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Molecular mechanism of thyroid carcinogenesis has been well studied through the discovery of genetic abnormalities such as RET/PTC rearrangement and BRAF mutation, both of which constitutively activate MAP kinase pathway and are frequently found in papillary thyroid cancer. The TP53 mutation is thought to play a critical role in transformation of differentiated thyroid cancer into anaplastic thyroid cancer. Besides these genetic alterations, cancer stem cell theory has recently been applied to thyroid field. A better understanding of thyroid cancer stem cell may not only ameliorate our comprehension of thyroid cancer biology, but also open the possibility of innovative diagnostic procedures and development of novel targeted therapies. In this article, we mainly review thyroid carcinogenesis based on the evidence of radiation-induced cancer and cancer stem cell hypothesis.

A number of genetic abnormalities in oncogenes or anti-oncogenes have been identified in association with thyroid carcinogenesis. Especially, oncogenes such as ras mutation, ret/PTC and Braf mutation that constitutively activate MAP kinase pathway a refrequently found in papillary thyroid cancer. The p53 mutation aggravates differentiated thyroid cancers to anaplastic thyroid cancer. These gene alterations are studied not only to understand basically the mechanisms of oncogenesis but also to develop clinically genetic diagnosis or molecular target therapy. In this article, we review the genetic diagnostic methods and phenotype-genotype relationship of human thyroid cancers.