Thyroid cancer is a frequent endocrine related malignancy with continuous increasing incidence. There has been moving development in understanding its molecular pathogenesis recently mainly through the explanation of the original role of several key signaling pathways and related molecular distributors. Central to these mechanisms are the genetic and epigenetic alterations in these pathways, such as mutation and DNA rearrangements. That does not mean, however, that all the somatic abnormalities here in a cancer genome have been involved in development of the cancer and just driver mutations are concerned in tumor initiation. By way of illustrations, MAPK pathway which is motivated by BRAFV600E and RAS and RET / PTC rearrangements are suggesting driver genetic alterations in follicular derived thyroid cancers which are considered in this review.
Thyroid carcinogenesis is a complicated process in which various genetic alterations happen. All these genetic mutations and rearrangements are not equally important, because some of them are driver mutations and the others are passenger mutations. The focus of this review is over the most important driver mutations in follicular derived thyroid cancers.