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Abstract
Tumor development within the human thyroid gland provides an attractive experimental model with which to consider the pathogenesis of carcinoma, the most common and clinically significant cancer. Thyroid tumors are readily accessible to morphological and molecular study because their primary treatment is surgical. Investigations of thyroid cancer have expanded our knowledge of carcinoma biology. Thyroid carcinoma is the only adult epithelial malignancy in which specific chromosomal rearrangements have been identified. 1-3 RET and PPARγ rearrangements in thyroid carcinoma create fusion proteins that are hypothesized to play fundamental roles in thyroid oncogenesis. 3,4 The fusion protein pathways are prime targets for new strategies directed at improving thyroid cancer diagnosis and treatment. 5-7
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