Abstract
Cancer arises as a result of a multi-step evolutionary process that is manifested on a genetically and epigenetically heterogeneous population of cells and currently is one of the leading causes of morbidity and mortality worldwide (1,2). In a Darwinian sense, “survival of the fittest” correlates with the selection of the most proliferative, invasive and tumorigenic cell type (3). Despite recent advances in diagnosis as well as development of targeted therapies and therapeutic interventions, there is a projection for a 50% increase in new cancer cases and a 60% increase in cancer associated deaths in the following two decades according to the World Health Organization (WHO). As the majority of cancer related deaths are due to the development of metastatic disease, this greatly reflects our limited understanding of the key processes that drive human cancer and lead to disease progression. Moreover, it highlights the ineffectiveness of current therapies that are most commonly followed by the development of resistance, as well as the inability to reinstate tumor suppressor gene function.
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