Redefining Cancer Stem Cells: Essential Insights for Targeted Therapy

Cancer resistance/recurrence, have both been linked to the presence of a tumor subpopulation of cells known as cancer stem-cells (CSCs). Current biomarkers used to define CSCs are often those markers which are either over-expressed in cancer cells, as compared to their normal counterpart cells, or shared with normal stem-cells (NSC) and other cell types.
Examples include HER2 and AFP, respectively. Targeting such biomarkers has been shown inefficient especially in those cases of resistance and relapse. Therefore the need to redefine stemness in cancer cells imposes itself. To shape and show their own identity, cancer cells must be endowed with biomarkers proper to cancer cells but absent in normal cells. Without such a sine qua non condition, our approach to cancer therapy and cure will remain elusive. Identifying these biomarkers, proper to cancer cells, and deciphering their biochemical action, will explain how cancer cells modulate their resistance to panoplies of anti-cancer therapies currently used in clinics. Moreover these findings will help design more appropriate anti-cancer drugs directed against cancer stem-cells themselves. The question is how to identify those biomarkers that could be present in cancer cells but not in normal cells?
The role of DNA mutations in the onset of cancer has been reexamined by several scientists, leading to think that specific cancer biomarkers could be of protein origin. This work discusses the hypothetic protein-centered model for cancer genesis as an approach to detect CSCs specific markers and the role of chronic inflammation in the rise and maintenance of CSCs.