ArticleISRN oncology2012
The stemness phenotype model.
Article in ISRN oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed.
- Electrical Impedance Spectroscopy as a Tool to Detect the Epithelial to Mesenchymal Transition in Prostate Cancer Cells.Biosensors · 2024Article
- Cancer Stem Cells and Treatment of Cancer: An Update and Future Perspectives.Current stem cell research & therapy · 2024Review
- Phenotypic Characterization of 2D and 3D Prostate Cancer Cell Systems Using Electrical Impedance Spectroscopy.Biosensors · 2023Article
- The Emerging Role of Tumor Microenvironmental Stimuli in Regulating Metabolic Rewiring of Liver Cancer Stem Cells.Cancers · 2022Review
- Cancer Stem Cells in Tumor Modeling: Challenges and Future Directions.Advanced nanobiomed research · 2021Article
- Alternative models of cancer stem cells: The stemness phenotype model, 10 years later.World journal of stem cells · 2021Review
- Cancer stem cells and macrophages: molecular connections and future perspectives against cancer.Oncotarget · 2021Review
- Cancer Stem Cells-Key Players in Tumor Relapse.Cancers · 2021Review
- Electrical Impedance Spectroscopy for Monitoring Chemoresistance of Cancer Cells.Micromachines · 2020Review
- Targeting Tumorigenicity of Breast Cancer Stem Cells Using SAHA/Wnt-b Catenin Antagonist Loaded Onto Protein Corona of Gold Nanoparticles.International journal of nanomedicine · 2020Article
- Cancer Cell Plasticity: Rapid Reversal of Chemosensitivity and Expression of Stemness Markers in Lung and Breast Cancer Tumorspheres.Journal of cellular physiology · 2017Article
- MICU1 drives glycolysis and chemoresistance in ovarian cancer.Nature communications · 2017Article
- Stem Cell Plasticity and Niche Dynamics in Cancer Progression.IEEE transactions on bio-medical engineering · 2017Article
- RNAi for contactin 2 inhibits proliferation of U87-glioma stem cells by downregulating AICD, EGFR, and HES1.OncoTargets and therapy · 2017Article
- Bidirectional interconversion of stem and non-stem cancer cell populations: A reassessment of theoretical models for tumor heterogeneity.Molecular & cellular oncology · 2016Review
- Formation of Tumorspheres with Increased Stemness without External Mitogens in a Lung Cancer Model.Stem cells international · 2016Article
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- Cisplatin-resistant cells in malignant pleural mesothelioma cell lines show ALDH(high)CD44(+) phenotype and sphere-forming capacity.BMC cancer · 2014Article
- An overview of the role of cancer stem cells in spine tumors with a special focus on chordoma.World journal of stem cells · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The identification of a fraction of cancer stem cells (CSCs) associated with resistance to chemotherapy in most solid tumors leads to the dogma that eliminating this fraction will cure cancer. Experimental data has challenged this simplistic and optimistic model. Opposite to the classical cancer stem cell model, we introduced the stemness phenotype model (SPM), which proposed that all glioma cells possess stem cell properties and that the stemness is modulated by the microenvironment. A key prediction of the SPM is that to cure gliomas all gliomas cells (CSCs and non-CSCs) should be eliminated at once. Other theories closely resembling the SPM and its predictions have recently been proposed, suggesting that the SPM may be a useful model for other type of tumors. Here, we review data from other tumors that strongly support the concepts of the SPM applied to gliomas. We include data related to: (1) the presence of a rare but constant fraction of CSCs in established cancer cell lines, (2) the clonal origin of cancer, (3) the symmetrical division, (4) the ability of "non-CSCs" to generate "CSCs," and (5) the effect of the microenvironment on cancer stemness. The aforenamed issues that decisively supported the SPM proposed for gliomas can also be applied to breast, lung, prostate cancer, and melanoma and perhaps other tumors in general. If the glioma SPM is correct and can be extrapolated to other types of cancer, it will have profound implications in the development of novel modalities for cancer treatment.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.