Cancer stemness

Cancer stemness refers to the biological state of a subpopulation of tumor cells, known as cancer stem cells (CSCs), characterized by the ability to self-renew and differentiate into multiple cell lineages within a tumor (PMID: 29775444). This phenotypic trait is not a single molecular target but rather a result of dysregulated signaling through conserved pathways such as Wnt/β-catenin, Notch, Hedgehog, and JAK/STAT (PMID: 31057328). Cancer stemness is a major contributor to tumor progression, driving both the initiation of primary tumors and the colonization of distant metastatic sites (PMID: 30046173). Importantly, these stem-like cells are often quiescent and possess enhanced DNA repair mechanisms, making them highly resistant to standard cytotoxic therapies and a primary cause of cancer recurrence (PMID: 31610933). Pharmaceutical development in this area involves targeting specific proteins—such as the Smoothened receptor in the Hedgehog pathway or Delta-like ligands in the Notch pathway—to disrupt the maintenance of the CSC niche (PMID: 34185191). Despite the therapeutic potential, a significant challenge remains in sparing normal somatic stem cells that utilize these same pathways for tissue homeostasis and repair (PMID: 31057328).

Other names

Tumor stemnessStem-like stateCancer stem cell phenotypeStemness-associated signaling

Inhibition of evolutionary conserved signaling pathways (Wnt, Notch, Hedgehog, JAK/STAT) that regulate the maintenance, self-renewal, and survival of the cancer stem cell subpopulation.