Tumor-initiating cells are not enriched in cisplatin-surviving BRCA1;p53-deficient mammary tumor cells in vivo

Kersbergen, Ariena; Diepen, Frank van; Pfauth, Anita; Jonkers, Jos; Borst, Piet; Rottenberg, Sven

doi:10.4161/cc.9.18.13002

Cited by 24 publications

(22 citation statements)

References 50 publications

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“…These data indicate that resistance to cytotoxic compounds could be used to enrich CSCs from a tumor mass [186][187][188][189]. However, Pajic et al did not observe CSC enrichment in breast cancer 1 (BRCA1)-and p53-deficient breast cancers after cisplatin treatment [190].…”

Section: Cytotoxic and Hypoxic Resistancementioning

confidence: 94%

Strategies for Isolating and Enriching Cancer Stem Cells: Well Begun Is Half Done

Duan

Qiu

et al. 2013

Stem Cells and Development

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Cancer stem cells (CSCs) constitute a subpopulation of cancer cells that have the potential for self-renewal, multipotent differentiation, and tumorigenicity. Studies on CSC biology and CSC-targeted therapies depend on CSC isolation and/or enrichment methodologies. Scientists have conducted extensive research in this field since John Dick's group successfully isolated CSCs based on the expression of the CD34 and CD38 surface markers. Progress in CSC research has been greatly facilitated by the enrichment and isolation of these cells. In this review, we summarize the current strategies used in our and other laboratories for CSC isolation and enrichment, including methods based on stem cell surface markers, intracellular enzyme activity, the concentration of reactive oxygen species, the mitochondrial membrane potential, promoter-driven fluorescent protein expression, autofluorescence, suspension/adherent culture, cell division, the identification of side population cells, resistance to cytotoxic compounds or hypoxia, invasiveness/adhesion, immunoselection, and physical property. Although many challenges remain to be overcome, it is reasonable to believe that more reliable, efficient, and convenient methods will be developed in the near future.

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Section: Cytotoxic and Hypoxic Resistancementioning

confidence: 94%

Strategies for Isolating and Enriching Cancer Stem Cells: Well Begun Is Half Done

Duan

Qiu

et al. 2013

Stem Cells and Development

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“…Moreover, residual disease is usually poorly accessible to detailed analysis, and often the analysis does not include an evaluation of EMT. In the few model systems in which this was verified, no EMT was found [66] and EMT therefore does not appear to provide a general explanation for residual disease.Are CSCs responsible for the therapy-resistant fraction resulting in residual disease? This is obviously the key question.…”

Section: Are Cancer Stem Cells the Key To Residual Disease?mentioning

confidence: 99%

Cancer drug pan-resistance: pumps, cancer stem cells, quiescence, epithelial to mesenchymal transition, blocked cell death pathways, persisters or what?

2012

Self Cite

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Although chemotherapy of tumours has scored successes, drug resistance remains the major cause of death of cancer patients. Initial treatment often leaves residual disease, from which the tumour regrows. Eventually, most tumours become resistant to all available chemotherapy. I call this pan-resistance to distinguish it from multi-drug resistance, usually describing resistance caused by upregulation of drug transporters, such as P-glycoprotein. In this review, I discuss mechanisms proposed to explain both residual disease and pan-resistance. Although plausible explanations are at hand for residual disease, pan-resistance is still a mystery. My conclusion is that it is time for a major effort to solve this mystery using the new genetically modified mouse tumour models that produce real tumours resembling cancer in human patients.

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“…PTEN can be mutated or silenced by various mechanisms in human cancer and clearly this pathway plays important roles in breast and other cancers and the generation of cancer stem cells. [105][106][107][108][109][110] Mutations occur which either delete the PTEN gene or alter its activity. Sometimes these mutations actually make the cells sensitive to Akt and mTOR inhibitors as the growth of the cells becomes dependent upon elevated Akt levels and downstream mTOR and p70S6K activities.…”

confidence: 99%

Involvement of Akt and mTOR in chemotherapeutic- and hormonal-based drug resistance and response to radiation in breast cancer cells

et al. 2011

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Tumor-initiating cells are not enriched in cisplatin-surviving BRCA1;p53-deficient mammary tumor cells in vivo

Cited by 24 publications

References 50 publications

Strategies for Isolating and Enriching Cancer Stem Cells: Well Begun Is Half Done

Strategies for Isolating and Enriching Cancer Stem Cells: Well Begun Is Half Done

Cancer drug pan-resistance: pumps, cancer stem cells, quiescence, epithelial to mesenchymal transition, blocked cell death pathways, persisters or what?

Involvement of Akt and mTOR in chemotherapeutic- and hormonal-based drug resistance and response to radiation in breast cancer cells

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