Biología molecular del carcinoma de tiroides de estirpe folicular. Bases moleculares en la oncogénesis tiroidea

According to current data, it seems probable that there is no  interruption in the evolution of different follicular thyroid neoplasm.  Probably transforming events responsible for the transition from normal  to tumor cells start with molecular changes that determine the  appearance of follicular adenoma. Later changes propitiate the  development of follicular cancer. It is likely that the generation of  papillary carcinoma follows a different pathway without passing  through a previous phase of follicular adenoma. Subsequently, genetic  changes render the cell prone to a failure to differentiate, culminating  in the development of anaplastic cancer. Those incidental molecular  changes result in a dramatic worsening in the prognosis of thyroid  cancer. Research into thyroid tumors is likely to be instructive in view  of the spectrum they span, from benign adenomas to poorly  differentiated carcinomas.   It has been proven that molecular alterations in thyroid tumor cells  are predisposed by genome instability. Usually changes of protooncogenes  represent an early event whereas mutations of suppressant  genes are usually a late phenomenon. The onset of aggressive or  invasive behavior may be studied, and perhaps can be predicted in  the future, by molecular changes.   The clinical application of the growing understanding of gene  alterations involved in thyroidal oncogenesis is becoming a reality.  Such knowledge might contribute, in the near future, to greater  diagnostic accuracy and effective treatment for thyroid malignancies.