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

研究成果: 雜誌貢獻回顧型文獻

10 引文 斯高帕斯(Scopus)

摘要

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.
原文英語
頁(從 - 到)7-12
頁數6
期刊Hormones and Cancer
6
發行號1
DOIs
出版狀態已發佈 - 2014

ASJC Scopus subject areas

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

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