title: Cancer stem cells: targeting tumors at the source.
abstract: The cancer stem cell hypothesis states that tumors rely exclusively on the continued proliferation of a subset of cancer cells that originated from normal adult stem cells. These cells have two key traits: multipotency, and self-renewal. The prolonged lifespan of stem cells makes them perfect candidates for the accumulation of carcinogenic mutations that would convert them into cancer stem cells (CSCs) no longer responsive to the many regulatory pathways in place that are responsible for tight governance of proliferation and differentiation in normal stem cells. Comprehending what these regulatory pathways are, and how their derailment contributes to oncogenic transformation, can hold the key to finding new strategies to target CSCs in order to effectively treat cancer. Additionally, what environmental factors are involved in promoting or suppressing CSC tumorigenicity requires attention. The possibility that some cancers may have clonal origins in non-stem cell populations that were able to acquire stem cell-like properties, and the lack of complete cell autonomy in carcinogenesis, suggests that the CSC hypothesis is continually evolving. Continued research in this field can shed light on how effective selective elimination of CSCs as opposed to generalized targeting of cancer cells will be in the treatment of cancer.
authors.affiliation: Department of Hematology Cancer Center, Xuzhou Central Hospital, Xuzhou, Jiangsu, China. zpying58@126.com.
authors.forename: P-Y
authors.initials: PY
authors.lastname: Zhang
authors.forename: Y-J
authors.initials: YJ
authors.lastname: Yang
authors.forename: Y
authors.initials: Y
authors.lastname: Xue
authors.forename: J
authors.initials: J
authors.lastname: Fu
authors.forename: C-X
authors.initials: CX
authors.lastname: Zhang
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.forename: Y
authors.initials: Y
authors.lastname: Yang
authors.forename: H
authors.initials: H
authors.lastname: Shi
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects / Q000235:genetics; D002471:Cell Transformation, Neoplastic / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D016503:Drug Delivery Systems / Q000639:trends; D018390:Gene Targeting / Q000639:trends; D006801:Humans; D009369:Neoplasms / Q000175:diagnosis / Q000378:metabolism / Q000628:therapy; D014411:Neoplastic Stem Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D010641:Phenotype; D013234:Stem Cells / Q000187:drug effects / Q000473:pathology