ReviewHormones & cancer2014
Modulation of sodium iodide symporter in thyroid cancer.
Review in Hormones & cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Salivary gland dynamic imaging combined with tomosynthesis fusion imaging for evaluating postoperative salivary gland function changes in patients with differentiated thyroid cancer undergoing initialQuantitative imaging in medicine and surgery · 2026Article
- Predictive Factors of Radioactive Iodine Therapy Refractoriness in Patients with Differentiated Thyroid Carcinoma.World journal of nuclear medicine · 2024Article
- The Cross-Talk between Polyphenols and the Target Enzymes Related to Oxidative Stress-Induced Thyroid Cancer.Oxidative medicine and cellular longevity · 2022Review
- MAPK Inhibition Requires Active RAC1 Signaling to Effectively Improve Iodide Uptake by Thyroid Follicular Cells.Cancers · 2021Article
- Tumor microenvironment affects exogenous sodium/iodide symporter expression.Translational oncology · 2021Article
- Downregulation of Rap1GAP Expression Activates the TGF-BioMed research international · 2021Article
- FOXA1 Regulation Turns Benzamide HDACi Treatment Effect-Specific in BC, Promoting NIS Gene-Mediated Targeted Radioiodine Therapy.Molecular therapy oncolytics · 2020Article
- Physiological and Pathophysiological Roles of Ion Transporter-Mediated Metabolism in the Thyroid Gland and in Thyroid Cancer.OncoTargets and therapy · 2020Review
- TNFα-mediated activation of NF-κB downregulates sodium-iodide symporter expression in thyroid cells.PloS one · 2020Article
- Dedifferentiation patterns in DTC: is PDTC an intermediate state between DTC and ATC?International journal of clinical and experimental pathology · 2019Article
- A Nonpump Function of Sodium Iodide Symporter in Thyroid Cancer via Cross-talk with PTEN Signaling.Cancer research · 2018Article
- Improved radioiodine-131 imaging of prostatic carcinoma using the sodium iodide symporter gene under control of the survivin promoter.International journal of clinical and experimental pathology · 2018Article
- Flavonoids, Thyroid Iodide Uptake and Thyroid Cancer-A Review.International journal of molecular sciences · 2017Review
- Effects of BRAF(V600E) mutation on Na(+)/I(-) symporter expression in papillary thyroid carcinoma.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2016Article
- FoxP3 in papillary thyroid carcinoma induces NIS repression through activation of the TGF-β1/Smad signaling pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Modulation of thyroidal radioiodide uptake by oncological pipeline inhibitors and Apigenin.Oncotarget · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Radioactive iodine (RAI) is a key therapeutic modality for thyroid cancer. Loss of RAI uptake in thyroid cancer inversely correlates with patient's survival. In this review, we focus on the challenges encountered in delivering sufficient doses of I-131 to eradicate metastatic lesions without increasing the risk of unwanted side effects. Sodium iodide symporter (NIS) mediates iodide influx, and NIS expression and function can be selectively enhanced in thyroid cells by thyroid-stimulating hormone. We summarize our current knowledge of NIS modulation in normal and cancer thyroid cells, and we propose that several reagents evaluated in clinical trials for other diseases can be used to restore or further increase RAI accumulation in thyroid cancer. Once validated in preclinical mouse models and clinical trials, these reagents, mostly small-molecule inhibitors, can be readily translated into clinical practice. We review available genetically engineered mouse models of thyroid cancer in terms of their tumor development and progression as well as their thyroid function. These mice will not only provide important insights into the mechanisms underlying the loss of RAI uptake in thyroid tumors but will also serve as preclinical animal models to evaluate the efficacy of candidate reagents to selectively increase RAI uptake in thyroid cancers. Taken together, we anticipate that the optimal use of RAI in the clinical management of thyroid cancer is yet to come in the near future.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.