Using approaches first applied in human leukemias, recent progress has been made in the identification of putative cancer stem cells in several different carcinomas and other solid cancers. Additional studies have suggested that cancer stem cells may be derived not only from transformation of quiescent, long-term stem cells but also from short-lived progenitors that then obtain the ability to undergo self-renewal. Therefore, the heterogeneity observed in many types of human cancers may reflect the activation of specific oncogenes and/or loss of specific tumor suppressor genes and the different stem and/or progenitor cell populations in which these genetic or epigenetic events occur. Similarities have been observed in the pathways regulating stem cell homing and metastasis, and increasing evidence also suggests that treatment failure and the recurrence of human cancer may reflect the intrinsic quiescence and drug resistance of cancer stem cells.
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