Animal Models of Thyroid Carcinogenesis

Conclusions

This animal model clearly supports the concept that in thyroid carcinogenesis, there is a very long latency period between the mutational event and the developement of malignant changes. This contradicts previous studies using a higher stimulation of thyrocyte proliferation by iodine deficiency, where malignancies were detected after much shorter time intervals (Axelrad & Leblond 1955). Large doses of iodine may induce thyroid carcinomas (Correa & Welsh 1960). We showed that mild iodine excess is not necessarily associated with the formation of thyroid malignant neoplasms, but when combined with a mutagen, carcinomas arise with high frequency. These data on mild forms of high iodine intake thus put a note of caution to a long term-use of high iodine. It was shown that euthyreosis is best protection against thyroid cancer before environmental hazards are effective.

The well-defined setting in these experiments clearly demonstrates that mutational lesions acquired by radiation are clinically silent over a long period of time. It is tempting to use such a model to search for candidate genes altered by mutagens, but which are not changed in thyroid adenomas found under control conditions. The definition of such changes may then have important implications for the characterization of the malignant potential of a given adenoma well before cytological or histological changes occur.