
This AOP is licensed under a Creative Commons Attribution 4.0 International License.
Aop: 303
Title
Frustrated phagocytosis-induced lung cancer
Short name
Graphical Representation
Point of Contact
Contributors
- Carole Seidel
- Sarah Valentino
- Laurent GATE
- Arthur Author
Status
Author status | OECD status | OECD project | SAAOP status |
---|---|---|---|
Under development: Not open for comment. Do not cite | Under Development | 1.86 | Included in OECD Work Plan |
This AOP was last modified on July 16, 2022 18:37
Revision dates for related pages
Page | Revision Date/Time |
---|---|
Frustrated phagoytosis | August 13, 2019 04:48 |
Release, Cytokine | September 16, 2017 10:14 |
Increased, recruitment of inflammatory cells | January 25, 2022 15:52 |
Increased, Reactive oxygen species | November 27, 2017 13:15 |
Increased, DNA damage and mutation | August 13, 2019 05:41 |
Increase, Cell Proliferation | June 23, 2021 12:28 |
Lung cancer | August 13, 2019 05:34 |
Frustrated phagoytosis leads to Release, Cytokine | August 13, 2019 05:25 |
Release, Cytokine leads to Recruitment of inflammatory cells | July 03, 2019 11:52 |
Recruitment of inflammatory cells leads to Increased, Reactive oxygen species | July 03, 2019 11:53 |
Increased, Reactive oxygen species leads to Increased, DNA damage and mutation | July 03, 2019 11:53 |
Increased, DNA damage and mutation leads to Increase, Cell Proliferation | July 03, 2019 11:53 |
Increase, Cell Proliferation leads to Lung cancer | July 03, 2019 11:53 |
High aspect ratio material | August 13, 2019 04:38 |
Abstract
Inhalation of materials, including fibres and particles, represents the main route of occupational exposure. The main issue is the biopersistance of these materials in lungs that could lead to chronic pulmonary pathologies such as fibrosis and cancer. Lung tumour is one of the most prevalent cancer in the world and, in general, is often detected at a late stage.
The knowledge related to the induction of lung disease following asbestos exposure led to study the toxicity of high aspect ratio materials (HARMs) in general. It is now well documented that exposure to HARMs could lead to pulmonary inflammation and ROS overproduction. Some studies suggest that lung biopersistence of HARMs is associated with frustrated phagocytosis and material length. The identified gaps regarding the induction of lung cancer following the exposure to HARMs is mainly on the interaction with cells, and no study demonstrated all the key events presented here in the same samples.
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 | 1668 | Frustrated phagoytosis | Frustrated phagoytosis |
KE | 87 | Release, Cytokine | Release, Cytokine |
KE | 1497 | Increased, recruitment of inflammatory cells | Recruitment of inflammatory cells |
KE | 1115 | Increased, Reactive oxygen species | Increased, Reactive oxygen species |
KE | 1669 | Increased, DNA damage and mutation | Increased, DNA damage and mutation |
KE | 870 | Increase, Cell Proliferation | Increase, Cell Proliferation |
AO | 1670 | Lung cancer | Lung cancer |
Relationships Between Two Key Events (Including MIEs and AOs)
Title | Adjacency | Evidence | Quantitative Understanding |
---|
Network View
Prototypical Stressors
Life Stage Applicability
Life stage | Evidence |
---|---|
Adult |
Taxonomic Applicability
Term | Scientific Term | Evidence | Link |
---|---|---|---|
mammals | mammals | NCBI |
Sex Applicability
Sex | Evidence |
---|---|
Unspecific |
Overall Assessment of the AOP
Domain of Applicability
This AOP is applicable to adult (at least to mature lung tissue), to many vertebrate taxons, and to both genders.