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Aop: 112

AOP Title

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Increased dopaminergic activity leading to endometrial adenocarcinomas (in Wistar rat)

Short name:

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Dopaminergic activity- endometrial carcinoma

Graphical Representation

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Click to download graphical representation template

Authors

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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 (wood.charles@epa.gov)

Point of Contact

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Charles Wood   (email point of contact)

Contributors

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  • Charles Wood

Status

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Author status OECD status OECD project SAAOP status
Under development: Not open for comment. Do not cite 1.29 Under Development


This AOP was last modified on January 27, 2018 15:34

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Revision dates for related pages

Page Revision Date/Time
Increase, Dopaminergic activity September 16, 2017 10:16
Decreased, Prolactin September 16, 2017 10:16
Increased, Estrogen receptor (ER) activity December 03, 2016 16:37
Decreased, Progesterone from corpus luteum September 16, 2017 10:16
Increase, Hyperplasia (glandular epithelial cells of endometrium) September 16, 2017 10:16
Increase, Endometrial adenocarcinomas September 16, 2017 10:16
Increase, Dopaminergic activity leads to Decreased, Prolactin December 03, 2016 16:37
Decreased, Prolactin leads to Increased, Estrogen receptor (ER) activity December 03, 2016 16:37
Increased, Estrogen receptor (ER) activity leads to Decreased, Progesterone from corpus luteum December 03, 2016 16:37
Increase, Hyperplasia (glandular epithelial cells of endometrium) leads to Increase, Endometrial adenocarcinomas December 03, 2016 16:38
Decreased, Progesterone from corpus luteum leads to Increase, Hyperplasia (glandular epithelial cells of endometrium) December 03, 2016 16:38

Abstract

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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.


Background (optional)

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Summary of the AOP

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Events: Molecular Initiating Events (MIE)

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Key Events (KE)

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Adverse Outcomes (AO)

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Sequence Type Event ID Title Short name
1 MIE 746 Increase, Dopaminergic activity Increase, Dopaminergic activity
2 KE 747 Decreased, Prolactin Decreased, Prolactin
3 KE 748 Increased, Estrogen receptor (ER) activity Increased, Estrogen receptor (ER) activity
4 KE 749 Decreased, Progesterone from corpus luteum Decreased, Progesterone from corpus luteum
5 KE 772 Increase, Hyperplasia (glandular epithelial cells of endometrium) Increase, Hyperplasia (glandular epithelial cells of endometrium)
6 AO 773 Increase, Endometrial adenocarcinomas Increase, Endometrial adenocarcinomas

Relationships Between Two Key Events
(Including MIEs and AOs)

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Title Adjacency Evidence Quantitative Understanding
Increase, Dopaminergic activity leads to Decreased, Prolactin adjacent
Decreased, Prolactin leads to Increased, Estrogen receptor (ER) activity adjacent
Increased, Estrogen receptor (ER) activity leads to Decreased, Progesterone from corpus luteum adjacent
Increase, Hyperplasia (glandular epithelial cells of endometrium) leads to Increase, Endometrial adenocarcinomas adjacent
Decreased, Progesterone from corpus luteum leads to Increase, Hyperplasia (glandular epithelial cells of endometrium) adjacent

Network View

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Stressors

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Life Stage Applicability

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Taxonomic Applicability

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Term Scientific Term Evidence Link
Rattus norvegicus Rattus norvegicus NCBI

Sex Applicability

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Sex Evidence
Female

Overall Assessment of the AOP

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Domain of Applicability

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Essentiality of the Key Events

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Evidence Assessment

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Quantitative Understanding

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Considerations for Potential Applications of the AOP (optional)

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References

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Gunin, A. G., Emelianov, V., Tolmachev, A. S., & Tolmacheva, A. (2002). Effect of prolactin and dopaminergic drugs on uterine response to chronic estrogen exposure. J Endocrinol, 172(1), 61-69.

Harleman, J. H., Hargreaves, A., Andersson, H., & Kirk, S. (2012). A review of the incidence and coincidence of uterine and mammary tumors in Wistar and Sprague-Dawley rats based on the RITA database and the role of prolactin. Toxicol Pathol, 40(6), 926-930. doi: 10.1177/0192623312444621

O'Connor, J. C., Plowchalk, D. R., Van Pelt, C. S., Davis, L. G., & Cook, J. C. (2000). Role of prolactin in chloro-S-triazine rat mammary tumorigenesis. Drug Chem Toxicol, 23(4), 575-601. doi: 10.1081/DCT-100101972