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 |
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頁(從 - 到) | 7-12 |
頁數 | 6 |
期刊 | Hormones and Cancer |
卷 | 6 |
發行號 | 1 |
DOIs | |
出版狀態 | 已發佈 - 2月 2014 |
ASJC Scopus subject areas
- 內分泌學、糖尿病和代謝
- 腫瘤科
- 內分泌
- 內分泌和自主系統
- 癌症研究