Thyroid follicular cell proliferation

Hood A, Hashmi R, Klaassen CD. 1999. Effects of microsomal enzyme inducers on thyroid-follicular cell proliferation, hyperplasia, and hypertrophy. Toxicol Appl Pharmacol 160 163-170. 

Hood, A., M. L. Allen, Y. Liu, J. Liu, and C. D. Klaassen. 2003. Induction of T(4) UDP-GT activity, serum thyroid stimulating hormone, and thyroid follicular cell proliferation in mice treated with microsomal enzyme inducers. Toxicology and Applied Pharmacology 188 6-13. 

Smith, P., Wyndford-Thomas, D., Stringer, B.M.J., Williams, E.D., 1986, Growth factor control of rat thyroid follicular cell proliferation. Endocrinology 119 1439. 

The decrease of T4 concentration with the increased thyroid weight and enhanced thyroid follicular cell hypertrophy [28, 29] was induced by an increased activity of a liver enzyme (UDPG-transferase) involved in peroxisome proliferation [33, 35, 36]. This mechanism is also specific to rodents. Therefore, thyroidal effects that were observed in the studies in rats and mice are considered unlikely to be relevant to human health. 

The t(2 3)(ql3 p25) translocation, found in a subset of thyroid follicular carcinomas, results in fusion of the DNA binding domains of the thyroid transcription factor PAX-8 to domains A-F of the peroxisome proliferation-activated receptor (PPAR) y 1 (Hg. 10.13). Studies using PCR and immunohistochemistry demonstrated that most follicular carcinomas positive for PPAR Y were widely invasive while tumors lacking the rearrangement were PPAR y negative. Papillary carcinomas and Hurthle cell tumors were negative. Other studies, however, have reported positivity both in follicular carcinomas and adenomas. 

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