Heterogeneity within particular cancers arises from different cell types of which a tumor is comprised, as well as from genetic and epigenetic factors that differ amongst the cancer cells themselves. This gives rise to a disease that displays a wide variety of phenotypes. In recent years, two theoretical models (supported by experimental evidence) of cancer growth and progression to a metastatic disease, have gained prominence. These are (i) models of clonal evolution and (ii) models based on the so-called cancer stem cell hypothesis. In the former, microenvironmental selection pressures are thought to drive mutations that generate clonal formations best suited to the particular microenvironment and these determine the tumor phenotype. In the latter theory, cancer stem cells (CSCs) with similar genetic backgrounds can be organized in a hierarchy corresponding to their tumorigenic potential. Thus, CSCs appear at the top of the hierarchy and are believed to drive the tumor initiating and metastatic capabilities of the majority of cancers. A characteristic feature of these types of models is the apparent unidirectional nature of disease development and progression. In these models, CSCs undergo symmetric division to replenish the CSC pool, asymmetric division to produce one CSC and one differentiated (non-CSC) daughter cell, or irreversible symmetric division into daughter cells (non-CSCs) with low tumorigenic potential. However, recent work from the Weinberg group and others strongly points to yet another possibility which supports a new model of tumorigenicity. The experimental evidence suggests significant potential plasticity that links the non-CSC and CSC compartments, so that non-CSCs can reacquire a CSC phenotype and vice-versa. Thus, under this CSC-Plasticity model, it appears that some tumors may be driven by these bidirectional interchanges which are common and essential components of its tumorigenicity. There is mounting evidence implicating the plasticity of cancer cells, in particular, as giving rise to aggressive CSCs which are created anew within a tumor. There is much current interest in clinical oncology on the therapeutic targeting of CSCs, and this workshop will include talks discussing not only clonal evolution, microenvironmental selection pressures, CSCs, CSC-plasticity but also implications for the development of future therapies.