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

doi:10.1007/s12672-014-0204-z

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 journal › Review article › peer-review

14 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 language	English
Pages (from-to)	7-12
Number of pages	6
Journal	Hormones and Cancer
Volume	6
Issue number	1
DOIs	https://doi.org/10.1007/s12672-014-0204-z
Publication status	Published - Feb 2014

ASJC Scopus subject areas

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

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1007/s12672-014-0204-z

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

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.",

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AU - Lin, Hung Yun

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

Abstract

ASJC Scopus subject areas

UN SDGs

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