Stemness combines the ability of a cell to perpetuate its lineage, to give rise to differentiated cells, and to interact with its environment to maintain a balance between quiescence, proliferation, and regeneration. While adult Stem Cells display these properties when participating in tissue homeostasis, Cancer Stem Cells (CSCs) behave as their malignant equivalents. CSCs display stemness in various circumstances, including the sustaining of cancer progression, and the interaction with their environment in search for key survival factors. As a result, CSCs can recurrently persist aftertherapy.[1]

Mechanistic studies have indicated that dysfunction of several developmental and homeostatic stemness signaling pathways may support unregulated self-renewal and differentiation that drive CSC functions. The growing list of dysfunctional signaling pathways in CSCs include the Janus-activated kinase/signal transducer and activator of transcription (JAK/STAT), Hedgehog, Wnt, Notch, phosphatidylinositol 3-kinase/phosphatase and tensin homolog (PI3K/PTEN), and nuclear factor-kB (NF-kB).[2]