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AOP: 578
Title
AhR activation leading to cancer progression via immunosuppression
Short name
Graphical Representation
Point of Contact
Contributors
- Léo SPORTES-MILOT
- Etienne Blanc
- Xavier COUMOUL
Coaches
- Annamaria Colacci
- Julija Filipovska
OECD Information Table
| OECD Project # | OECD Status | Reviewer's Reports | Journal-format Article | OECD iLibrary Published Version |
|---|---|---|---|---|
This AOP was last modified on February 25, 2026 04:39
Revision dates for related pages
| Page | Revision Date/Time |
|---|---|
| Activation, AhR | May 31, 2025 07:56 |
| Over-expression of PD-L1 in cancer cells | September 30, 2025 12:12 |
| Increased of Treg/Th17 cell ratio | February 24, 2026 11:48 |
| CTL cytotoxic activity disruption | February 24, 2026 11:49 |
| Increased, tumor growth | February 29, 2024 06:05 |
| Activation, AhR leads to Over-expression of PD-L1 in cancer cells | February 25, 2026 04:37 |
| Over-expression of PD-L1 in cancer cells leads to Dysregulation of Treg/Th17 cell ratio | February 25, 2026 08:45 |
| Dysregulation of Treg/Th17 cell ratio leads to CTL cytotoxicity | May 22, 2025 12:01 |
| CTL cytotoxicity leads to tumor growth | June 10, 2025 09:59 |
| 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) | February 09, 2017 14:32 |
Abstract
Due to the evolution of our society, numerous chemical compounds are created, produced, and released into the environment. However, the impact on the environment and human health remains to be demonstrated for many of them. The AhR receptor is known to be an essential receptor in the metabolism of these xenobiotics. Moreover, AhR regulates many cellular signaling pathways, notably in immunity. Thus, the over-activation of AhR could lead to harmful effects. This AOP focuses on the mechanisms linking AhR activation (MIE) and immunosuppression that can lead to tumor progression (AO).
A literature analysis using artificial intelligences such as AOP-helpfinder or Perplexity highlighted 55 articles. After analyzing these articles, clear links between AhR activation, PD-L1 (Program Death Ligand) expression, the impact on lymphocytes, and finally cancer progression were identified as KEs and KER.
These analyses bring together scientific results in vitro and in vivo, several types of cancers in humans and animals, as well as reviews and articles.
AOP Development Strategy
Context
Strategy
Summary of the AOP
Events:
Molecular Initiating Events (MIE)
Key Events (KE)
Adverse Outcomes (AO)
| Type | Event ID | Title | Short name |
|---|
| MIE | 18 | Activation, AhR | Activation, AhR |
| KE | 2323 | Over-expression of PD-L1 in cancer cells | Over-expression of PD-L1 in cancer cells |
| KE | 2324 | Increased of Treg/Th17 cell ratio | Dysregulation of Treg/Th17 cell ratio |
| KE | 2326 | CTL cytotoxic activity disruption | CTL cytotoxicity |
| AO | 1971 | Increased, tumor growth | tumor growth |
Relationships Between Two Key Events (Including MIEs and AOs)
| Title | Adjacency | Evidence | Quantitative Understanding |
|---|
Network View
Prototypical Stressors
Life Stage Applicability
Taxonomic Applicability
Sex Applicability
Overall Assessment of the AOP
Domain of Applicability
Essentiality of the Key Events
Evidence Assessment
Known Modulating Factors
| Modulating Factor (MF) | Influence or Outcome | KER(s) involved |
|---|---|---|