Recurrence of Differentiated Thyroid Carcinoma During Full TSH Suppression: Is the Tumor Now Thyroid Hormone Dependent?

Paul J. Davis, Aleck Hercbergs, Mary K. Luidens, Hung Yun Lin

Research output: Contribution to journalReview article

9 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)7-12
Number of pages6
JournalHormones and Cancer
Volume6
Issue number1
DOIs
Publication statusPublished - 2014

ASJC Scopus subject areas

  • Oncology
  • Cancer Research
  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Endocrine and Autonomic Systems

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