Endogenous anticancer mechanism differentiation

Abstract

It has been recently shown that within heterogeneous tumor masses a small population of less differentiated transformed cells has the ability to self-renew and regenerate the bulk of the tumor. Their similarities with normal stem cells in terms of gene expression patterns, proliferative capacity and surface markers rendered them the name of cancer stem-like cells (CSC), and these are thought to be the tumor initiating cells (TIC). Their limited susceptibility to classical anti-tumor therapy help explain the high incidence of cancer-treatment relapses observed in selected malignancies. Much effort is being directed towards the understanding of factors that maintain CSC survival and their self-renewal capacity, with the goal that these same signaling pathways can be harnessed for treatments that aim at inducing CSC differentiation. This review will discuss the CSC theory, its implications, potential signaling pathways responsible for maintaining their undifferentiated and pluripotent states, and new venues being explored to target these cells in modern cancer therapy.

Novel and emerging targeted-based cancer therapy agents and methods

“…By inducing CSCs differentiation, cells will become more susceptible to anti-tumor therapy, and lose their ability to rebuild the tumor later. As described 37 years ago, retinoic acid (RA) is an appropriate molecule that induces cellular differentiation in embryonal carcinoma cell lines [135] through the upregulation of genes that promotes differentiation, like α-fetoprotein [136,137] and downregulation of pluripotency-associated ones like Oct4 or telomerase [138].…”