Plasticity of melanoma and EMT-TF reprogramming

For several decades, tumour progression has been considered as linear process involving clonal selection of most aggressive cell variants. Within the framework of this concept, multiple attempts have been made to identify genes specifically activated at late cancer stages and involved in cancer metastases. However, there are no experimental evidences supporting the existence of such purely “metastatic genes”, and metastatic behaviour is likely to be induced by the same mutationally-activated pathways that cause neoplastic transformation. In line with this view is the parallel model of tumour progression and metastases. It proposes that at least in some cancer types early metastatic spread is concomitant with oncogenic transformation, i.e. the same genetic insults are responsible for the tumourigenicity and metastatic