Biología molecular del carcinoma de tiroides de estirpe folicular. Bases moleculares en la oncogénesis tiroidea
2017
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.
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