This is a legacy representation of this AOP. Please see the current version here:
Cancer AOP group. National Health and Environmental Effects Research Laboratory, Office of Research and Development, Integrated Systems Toxicology Division, US Environmental Protection Agency, Research Triangle Park, NC. Corresponding author for wiki entry (email@example.com)
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This AOP page was last modified on 12/11/2016.
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This putative adverse outcome pathway (AOP) outlines potential key events leading to a tumor outcome in standard carcinogenicity models. This information is based largely on modes of action described previously in cited literature sources and is intended as a resource template for AOP development and data organization. Presentation in this Wiki does not indicate EPA acceptance of a particular pathway for a given reference agent, only that the information has been proposed in some manner. In addition, this putative AOP relates to the model species indicated and does not directly address issues of human relevance
Summary of the AOP
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Molecular Initiating Event
|Molecular Initiating Event||Support for Essentiality|
|Uptake of inorganic iodide, Decreased|
|Event||Support for Essentiality|
|Serum thyroid hormone (T4/T3), Decrease|
|Thyroid-stimulating hormone (TSH), Increase|
|Hypertrophy and proliferation (follicular cell), Increase|
|Hyperplasia (follicular cells), Increase|
|Adenomas/carcinomas (follicular cell), Increase|
Relationships Among Key Events and the Adverse Outcome
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Life Stage Applicability
|Rattus norvegicus||Rattus norvegicus||NCBI|
|Mus musculus||Mus musculus||NCBI|
Overall Assessment of the AOP
Domain of Applicability
Life Stage Applicability,
Elaborate on the domains of applicability listed in the summary section above. Specifically, provide the literature supporting, or excluding, certain domains.
Essentiality of the Key Events
Molecular Initiating Event Summary,
Key Event Summary
Provide an overall assessment of the essentiality for the key events in the AOP. Support calls for individual key events can be included in the molecular initiating event, key event, and adverse outcome tables above.
Weight of Evidence Summary
Provide an overall summary of the weight of evidence based on the evaluations of the individual linkages from the Key Event Relationship pages.
Provide an overall discussion of the quantitative information available for this AOP. Support calls for the individual relationships can be included in the Key Event Relationship table above.
Considerations for Potential Applications of the AOP (optional)
Dellarco, V. L., McGregor, D., Berry, S. C., Cohen, S. M., & Boobis, A. R. (2006). Thiazopyr and thyroid disruption: case study within the context of the 2006 IPCS Human Relevance Framework for analysis of a cancer mode of action. Crit Rev Toxicol, 36(10), 793-801. doi: 10.1080/10408440600975242
U.S. Environmental Protection Agency, R. A. F. (Mar. 1998). Assessment of Thyroid Follicular Cell Tumors. Washington, DC.
Hurley, P. M. (1998). Mode of carcinogenic action of pesticides inducing thyroid follicular cell tumors in rodents. Environ Health Perspect, 106(8), 437-445.
Wolff, J. (1998). Perchlorate and the thyroid gland. Pharmacol Rev, 50(1), 89-105.