The objective of this study was to determine the effects of sunitinib on signal transduction pathways and on gene expression of iodide-metabolizing proteins in papillary cancer cells with the RET/PTC1 rearrangement.     ///    "Sunitinib treatment of RET/PTC1 cell lines, in combination, with forskolin induced expression of the sodium (Na)/iodide (I) symporter (NIS) and the transcription factors that bind the NIS upstream enhancer. "    ///    Incubation of RET/PTC1 cells with 1 microM sunitinib inhibited their migration potential and transformed their morphology.     ///    The mean 50% lethal concentration in the RET/PTC1 subclones was 1.81 microM.     ///    Sunitinib inhibited proliferation of RET/PTC1 subclones in a time- and dose-related manner.     ///    "Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells.. "