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논문 기본 정보

자료유형
학술저널
저자정보
Jierui Liu (Peking Union Medical College Hospital) Yanqing Liu (Peking Union Medical College Hospital) Yan-Song Lin (Department of Nuclear Medicine Peking Union Medical College Hospital) Jun Liang (Peking University)
저널정보
대한내분비학회 Endocrinology and Metabolism Endocrinology and Metabolism Vol.34 No.3
발행연도
2019.1
수록면
215 - 225 (11page)

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초록· 키워드

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The retained functionality of the sodium iodide symporter (NIS) expressed in differentiated thyroid cancer (DTC) cells allows thefurther utilization of post-surgical radioactive iodine (RAI) therapy, which is an effective treatment for reducing the risk of recurrence, and even the mortality, of DTC. Whereas, the dedifferentiation of DTC could influence the expression of functional NIS,thereby reducing the efficacy of RAI therapy in advanced DTC. Genetic alternations (such as BRAF and the rearranged during transfection [RET]/papillary thyroid cancer [PTC] rearrangement) have been widely reported to be prominently responsible for the onset,progression, and dedifferentiation of PTC, mainly through activating the mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K) signaling cascades. These genetic alternations have been suggested to associate with the reduced expression of iodide-handling genes in thyroid cancer, especially the NIS gene, disabling iodine uptake and causing resistance to RAItherapy. Recently, novel and promising approaches aiming at various targets have been attempted to restore the expression of theseiodine-metabolizing genes and enhance iodine uptake through in vitro studies and studies of RAI-refractory (RAIR)-DTC patients. In this review, we discuss the regulation of NIS, known mechanisms of dedifferentiation including the MAPK and PI3K pathways,and the current status of redifferentiation therapy for RAIR-DTC patients.

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