Radioactive Iodine-Refractory Differentiated Thyroid Cancer and Redifferentiation Therapy
The retained functionality of the sodium iodide symporter (NIS) expressed in differentiated thyroid cancer (DTC) cells allows the further 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...
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| Format: | Article |
| Language: | English |
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Korean Endocrine Society
2019-09-01
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| Series: | Endocrinology and Metabolism |
| Subjects: | |
| Online Access: | https://e-enm.org/Synapse/Data/PDFData/2008ENM/enm-34-215.pdf |
| _version_ | 1818357455977971712 |
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| author | Jierui Liu Yanqing Liu Yansong Lin Jun Liang |
| author_facet | Jierui Liu Yanqing Liu Yansong Lin Jun Liang |
| author_sort | Jierui Liu |
| collection | DOAJ |
| description | The retained functionality of the sodium iodide symporter (NIS) expressed in differentiated thyroid cancer (DTC) cells allows the further 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 RAI therapy. Recently, novel and promising approaches aiming at various targets have been attempted to restore the expression of these iodine-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. |
| first_indexed | 2024-12-13T20:13:23Z |
| format | Article |
| id | doaj.art-646f5aca73f64a7cab51ade749d8f488 |
| institution | Directory Open Access Journal |
| issn | 2093-596X 2093-5978 |
| language | English |
| last_indexed | 2024-12-13T20:13:23Z |
| publishDate | 2019-09-01 |
| publisher | Korean Endocrine Society |
| record_format | Article |
| series | Endocrinology and Metabolism |
| spelling | doaj.art-646f5aca73f64a7cab51ade749d8f4882022-12-21T23:32:53ZengKorean Endocrine SocietyEndocrinology and Metabolism2093-596X2093-59782019-09-0134321522510.3803/EnM.2019.34.3.215Radioactive Iodine-Refractory Differentiated Thyroid Cancer and Redifferentiation TherapyJierui Liu0Yanqing Liu1Yansong Lin2Jun Liang3Department of Nuclear Medicine, Peking Union Medical College Hospital, Beijing, .ChinaDepartment of Nuclear Medicine, Peking Union Medical College Hospital, Beijing, .ChinaDepartment of Nuclear Medicine, Peking Union Medical College Hospital, Beijing, .ChinaDepartment of Oncology, Peking University International Hospital, Beijing, .ChinaThe retained functionality of the sodium iodide symporter (NIS) expressed in differentiated thyroid cancer (DTC) cells allows the further 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 RAI therapy. Recently, novel and promising approaches aiming at various targets have been attempted to restore the expression of these iodine-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.https://e-enm.org/Synapse/Data/PDFData/2008ENM/enm-34-215.pdfthyroid neoplasmssodium-iodide symporterisotopes |
| spellingShingle | Jierui Liu Yanqing Liu Yansong Lin Jun Liang Radioactive Iodine-Refractory Differentiated Thyroid Cancer and Redifferentiation Therapy Endocrinology and Metabolism thyroid neoplasms sodium-iodide symporter isotopes |
| title | Radioactive Iodine-Refractory Differentiated Thyroid Cancer and Redifferentiation Therapy |
| title_full | Radioactive Iodine-Refractory Differentiated Thyroid Cancer and Redifferentiation Therapy |
| title_fullStr | Radioactive Iodine-Refractory Differentiated Thyroid Cancer and Redifferentiation Therapy |
| title_full_unstemmed | Radioactive Iodine-Refractory Differentiated Thyroid Cancer and Redifferentiation Therapy |
| title_short | Radioactive Iodine-Refractory Differentiated Thyroid Cancer and Redifferentiation Therapy |
| title_sort | radioactive iodine refractory differentiated thyroid cancer and redifferentiation therapy |
| topic | thyroid neoplasms sodium-iodide symporter isotopes |
| url | https://e-enm.org/Synapse/Data/PDFData/2008ENM/enm-34-215.pdf |
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