Abstract

Metastatic melanoma is a fatal malignancy which is remarkably resistant to treatment. It is not entirely clear what determines transition from primary local to metastatic melanoma. Recent gene profiling studies shed light onto the complexity of pathogenesis of melanoma progression. An interaction between cell cycle signaling, adhesion pathways and epithelial-mesenchimal transition program appears to be critical in the development of metastatic disease. An isolated deregulation of either of those pathways may not be sufficient to initiate tumor evolution towards an aggressive phenotype. Here we review how they act in concert to make such a transition possible.

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