Convergence of normal stem cell and cancer stem cell developmental stage: Implication for differential therapies

Li, Shengwen Calvin; Lee, Katherine L; Luo, Jane; Zhong, Jiang; Loudon, William G.

doi:10.4252/wjsc.v3.i9.83

Cited by 8 publications

(10 citation statements)

References 46 publications

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“…The transition from neural stem cells to cancer cells [25] may be activated by expression of some cancer driver, characteristic of dominant clones (single cells), but not in every cell [26]. Cancer cell phenotypes may be derived from such a few dominant single cells with a continuum from single driver stem cells to cancer cells.…”

Section: Discussionmentioning

confidence: 99%

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Cancer stem cells from a rare form of glioblastoma multiforme involving the neurogenic ventricular wall

et al. 2012

Cancer Cell Int

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BackgroundThe cancer stem cell (CSC) hypothesis posits that deregulated neural stem cells (NSCs) form the basis of brain tumors such as glioblastoma multiforme (GBM). GBM, however, usually forms in the cerebral white matter while normal NSCs reside in subventricular and hippocampal regions. We attempted to characterize CSCs from a rare form of glioblastoma multiforme involving the neurogenic ventricular wall.MethodsWe described isolating CSCs from a GBM involving the lateral ventricles and characterized these cells with in vitro molecular biomarker profiling, cellular behavior, ex vivo and in vivo techniques.ResultsThe patient’s MRI revealed a heterogeneous mass with associated edema, involving the left subventricular zone. Histological examination of the tumor established it as being a high-grade glial neoplasm, characterized by polygonal and fusiform cells with marked nuclear atypia, amphophilic cytoplasm, prominent nucleoli, frequent mitotic figures, irregular zones of necrosis and vascular hyperplasia. Recurrence of the tumor occurred shortly after the surgical resection. CD133-positive cells, isolated from the tumor, expressed stem cell markers including nestin, CD133, Ki67, Sox2, EFNB1, EFNB2, EFNB3, Cav-1, Musashi, Nucleostemin, Notch 2, Notch 4, and Pax6. Biomarkers expressed in differentiated cells included Cathepsin L, Cathepsin B, Mucin18, Mucin24, c-Myc, NSE, and TIMP1. Expression of unique cancer-related transcripts in these CD133-positive cells, such as caveolin-1 and −2, do not appear to have been previously reported in the literature. Ex vivo organotypic brain slice co-culture showed that the CD133+ cells behaved like tumor cells. The CD133-positive cells also induced tumor formation when they were stereotactically transplanted into the brains of the immune-deficient NOD/SCID mice.ConclusionsThis brain tumor involving the neurogenic lateral ventricular wall was comprised of tumor-forming, CD133-positive cancer stem cells, which are likely the driving force for the rapid recurrence of the tumor in the patient.

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Section: Discussionmentioning

confidence: 99%

“…We have shown that normal stem cells and cancer cells share p53 signaling pathways [24], implying the convergence of stem cells and cancer for signaling pathways [25]. These results prompted us to hypothesize that the convergence of stem cells and cancer may drive tumor recurrence by subclonal switchboard signal activation [26].…”

Section: Introductionmentioning

confidence: 99%

Cancer stem cells from a rare form of glioblastoma multiforme involving the neurogenic ventricular wall

et al. 2012

Cancer Cell Int

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“…Increased lines of evidence show “inappropriate context” ( i.e ., environment) in stem cell development may contribute to cancer development through their interactions with abnormal environmental elements such as inflammation. We pointed out that the crosstalk for tumorigenesis may have a critical stage characterized as a “therapeutic window”, which can be identified by association of molecular, biochemical and biological events in the converge developmental stages of different types of stem cells [ e.g ., normal stem cells (NSC), CSC and embryonic stem cells][ 37 ]. Such convergence of NSC and CSC demands spatiotemporal confinement of boundary for breaching to malignancy in response to stress (tissue injury/wound healing).…”

Section: Evidence To Support the Hypothesismentioning

confidence: 99%

“…Big data based on supercomputing, such as the team led by University of Washington’s David Baker in collaboration with researchers at the United States Department of Energy Joint Genome Institute (DOE JGI), can lead to an integrated comprehensive approach to cancer. Part of this integration is a lifetime imaging system that can define the convergence of normal stem cell and cancer stem cell developmental stages to determine appropriate therapies and assess their effects[ 37 ], for example, in monitoring maintenance immunotherapy[ 45 ]. Spatiotemporal monitoring of single cells will be high demand in the future because cancer originates from a single cell.…”

Section: Poac Demands For Development Of Innovative Detection Technolmentioning

confidence: 99%

Spatiotemporal switching signals for cancer stem cell activation in pediatric origins of adulthood cancer: Towards a watch-and-wait lifetime strategy for cancer treatment

Li¹,

Kabeer²

2018

WJSC

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Pediatric origin of cancer stem cell hypothesis holds great promise and potential in adult cancer treatment, however; the road to innovation is full of obstacles as there are plenty of questions left unanswered. First, the key question is to characterize the nature of such stem cells (concept). Second, the quantitative imaging of pediatric stem cells should be implemented (technology). Conceptually, pediatric stem cell origins of adult cancer are based on the notion that plasticity in early life developmental programming evolves local environments to cancer. Technologically, such imaging in children is lacking as all imaging is designed for adult patients. We postulate that the need for quantitative imaging to measure space-time changes of plasticity in early life developmental programming in children may trigger research and development of the imaging technology. Such quantitative imaging of pediatric origin of adulthood cancer will help develop a spatiotemporal monitoring system to determine cancer initiation and progression. Clinical validation of such speculative hypothesis-that cancer originates in a pediatric environment-will help implement a wait-and-watch strategy for cancer treatment.

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“…The similarities in developmental stages, receptor expression patterns and self-renewal capacities of normal stem cells and CSCs raise the possibility that malignantly transformed normal stem cells may be a source of CSCs during tumor initiation [ 10 , 11 ]. In tumors that follow the CSC model, cancer cells can exist in different states of differentiation with a CSC population of relatively high replicative potential (producing highly proliferating transit-amplifying cells), which can contribute to intratumoral heterogeneity in the parent tumor [ 9 , 12 , 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Extracellular Vesicle-Based Communication May Contribute to the Co-Evolution of Cancer Stem Cells and Cancer-Associated Fibroblasts in Anti-Cancer Therapy

Valcz¹,

Buzás

Sebestyén

et al. 2020

Cancers

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Analogously to the natural selective forces in ecosystems, therapies impose selective pressure on cancer cells within tumors. Some tumor cells can adapt to this stress and are able to form resistant subpopulations, parallel with enrichment of cancer stem cell properties in the residual tumor masses. However, these therapy-resistant cells are unlikely to be sufficient for the fast tumor repopulation and regrowth by themselves. The dynamic and coordinated plasticity of residual tumor cells is essential both for the conversion of their regulatory network and for the stromal microenvironment to produce cancer supporting signals. In this nursing tissue “niche”, cancer-associated fibroblasts are known to play crucial roles in developing therapy resistance and survival of residual stem-like cells. As paracrine messengers, extracellular vesicles carrying a wide range of signaling molecules with oncogenic potential, can support the escape of some tumor cells from their deadly fate. Here, we briefly overview how extracellular vesicle signaling between fibroblasts and cancer cells including cancer progenitor/stem cells may contribute to the progression, therapy resistance and recurrence of malignant tumors.

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Convergence of normal stem cell and cancer stem cell developmental stage: Implication for differential therapies

Cited by 8 publications

References 46 publications

Cancer stem cells from a rare form of glioblastoma multiforme involving the neurogenic ventricular wall

Cancer stem cells from a rare form of glioblastoma multiforme involving the neurogenic ventricular wall

Spatiotemporal switching signals for cancer stem cell activation in pediatric origins of adulthood cancer: Towards a watch-and-wait lifetime strategy for cancer treatment

Extracellular Vesicle-Based Communication May Contribute to the Co-Evolution of Cancer Stem Cells and Cancer-Associated Fibroblasts in Anti-Cancer Therapy

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