Radiation-induced damage is a complex network of interlinked signaling pathways, which may result in apoptosis, cell cycle arrest, DNA repair, and cancer. The development of thyroid cancer in response to radiation, from nuclear catastrophes to chemotherapy, has long been an object of study. A basic overview of the ionizing and non-ionizing radiation effects of the sensitivity of the thyroid gland on radiation and cancer development has been provided. In this review, we focus our attention on experiments in cell cultures exposed to ionizing radiation, ultraviolet light, and proton beams. Studies on the involvement of specific genes, proteins, and lipids are also reported. This review also describes how lipids are regulated in response to the radiation-induced damage and how they are involved in thyroid cancer etiology, invasion, and migration and how they can be used as both diagnostic markers and drug targets.
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Publication date: 18 April 2017 Source: Cell Reports, Volume 19, Issue 3 Author(s): David Estoppey, Chia Min Lee, Marco Janoschke, Boon He...
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Abstract Functionalised electrospun polyamide-6 (PA-6) nanofibres incorporating gadolinium oxide nanoparticles conjugated to zinc tetracar...
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Cytokine-dependent renewal of stem cells is a fundamental requisite for tissue homeostasis and regeneration. Spermatogonial progenitor cells...
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Abstract This paper addresses the hybrid consensus-based formation keeping problem for nonholonomic mobile robots in the presence of a nov...
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Induced overexpression of CD44 associated with resistance to apoptosis on DNA damage response in human head and neck squamous cell carc...
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Current treatments for generalized pustular psoriasis are unsatisfactory. We applied recently-developed techniques for transcriptomic analys...
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Downregulation of mouse CCR3 by lentiviral shRNA inhibits proliferation and induces apoptosis of mouse eosinophils. Mol Med Rep. 2016 ...
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