COP1 and cancer: TrkAIII oncogenic activity, confirmed by its capacity to transform NIH3T3 cells and promote oncogenic behaviour in neuroblastoma models, results from: receptor re-localization to pre-Golgi membranes, centrosomes and mitochondria; regulated ligand-independent activation within COP1/ERGIC membranes; PI3K/Akt/NF-κB survival-signalling; induction of a survival adapted ER-stress response; increased SOD2 expression enhancing resistance to oxidative-stress and promotion of a more angiogenic cancer stem cell-like phenotype.