6 × CR705, WT, vs 6 × CR705, AHRKO,Groups 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: Loss of aryl hydrocarbon receptor reduces pancreatic tumor growth by increasing immune cell infiltrationBiochemical pharmacology · 2025

Summary (written by the submitters)

Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease which despite large research efforts remains poorly understood. Many studies provide evidence that the aryl hydrocarbon receptor (AHR) plays a critical role in the pathogenesis of several cancers and represents new anti-cancer therapeutic target. The role of AHR in PDAC is, however, unclear since AHR has been reported to exhibit both pro- and anti-tumor activities.

Read the full summary ↓

In this study we evaluated the role of AHR in murine PDAC cells in vitro and in vivo. Loss of AHR did not affect cell proliferation compared with wildtype (WT). Consistent with these findings, no differences in tumor development between WT and AhrKO cells were observed in immunocompromised mice. However, tumors from AhrKO cells grew more slowly than tumors from WT cells in immune competent mice. RNA sequencing of the tumors resulted in 1009 genes upregulated and 477 genes downregulated in AhrKO tumors compared with WT tumors. Pathway analysis identified immunoregulatory interactions, interferon signaling, interleukin signaling and PD1 signaling among the top upregulated pathways. Increased infiltration of CD45+ cells and higher numbers of CD8+ T-cells and F4/80+ cells were observed in AhrKO tumors. Analysis of the F4/80+ cell populations revealed a lower percentage of anti-inflammatory (M2) macrophages in AhrKO tumors. Ahr deficiency in macrophages (LysMCre) or lymphocytes (RorcCre) did not alter tumor development of WT cells compared with WT C57BL/6 mice. AhrKO tumors in RorcCre mice, but not in LysMCre mice had significantly lower tumor weights normalized to body weights compared with AhrKO tumors in WT mice. These findings show that tumors derived from AhrKO pancreatic cancer cells exhibit a proinflammatory gene responses that contribute to increased immune cell infiltration and reduced tumor growth. They also suggesting that loss of AHR in lymphocytes together Ahr loss in cancer cells further reduces tumor growth.

Published in

Loss of aryl hydrocarbon receptor reduces pancreatic tumor growth by increasing immune cell infiltration

Kannen V, Olafsen NE, Das S et al. · Biochemical pharmacology 2025 · PMID 40090596 · doi:10.1016/j.bcp.2025.116872

This dataset

Open GSE279893 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 GSE279893_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 PRJNA1175267 and SRA study SRP539655. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40090596) ↗

Study design

6 × CR705, WT, vs 6 × CR705, AHRKO,

Supports a between-group comparison across 12 samples.

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

GSM8582637 CR705, WT, Rep1 CR705, WT,
GSM8582638 CR705, WT, Rep2 CR705, WT,
GSM8582639 CR705, WT, Rep3 CR705, WT,
GSM8582640 CR705, WT, Rep4 CR705, WT,
GSM8582641 CR705, WT, Rep5 CR705, WT,
GSM8582642 CR705, WT, Rep6 CR705, WT,
GSM8582643 CR705, AHRKO, Rep1 CR705, AHRKO,
GSM8582644 CR705, AHRKO, Rep2 CR705, AHRKO,
GSM8582645 CR705, AHRKO, Rep3 CR705, AHRKO,
GSM8582646 CR705, AHRKO, Rep4 CR705, AHRKO,
GSM8582647 CR705, AHRKO, Rep5 CR705, AHRKO,
GSM8582648 CR705, AHRKO, Rep6 CR705, AHRKO,

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