Over the last decades, the
cancer survival rate has increased due to personalized
therapies, the discovery of targeted
therapeutics and novel biological agents, and the application of
palliative treatments. Despite these advances,
tumor resistance to
chemotherapy and radiation and rapid progression to metastatic disease are still seen in many patients. Evidence has shown that cancer stem cells (CSCs), a sub-population of cells that share many common characteristics with somatic stem cells (SSCs), contribute to this therapeutic failure. The most critical properties of CSCs are their self-renewal ability and their capacity for differentiation into heterogeneous populations of
cancer cells. Although CSCs only constitute a low percentage of the total
tumor mass, these cells can regrow the
tumor mass on their own. Initially identified in
leukemia, CSCs have subsequently been found in
cancers of the breast, the colon, the pancreas, and the brain. Common genetic and phenotypic features found in both SSCs and CSCs, including upregulated signaling pathways such as Notch, Wnt, Hedgehog, and TGF-β. These pathways play fundamental roles in the development as well as in the control of cell survival and cell fate and are relevant to therapeutic targeting of CSCs. The differences in the expression of
membrane proteins and exosome-delivered
microRNAs between SSCs and CSCs are also important to specifically target the stem cells of the
cancer. Further research efforts should be directed toward elucidation of the fundamental differences between SSCs and CSCs to improve existing
therapies and generate new clinically relevant
cancer treatments.