Principles of stem cell biology and cancer: future applications and therapeutics. Edited by T. Regad, T. J. Sayers and R. C. Rees. John Wiley & Sons (2015)

Part II. Cancer stem cells

Experimental identification of cancer stem cells (CSCs) in acute myeloid leukaemia (Lapidot et al., 1994) was followed by the isolation and functional characterization of CSCs in solid tumours, including breast (Al-Hajj et al., 2003), brain (Hemmati et al., 2003), colon (O’Brien et al., 2007), melanoma (Fang et al., 2005), pancreatic (Hermann et al., 2007), prostate (Collins et al., 2005), ovarian (Bapat et al., 2005), lung (Ho et al., 2007) and gastric (Fukuda et al., 2009) cancers. Thus, accumulating evidence over the past decade suggests that many human cancers are driven by CSCs, which share many properties with their normal counterparts. Like normal stem cells, CSCs retain properties of self-renewal and lineage differentiation, contributing to tumour heterogeneity. According to the CSC hypothesis, tumours are organized in a hierarchical fashion, whereby self-renewing CSCs drive tumourigenesis or differentiated cells constitute the tumour bulk (O’Brien et al., 2010). Although the existence of CSCs in multiple human tumours has been firmly established, the functional and clinical significance of these cells are currently under intensive investigation (Shipitsin and Polyak, 2008). CSCs are also regulated by various extrinsic and intrinsic signalling pathways, which govern their self-renewal and lineage differentiation (Charafe-Jauffret et al., 2008). Alterations in these pathways may result in stem cell expansion, an event implicated in malignant transformation. The intricate crosstalk between the CSCs and their microenvironment has been an area of interest in recent years. Investigations have led to new insights into the nature of these bidirectional interactions, which play a critical role in tumour development and progression.

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