Both CD44+CD24− and CD44+CD24+ cell populations are tumor initiating cells; however, CSC are most highly enriched using the marker profile CD44+CD49fhiCD133/2hi. CSCs have been reported in many brain tumors. Stem-like tumor cells have been identified using cell surface markers including CD133, SSEA-1 (stage-specific embryonic antigen-1), EGFR and CD44. The use of CD133 for identification of brain tumor stem-like cells may be problematic because tumorigenic cells are found in both CD133+ and CD133− cells in some gliomas and some CD133+ brain tumor cells may not possess tumor-initiating capacity. CSCs were reported in human colon cancer. For their identification, cell surface markers such as CD133, CD44 and ABCB5, functional analysis including clonal analysis and Aldefluor assay were used. Using CD133 as a positive marker for colon CSCs generated conflicting results. The AC133 epitope, but not the CD133 protein, is specifically expressed in colon CSCs and its expression is lost upon differentiation. In addition, CD44+ colon cancer cells and additional sub-fractionation of CD44+EpCAM+ cell population with CD166 enhance the success of tumor engraftments. Multiple CSCs have been reported in prostate, lung and many other organs, including liver, pancreas, kidney or ovary. In prostate cancer, the tumor-initiating cells have been identified in CD44+ cell subset as CD44+α2β1+, TRA-1-60+CD151+CD166+ or ALDH+ cell populations. Putative markers for lung CSCs have been reported, including CD133+, ALDH+, CD44+ and oncofetal protein 5T4+. Metastasis Metastasis is the major cause of tumor lethality. However, not every tumor cell can metastasize. This potential depends on factors that determine growth, angiogenesis, invasion and other basic processes. Epithelial-mesenchymal transition In epithelial tumors, the epithelial-mesenchymal transition (EMT) is considered to be a crucial event. EMT and the reverse transition from mesenchymal to an epithelial phenotype (MET) are involved in embryonic development, which involves disruption of epithelial cell homeostasis and the acquisition of a migratory mesenchymal phenotype. EMT appears to be controlled by canonical pathways such as WNT and transforming growth factor β. EMT's important feature is the loss of membrane E-cadherin in adherens junctions, where β-catenin may play a significant role. Translocation of β-catenin from adherens junctions to the nucleus may lead to a loss of E-cadherin and subsequently to EMT. Nuclear β-catenin apparently can directly, transcriptionally activate EMT-associated target genes, such as the E-cadherin gene repressor SLUG (also known as SNAI2). Mechanical properties of the tumor microenvironment, such as hypoxia, can contribute to CSC survival and metastatic potential through stabilization of hypoxia inducible