Abstract
Well-standardized primary treatment and long-term management of differentiated thyroid carcinoma (DTC) include lowering or suppression of host thyrotropin (TSH) with exogenous L-thyroxine (T4). This treatment recognizes the trophic action of TSH on DTC cells. Suppression of endogenous TSH with T4 is continued in recurrent disease. However, T4 can induce proliferation of follicular and papillary thyroid carcinoma cell lines and of other human carcinoma cells. The proliferative mechanism is initiated at a cell surface receptor for T4 on integrin αvβ3, a receptor by which the hormone also inhibits p53-dependent apoptosis in tumor cells. In recurrent DTC with satisfactory suppression of endogenous TSH, we discuss here the possibility that the tumor is no longer TSH dependent and that T4 has become a critical growth factor for the cancer.
Highlights
Well-standardized primary treatment and longterm management of differentiated thyroid carcinoma (DTC) include lowering or suppression of host thyrotropin (TSH) with exogenous L-thyroxine (T4)
Initial and long-term management guidelines provided by the American Thyroid Association have worked to standardize the surgical, radioablative, and medical treatment of differentiated thyroid carcinoma (DTC) [16] and have drawn a number of substantial comments [63, 70, 73]
TSH is a growth factor for papillary and follicular thyroid cancer, and successful TSH suppression therapy assumes a functional TSH receptor (TSHR) in thyroid cells whose activity is minimized by the dearth of circulating TSH
Summary
Well-standardized primary treatment and longterm management of differentiated thyroid carcinoma (DTC) include lowering or suppression of host thyrotropin (TSH) with exogenous L-thyroxine (T4). TSH is a growth factor for papillary and follicular thyroid cancer, and successful TSH suppression therapy assumes a functional TSH receptor (TSHR) in thyroid cells whose activity is minimized by the dearth of circulating TSH. One such factor is thyroid hormone (see section) which has been shown to have proliferative effects on follicular and papillary thyroid carcinoma cells [48].
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