Molecular genetics of thyroid cancer

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Abstract
This review summarizes recent progress in understanding the somatic genetic events responsible for the multiple stages and pathways of development of tumors arising from the thyroid follicular cell. No new oncogenes have been added 10 the existing list of ras, ret, trk. gsp, and the thyroid-stimulating hormone receptor (TSHK) genes However, several new activating mutations of TSHR have been identified that are shedding light on its normal and pathological function. Unique features of the intracellular signal pathways employed by the ret gene product ore being uncovered that may explain the striking specificity of its activation for papillary thyroid cancer. In vitro gene transfer has provided direct experimental evidence for the role of ras and ret mutations as tumor initiators. Among the tumor suppressor genes, an important potential candidate — the APC gene — has been excluded. The correlation between p53 mutation and progression to undifferentiated cancer has been confirmed. In vitro studies have demonstrated the unusual ability of differentiated thyroid cancer to tolerate functional p53, a feature that may hold important general clues to the role of p53 in cancer progression.

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