Resistance To Taxanes
L. Greenberger, D. Sampath
Published 2006 · Chemistry
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Resistance to two taxanes, paclitaxel and docetaxel, is frequently observed in cancer patients and limits successful therapy. In experimental systems, resistance to paclitaxel and docetaxel are mediated by alterations in tubulin (the primary site of action of taxanes), proteins that interact with microtubules, energy-dependent efflux pumps, apoptotic proteins, and signal transduction pathways. Clinical correlations with some of these alterations exist, but have not been fully elucidated. Strategies to overcome or circumvent resistance to paclitaxel or docetaxel include inhibition of efflux pumps (which have largely proven to be unsuccessful), the use of novel taxanes or other chemically distinct classes of polymerizing agents that do not interact with drug efflux pumps (currently in clinical trials), and regulation of apoptotic or signal transduction pathways that would restore sensitivity to taxanes. Understanding the basis of resistance at the clinical level is likely to be difficult and complex, but holds the promise of providing a therapeutic opportunity specific to taxane-resistant cancer cells.
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The transcription factor ZEB1 promotes chemoresistance in prostate cancer cell lines
O. Orellana-Serradell (2019)
Telomere and Microtubule Targeting in Treatment-Sensitive and Treatment-Resistant Human Prostate Cancer Cells
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Recent findings and future directions for interpolar mitotic kinesin inhibitors in cancer therapy
S. M. Myers (2016)
The potential role of miRNAs and exosomes in chemotherapy in ovarian cancer.
Mona Alharbi (2018)
Efficacy of cabazitaxel in mouse models of pediatric brain tumors.
Emily J. Girard (2015)