ArticleBreast cancer research : BCR2014
Sequencing of breast cancer stem cell populations indicates a dynamic conversion between differentiation states in vivo.
Article in Breast cancer research : BCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed.
- Forward-reverse mutation cycles in cancer cell lines under chemical treatments.Human genomics · 2024Article
- Review
- Metabolic dependencies of metastasis-initiating cells in female breast cancer.Nature communications · 2023Article
- Tumor suppressor DEAR1 regulates mammary epithelial cell fate and predicts early onset and metastasis in triple negative breast cancer.Scientific reports · 2022Article
- Article
- Bladder cancer cells shift rapidly and spontaneously to cisplatin-resistant oxidative phosphorylation that is trackable in real time.Scientific reports · 2022Article
- Breast cancer as an example of tumour heterogeneity and tumour cell plasticity during malignant progression.British journal of cancer · 2021Review
- Review
- Epigenetic plasticity potentiates a rapid cyclical shift to and from an aggressive cancer phenotype.International journal of cancer · 2020Article
- What is the potential use of platelet-rich-plasma (PRP) in cancer treatment? A mini review.Heliyon · 2020Review
- Comparison of the Genomic Profile of Cancer Stem Cells and Their Non-Stem Counterpart: The Case of Ovarian Cancer.Journal of clinical medicine · 2020Review
- New Insights Into the Role of Phenotypic Plasticity and EMT in Driving Cancer Progression.Frontiers in molecular biosciences · 2020Review
- Interrogation of Phenotypic Plasticity between Epithelial and Mesenchymal States in Breast Cancer.Journal of clinical medicine · 2019Article
- Modeling differentiation-state transitions linked to therapeutic escape in triple-negative breast cancer.PLoS computational biology · 2019Article
- Systemic Metabolism, Its Regulators, and Cancer: Past Mistakes and Future Potential.Frontiers in endocrinology · 2019Review
- Differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer.Nature communications · 2018Article
- The viable circulating tumor cells with cancer stem cells feature, where is the way out?Journal of experimental & clinical cancer research : CR · 2018Review
- 3D modeling of cancer stem cell niche.Oncotarget · 2018Review
- Phenotypic Plasticity, Bet-Hedging, and Androgen Independence in Prostate Cancer: Role of Non-Genetic Heterogeneity.Frontiers in oncology · 2018Review
- Comparison of EpCAMCancer biology & therapy · 2018Article
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9 authors.
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Abstract
introductionThe cancer stem cell model implies a hierarchical organization within breast tumors maintained by cancer stem-like cells (CSCs). Accordingly, CSCs are a subpopulation of cancer cells with capacity for self-renewal, differentiation and tumor initiation. These cells can be isolated through the phenotypic markers CD44+/CD24-, expression of ALDH1 and an ability to form nonadherent, multicellular spheres in vitro. However, controversies to describe the stem cell model exist; it is unclear whether the tumorigenicity of CSCs in vivo is solely a proxy for a certain genotype. Moreover, in vivo evidence is lacking to fully define the reversibility of CSC differentiation.
methodsIn order to answer these questions, we undertook exome sequencing of CSCs from 12 breast cancer patients, along with paired primary tumor samples. As suggested by stem classical cell biology, we assumed that the number of mutations in the CSC subpopulation should be lower and distinct compared to the differentiated tumor cells with higher proliferation.
resultsOur analysis revealed that the majority of somatic mutations are shared between CSCs and bulk primary tumor, with similar frequencies in the two.
conclusionsThe data presented here exclude the possibility that CSCs are only a phenotypic consequence of certain somatic mutations, that is a distinct and non-reversible population of cells. In addition, our results imply that CSCs must be a population of cells that can dynamically switch from differentiated tumor cells, and vice versa. This finding increases our understanding of CSC function in tumor heterogeneity and the importance of identifying drugs to counter de-differentiation rather than targeting CSCs.
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