**3. Cancer stem cells**

Accumulating evidence strongly suggests that tumors are organized into cellular hierarchies initiated and maintained by a small pool of self-renewing cancer stem cells (CSCs) (Dick, 2008; Reya et al., 2001). CSCs are thought to be resistant to various cancer treatments because of their relative quiescence (Komarova & Wodarz., 2007). Cancer relapses may occur because the dormancy of CSCs protects them from elimination by various cancer therapies (Dick, 2008). In an acute myelogenous leukemia (AML) xenograft model, AML leukemic stem cells (LSCs) localized in the endosteal region of the BM show cellular quiescence and resistance to chemotherapy (Ishikawa et al., 2007; Saito et al., 2010). In patients with chronic myelogenous leukemia (CML), CD34+ progenitor cells contain dormant cells that are resistant to BCR/ABL tyrosine kinase inhibitors (Bhatia et al., 2003).

It is well documented that regulators of HSC maintenance are also involved in the development of leukemias (Rizo et al., 2006). A number of cancer-related proteins, such as Bmi1, c-Myc, p53, Gfi-1, and PTEN, are key participants in HSC regulation, demonstrating the close relationship between normal HSCs and CSCs. Therefore, further understanding the mechanisms regulating HSC fate is needed if we are to develop new strategies for targeting CSCs and successfully treat cancer.
