Tumour stem cells and drug resistance

By M. Dean, T. Fojo, S. Bates. Nature Reviews. Cancer, 2005

3,724 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/589506337476b1cf39953cd6dba84a2e626b29de

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Citations in the corpus

Cyclopamine‐Mediated Hedgehog Pathway Inhibition Depletes Stem‐Like Cancer Cells in Glioblastoma (2007, background): “It has been postulated that the recurrence of GBM following current therapies is due to the persistent presence of a small group of stem-like cancer cells within tumors that are relatively resistant to cell death (reviewed in [ 48 ]).”
Drug penetration in solid tumours (2006, background): “, and there is a large body of evidence indicating that hypoxic cells are relatively resistant to radiation treatment and can repopulate the tumour after radiotherapy; that is, there are stem cells in hypoxic regions of some tumour”
Nanomedicine therapeutic approaches to overcome cancer drug resistance (2013, neutral): “4B [49].”
MEF promotes stemness in the pathogenesis of gliomas (2012, neutral): “Moreover, GSCs are remarkably resistant to the chemotherapy and radiotherapy (Dean et al., 2005) used as standard first-line treatment of patients with malignant gliomas.”
Stochastic state transitions give rise to phenotypic equilibrium in populations of cancer cells. (2011, positive): “Such studies are of particular importance because of the observed resistance of cancer stem-like cells to chemoand radiation therapies (Bao et al., 2006; Dean et al., 2005; Diehn and Clarke, 2006; Eyler and Rich, 2008; Li et al., 2008; Woodward et al., 2007).”
Triple-Negative Breast Cancer: A Brief Review About Epidemiology, Risk Factors, Signaling Pathways, Treatment and Role of Artificial Intelligence (2022, background): “Furthermore, Wnt inhibitors can destroy drug-resistant cells and cancer stem cells (Dean et al., 2005).”
Autophagy and multidrug resistance in cancer (2017, background): “the main transporters [30]; (2) reducing drug uptake by influx transporters, such as solute carriers [31]; (3) boosting drug metabolism, including elimination by glutathione S-transferase and cytochrome P450 enzymes [32, 33]; (4) blocking apoptotic signaling pathways due to change in the expression ”
Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “Indeed, therapies that eradicate the bulk of tumour cells fail to kill cancer stem cells [227], mainly due to their quiescence and the expression of drug membrane transporters [228].”
Molecular definition of breast tumor heterogeneity. (2007, background): “…tumors contain a subpopulation of cells with stem-cell characteristics has generated renewed interest and excitement in part due to the assumption that ineffective targeting of this cell population is responsible for therapeutic failures and recurrences (Dean et al., 2005; Eckfeldt et al., 2005).”
The Hippo transducer TAZ confers cancer stem cell-related traits on breast cancer cells. (2011, background): “In addition to self-renewal, another characteristic of CSCs is their capacity to resist chemotherapy (Dean et al., 2005).”