scholarly journals Preclinical efficacy of the oncolytic measles virus expressing the sodium iodide symporter in iodine non-avid anaplastic thyroid cancer: a novel therapeutic agent allowing noninvasive imaging and radioiodine therapy

2012 ◽  
Vol 19 (9) ◽  
pp. 659-665 ◽  
Author(s):  
H V Reddi ◽  
P Madde ◽  
S J McDonough ◽  
M A Trujillo ◽  
J C Morris ◽  
...  
Autophagy ◽  
2016 ◽  
Vol 12 (7) ◽  
pp. 1195-1205 ◽  
Author(s):  
Theo S. Plantinga ◽  
Marika H. Tesselaar ◽  
Hans Morreau ◽  
Eleonora P. M. Corssmit ◽  
Brigith K. Willemsen ◽  
...  

2009 ◽  
Vol 17 (12) ◽  
pp. 2041-2048 ◽  
Author(s):  
Pavlos Msaouel ◽  
Ianko D Iankov ◽  
Cory Allen ◽  
Ileana Aderca ◽  
Mark J Federspiel ◽  
...  

2021 ◽  
Vol 22 (3) ◽  
pp. 1077
Author(s):  
Yoon Ju Choi ◽  
Jae-Eon Lee ◽  
Hyun Dong Ji ◽  
Bo-Ra Lee ◽  
Sang Bong Lee ◽  
...  

The silencing of thyroid-related genes presents difficulties in radioiodine therapy for anaplastic thyroid cancers (ATCs). Tunicamycin (TM), an N-linked glycosylation inhibitor, is an anticancer drug. Herein, we investigated TM-induced restoration of responsiveness to radioiodine therapy in radioiodine refractory ATCs. 125I uptake increased in TM-treated ATC cell lines, including BHT101 and CAL62, which was inhibited by KClO4, a sodium-iodide symporter (NIS) inhibitor. TM upregulated the mRNA expression of iodide-handling genes and the protein expression of NIS. TM blocked pERK1/2 phosphorylation in both cell lines, but AKT (protein kinase B) phosphorylation was only observed in CAL62 cells. The downregulation of glucose transporter 1 protein was confirmed in TM-treated cells, with a significant reduction in 18F-fluorodeoxyglucose (FDG) uptake. A significant reduction in colony-forming ability and marked tumor growth inhibition were observed in the combination group. TM was revealed to possess a novel function as a redifferentiation inducer in ATC as it induces the restoration of iodide-handling gene expression and radioiodine avidity, thereby facilitating effective radioiodine therapy.


2007 ◽  
Vol 5 (6) ◽  
pp. 631-640 ◽  
Author(s):  
Jacqueline Jonklaas

Normal thyrocytes and thyroid cancer cells are characterized by possession of a sodium iodide symporter. Radioiodine administration is a unique and powerful means of treating differentiated thyroid cancer because of the ability of thyroid cancer cells to concentrate beta-emitting radiolabeled iodine. Several manipulations, such as iodine depletion and thyroid hormone-stimulating hormone elevation, are used to enhance uptake of radiolabeled iodine by tumor cells. Adjuvant radioiodine therapy, given to patients without evidence of residual disease, enhances the sensitivity of subsequent surveillance and may decrease recurrence rates and mortality. However, its exact role in the management of low-risk patients merits further investigation. In contrast, radioactive iodine therapy used in patients with residual or metastatic disease clearly improves outcomes. Several studies show decreased recurrence and mortality rates in patients treated with radioiodine compared with those not receiving radioactive iodine. Adverse events from radioiodine therapy include salivary gland dysfunction, bone marrow suppression, and reproductive disturbances. Side effects of radioiodine therapy are generally greater when higher activities of radioiodine are used and may be transient or permanent. Secondary malignancies also may occur after radioiodine therapy. These side effects must be weighed against potential benefits, especially when radioactive iodine is used as adjuvant therapy. Stimulation of the expression of the sodium iodide symporter, or its introduction de novo into nonthyroid cells, is promising in treating poorly differentiated thyroid cancer and nonthyroid malignancies, respectively.


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