Cancer cells display profound intra- and interline variation following prolonged exposure to antimitotic drugs.
By Karen E Gascoigne, Stephen S. Taylor. Cancer Cell, 2008
840 citations recorded by the source corpus.
Subfields: Biophysics, Cell Biology, Structural Biology
View Paper: https://www.semanticscholar.org/paper/44c567a862a95d7a7249e940ff64c4ad35120ce3
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Citations in the corpus
- Mitotic catastrophe: a mechanism for avoiding genomic instability (2011, background): “Intriguingly, these variations depend only in part on the initiating stimulus and genetic background, with the inherent stochasticity of biochemical reactions having a prominent rol”
- Network pharmacology: the next paradigm in drug discovery. (2008, background): “Indeed, subtle differences in network stability and structure between cancer cells may explain the wide variance in cell fate that has been observed in individual cells of the same genetic lineag”
- Causes and consequences of aneuploidy in cancer (2012, background): “Furthermore, many CIN cancer cell lines that were previously thought to have SAC defects were recently shown by large-scale imaging experiments to have normally functioning checkpoint”
- A chromatin-mediated reversible drug tolerant state in cancer cell subpopulations (2010, background): “, 2006), and has been implicated in cancer cell fates following drug exposure in culture (Cohen et al., 2008; Gascoigne and Taylor, 2008).”
- How Taxol/paclitaxel kills cancer cells (2014, background): “Thus cell fate in response to mitotic arrest is stochastic and not determined genetically (Gascoigne and Taylor, 2008).”
- Cellular heterogeneity: when do differences make a difference? (2010, background): “…populations under carefully controlled laboratory conditions, the dynamics and responses of single cancer cells to drugs can vary widely (Cohen et al., 2008; Gascoigne and Taylor, 2008), and drug-tolerant states can arise transiently through reversible epigenetic changes (Sharma et al., 2010).”
- Boveri revisited: Chromosomal instability, aneuploidy and tumorigenesis (2009, neutral): “Direct measurements using live-cell imaging to visualize mitosis have revealed that, in response to spindle toxins, the duration of mitosis in CIN cells is at least as long as in chromosomally stable diploid cell”
- Evolution of the cancer stem cell model. (2014, background): “Substantial variation between daughter cells in response to antimitotic drugs has also been reported that is not the result of genetic differences, but rather due to competing intracellular networks involving caspase activation and cyclin B1 levels (Gascoigne and Taylor, 2008).”
- Biological and therapeutic impact of intratumor heterogeneity in cancer evolution. (2015, background): “In support of this, phenotypic behavior and fate of identical daughter cancer cells can be vastly different upon treatment despite identical genetic backgrounds (Gascoigne and Taylor, 2008).”