<b>Conclusions</b>: Our data demonstrate that vitamin C kills thyroid cancer cells by inhibiting MAPK/ERK and PI3K/AKT pathways via a ROS-dependent mechanism and suggest that pharmaceutical concentration of vitamin C has potential clinical use in thyroid cancer therapy.
<b>Conclusions</b>: Our data demonstrate that vitamin C kills thyroid cancer cells by inhibiting MAPK/ERK and PI3K/AKT pathways via a ROS-dependent mechanism and suggest that pharmaceutical concentration of vitamin C has potential clinical use in thyroid cancer therapy.
<b>Conclusions</b>: Our data demonstrate that vitamin C kills thyroid cancer cells by inhibiting MAPK/ERK and PI3K/AKT pathways via a ROS-dependent mechanism and suggest that pharmaceutical concentration of vitamin C has potential clinical use in thyroid cancer therapy.
<b>Conclusions</b>: Our data demonstrate that vitamin C kills thyroid cancer cells by inhibiting MAPK/ERK and PI3K/AKT pathways via a ROS-dependent mechanism and suggest that pharmaceutical concentration of vitamin C has potential clinical use in thyroid cancer therapy.
<b>Conclusions</b>: Our data demonstrate that vitamin C kills thyroid cancer cells by inhibiting MAPK/ERK and PI3K/AKT pathways via a ROS-dependent mechanism and suggest that pharmaceutical concentration of vitamin C has potential clinical use in thyroid cancer therapy.
<b>Conclusions</b>: Our data demonstrate that vitamin C kills thyroid cancer cells by inhibiting MAPK/ERK and PI3K/AKT pathways via a ROS-dependent mechanism and suggest that pharmaceutical concentration of vitamin C has potential clinical use in thyroid cancer therapy.
<b>Conclusions</b>: Our data demonstrate that vitamin C kills thyroid cancer cells by inhibiting MAPK/ERK and PI3K/AKT pathways via a ROS-dependent mechanism and suggest that pharmaceutical concentration of vitamin C has potential clinical use in thyroid cancer therapy.
<i>MIR182-5p</i> and <i>MIR20a-5p</i> were upregulated in human thyroid cancer and thyroid cancer experimental models and their effects on <i>Pax8</i> and <i>Bcl2</i> were rescued by <i>Klhl14-AS</i> overexpression, confirming <i>Klhl14-AS</i> as a ceRNA for both <i>Pax8</i> and <i>Bcl2</i>.
<i>In vivo</i>, BLU-667 potently inhibited growth of NSCLC and thyroid cancer xenografts driven by various <i>RET</i> mutations and fusions without inhibiting VEGFR2.
<i>In vivo</i>, BLU-667 potently inhibited growth of NSCLC and thyroid cancer xenografts driven by various <i>RET</i> mutations and fusions without inhibiting VEGFR2.
<i>In vivo</i>, BLU-667 potently inhibited growth of NSCLC and thyroid cancer xenografts driven by various <i>RET</i> mutations and fusions without inhibiting VEGFR2.
<i>MIR182-5p</i> and <i>MIR20a-5p</i> were upregulated in human thyroid cancer and thyroid cancer experimental models and their effects on <i>Pax8</i> and <i>Bcl2</i> were rescued by <i>Klhl14-AS</i> overexpression, confirming <i>Klhl14-AS</i> as a ceRNA for both <i>Pax8</i> and <i>Bcl2</i>.
<i>MIR182-5p</i> and <i>MIR20a-5p</i> were upregulated in human thyroid cancer and thyroid cancer experimental models and their effects on <i>Pax8</i> and <i>Bcl2</i> were rescued by <i>Klhl14-AS</i> overexpression, confirming <i>Klhl14-AS</i> as a ceRNA for both <i>Pax8</i> and <i>Bcl2</i>.
<sup>18</sup>F-FDG-avid thyroid incidentaloma (TI) is seen in approximately 2.5% of patients imaged for staging or response assessment of malignancy and represents thyroid cancer in approximately 35% of cases.
(1) We discuss how loss of TRAIL mediated apoptosis occurred in thyroid cancer cells and how different strategies can be used to restore apoptosis in resistant cancer cells; (2) We provide detailed account of seemingly opposite roles of NOTCH signaling in thyroid cancers; (3) TGF/SMAD mediated signaling also needs detailed research because of context dependent role in thyroid cancer.