Evolution of the Cancer Stem Cell Model

Kreso, Antonija; Dick, John E.

doi:10.1016/j.stem.2014.02.006

Cited by 1,936 publications

(1,766 citation statements)

References 151 publications

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“…Unlike normal stem cells, self-renewal is typically downregulated in CSCs (Kreso and Dick, 2014). Until now, CSCs are recognized to represent a distinct cell population that has the capacity of self-renewal and clonal long-term repopulation (Clarke et al, 2006;Nguyen et al, 2012).…”

Section: Cancer Stem Cellsmentioning

confidence: 99%

Emerging Roles of Krüppel-Like Factor 4 in Cancer and Cancer Stem Cells

Ding¹,

Liu²,

Li³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Cancer stem cells (CSCs) are rare subpopulations within tumors which are recognized as culprits in cancer recurrence, drug resistance and metastasis. However, the molecular mechanisms of how CSCs are regulated remain elusive. Krüppel-like factors (KLFs) are evolutionarily conserved zinc finger-containing transcription factors with diverse functions in cell differentiation, proliferation, embryogenesis and pluripotency. Recent progress has highlighted the significance of KLFs, especially KLF4, in cancer and CSCs. Therefore, for better therapeutics of cancer disease, it is crucial to develop a deeper understanding of the mechanisms of how KLF4 regulate CSC functions. Herein we summarized the current understanding of the transcriptional regulation of KLF4 in CSCs, and discussed the functional implications of targeting CSCs for potential cancer therapeutics.

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Section: Cancer Stem Cellsmentioning

confidence: 99%

Emerging Roles of Krüppel-Like Factor 4 in Cancer and Cancer Stem Cells

Ding¹,

Liu²,

Li³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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show abstract

“…However, a limitation of this model is it does not take into account the importance of non-genetic variations, minor clones, and potential functional interactions between clones and tumors [8]. The cancer stem cell model asserts that a small pool of cancer cells with self-renewal and differentiation capacity serve as “seeds” to promote tumor initiation, progression and recurrence [9]. A major drawback of this model is that it neglects heterogeneous DNA within the tumor [8].…”

Section: Introductionmentioning

confidence: 99%

Oncogenic transformation of normal breast epithelial cells co-cultured with cancer cells

Song

Zhou

et al. 2018

Cell Cycle

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The heterogeneity in human breast cancer poses a challenge for effective treatment. Better understanding of tumor initiation and development will help to resolve this problem. Current models explaining intratumoral diversity include cancer stem cells, clonal evolution and cancer cell dedifferentiation and reprogramming. Herein, a new model, cancer transmission, is proposed to explain cancer heterogeneity. We found breast cancer cells (MCF10A.NeuT) were capable of transforming normal mammary epithelial cells (MCF10A). The transformed cells exhibited cancerous properties including enhanced proliferation and migration, loss of apical-basal polarity and depolarized acini structure associated with epithelial-mesenchymal transition (EMT). The transformed MCF10A cells displayed distinct EMT characteristics compared to parental cells. We further showed that cancer cell-secreted factors were sufficient to induce cancerous transformation of normal cells. Furthermore, transformed cells were resistant to radiation treatment, providing new insights into mechanisms underlying therapeutic resistance.

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“…Deep phenotypic analysis of tumor-associated immune cells provides ample evidence that valuable information can be elucidated regarding the TME from cells embedded in and surrounding a cancer lesion (7). The initially rather static CSC concept was refined through the realization that even cells initially classified as nonstem cells can adopt a stem cell phenotype (8), and recent models indicate that the view of cells able to switch between various degrees of "stemness" may be more accurate (9).…”

Section: Introductionmentioning

confidence: 99%

Immunophenotyping and Transcriptomic Outcomes in PDX-Derived TNBC Tissue

Snowden

Hahn

Ferguson

et al. 2017

Molecular Cancer Research

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Cancer tissue functions as an ecosystem of a diverse set of cells that interact in a complex tumor microenvironment. Genomic tools applied to biopsies in bulk fail to account for this tumor heterogeneity, whereas single-cell imaging methods limit the number of cells which can be assessed or are very resource intensive. The current study presents methods based on flow cytometric analysis and cell sorting using known cell surface markers (CXCR4/CD184, CD24, THY1/CD90) to identify and interrogate distinct groups of cells in triple-negative breast cancer clinical biopsy specimens from patient-derived xenograft (PDX) models. The results demonstrate that flow cytometric analysis allows a relevant subgrouping of cancer tissue and that sorting of these subgroups provides insights into cancer cell populations with unique, reproducible, and functionally divergent gene expression profiles. The discovery of a drug resistance signature implies that uncovering the functional interaction between these populations will lead to deeper understanding of cancer progression and drug response. Implications: PDX-derived human breast cancer tissue was investigated at the single-cell level, and cell subpopulations defined by surface markers were identified which suggest specific roles for distinct cellular compartments within a solid tumor. Mol Cancer Res; 15(4); 429–38. ©2016 AACR.

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Evolution of the Cancer Stem Cell Model

Cited by 1,936 publications

References 151 publications

Emerging Roles of Krüppel-Like Factor 4 in Cancer and Cancer Stem Cells

Emerging Roles of Krüppel-Like Factor 4 in Cancer and Cancer Stem Cells

Oncogenic transformation of normal breast epithelial cells co-cultured with cancer cells

Immunophenotyping and Transcriptomic Outcomes in PDX-Derived TNBC Tissue

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