Cancer stem cells

Abstract

Heterogeneity within and between tumors is a well-known phenomenon that greatly complicates the diagnosis and treatment of cancer. A large body of research indicates that heterogeneity develops through time as tumor-initiating stem cells, also known as cancer stem cells (CSCs), evolve genetic or epigenetic alterations that allow them to differentiate into multiple tumor cell types. Similar to normal stem cells, CSCs can self-renew and possess long-term repopulation potential. However, unlike normal stem cells, CSCs are not subject to the usual controls that limit growth. Different models have been postulated to explain the heterogeneity of tumors, but it is widely agreed that interactions between tumor cells and their microenvironment create niches that promote CSC properties and enable their survival. Within the microenvironment, CSC self-renewal, replication, and differentiation are postulated to produce a hierarchy of cells constituting the tumor mass. Increased understanding of the factors that create and contribute to tumor heterogeneity may support the design of therapies that affect CSC function and their microenvironments.

microRNA: The Impact on Cancer Stemness and Therapeutic Resistance

“…The other is that differentiated tumor cells could return to CSCs and reacquire stemness properties with changes of the transcriptome. The reversible transformation between CSCs and differentiated tumor cells may better explain the heterogeneity of cancer cells [204]. The transcriptome means the entire set of transcripts in a cell or a certain population of cells.…”

The Interactions Between Cancer Stem Cells and the Innate Interferon Signaling Pathway

“…Nowadays, the most accepted CSC model proposes that, on the one hand, CSCs remain in a de-differentiated state, maintain their pluripotency and have unlimited self-renewal capacity. However, on the other hand, they can also differentiate into all possible cancer cell states that form a continuum, thus building the tumor hierarchy and giving rise to intratumoral heterogeneity (122). These unique abilities define CSCs as the sole drivers of tumorigenesis and tumor maintenance, and subsequently the cell entity that drives metastatic spread.…”

Apoptotic Signaling Pathways in Glioblastoma and Therapeutic Implications

“…This clonal divergence can be caused by the genetic instability intrinsic to cancer cells combined with the selective pressure elicited by therapeutic interventions [ 74 ]. Furthermore, intratumor heterogeneity is increased by cell plasticity, which allows glioblastoma cells to dedifferentiate to a stem cell-like state [ 75 ].…”