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An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
Published on: April 17, 2013
Thyroid follicular cell carcinogenesis
R N Hill1, L S Erdreich, O E Paynter
1Office of Pesticides and Toxic Substances, U.S. Environmental Protection Agency, Washington, D.C. 20460.
Summary
Thyroid-pituitary disruption in animals can cause thyroid tumors, often reversible by restoring hormonal balance. Human data is less certain, with ionizing radiation being the primary known carcinogen.
Area of Science:
- Endocrinology
- Toxicology
- Oncology
Background:
- Inhibition of thyroid-pituitary homeostasis is linked to thyroid follicular cell neoplasms in animal models.
- Long-term hormonal imbalances, particularly elevated thyroid stimulating hormone, drive tumor development.
- This process involves stages from cellular changes to benign and malignant growths.
Purpose of the Study:
- To review the relationship between thyroid-pituitary homeostasis and thyroid neoplasms.
- To compare findings in animal models with human data regarding thyroid carcinogens.
- To elucidate mechanisms of thyroid carcinogenesis.
Main Methods:
- Review of experimental animal data on thyroid-pituitary axis disruption and neoplasia.
- Analysis of chemical and physical agents affecting thyroid function and tumor development.
- Comparison of animal findings with human epidemiological and experimental evidence.
Main Results:
- In animals, thyroid neoplasms arise from sustained hormonal imbalances, often reversible.
- Most chemicals induce tumors by affecting thyroid hormone synthesis or degradation, not necessarily via genotoxicity.
- Ionizing radiation is the only confirmed human thyroid carcinogen; human sensitivity to hormonal disruption differs from animals.
Conclusions:
- Thyroid-pituitary axis disruption is a significant factor in animal thyroid carcinogenesis.
- Mechanisms involve hormonal imbalance and potentially genotoxicity for some agents.
- Human thyroid cancer development from hormonal disruption is less clear and likely involves lower sensitivity compared to animal models.
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