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This version published online on August 31, 2006
Endocrinology, doi:10.1210/en.2006-0926
A more recent version of this article appeared on March 1, 2007
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*Thyroid Cancer

Submitted on July 11, 2006
Accepted on August 24, 2006

THE PAX8/PPAR{gamma} ONCOGENE IN THYROID TUMORIGENESIS

Honey V. Reddi, Bryan McIver, Stefan K.G. Grebe, and Norman L. Eberhardt*

Department of Medicine, Division of Endocrinology, Department of Laboratory Medicine and Pathology, Department of Biochemistry and Molecular Biology, Mayo Clinic & Foundation, Rochester, MN 55905

* To whom correspondence should be addressed. E-mail: eberhardt{at}mayo.edu.

The American Cancer Society estimates 30,180 new cases of thyroid cancer in the USA in 2006. Of all thyroid cancers, 15-20% are follicular thyroid carcinoma (FTC), making this the second most common thyroid malignancy (after papillary carcinoma, PTC). A proportion of FTC has been found to be associated with a chromosomal translocation, t (2;3)(q13;p25), which fuses the thyroid-specific transcription factor PAX8 with the peroxisome proliferator-activated receptor gamma (PPAR{gamma}) nuclear receptor, a ubiquitously expressed transcription factor. This fusion event causes expression of a PAX8/PPAR{gamma} fusion protein (PPFP). PPFP is detected in ~30% of FTC. In this report we review data on the role of PPFP in FTC, its mechanism of oncogenesis and PPFP targeting as a strategy in thyroid cancer treatment.






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