2009
DOI: 10.1038/tpj.2008.20
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Identification of genes that confer tumor cell resistance to the Aurora B kinase inhibitor, AZD1152

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Cited by 34 publications
(31 citation statements)
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“…It is likely that an enhanced ability to progress through mitosis presents these cells with a significant growth advantage in the presence of these agents, perhaps mirroring the situation in inhibitor-exposed cancer patients. It will therefore be important to assess the long-term effects of drugresistant kinase expression in model systems and to determine whether cell survival is influenced by other factors in addition to kinase resistance, such as changes in p53 status or induction of multidrug resistance genes (53,54).…”
Section: Discussionmentioning
confidence: 99%
“…It is likely that an enhanced ability to progress through mitosis presents these cells with a significant growth advantage in the presence of these agents, perhaps mirroring the situation in inhibitor-exposed cancer patients. It will therefore be important to assess the long-term effects of drugresistant kinase expression in model systems and to determine whether cell survival is influenced by other factors in addition to kinase resistance, such as changes in p53 status or induction of multidrug resistance genes (53,54).…”
Section: Discussionmentioning
confidence: 99%
“…Additional molecular parameters are also critical for the efficacy of Aurora kinase inhibitors. For instance, for the Aurora-B inhibitor AZD1152, the avidin-biotin complex method transporters multidrug resistance 1 and breast cancer resistance protein were found to mediate resistance, indicating that this compound is a substrate for efflux pumps (42).…”
Section: Discussionmentioning
confidence: 99%
“…In cultured tumor cells, 2 prominent mechanisms of resistance to the taxanes are overexpression of drug efflux pumps and tubulin modifications (19)(20)(21). One strategy to overcome susceptibility to the effects of MDR would be to design a novel antimitotic drug candidate whose activity is not influenced by drug efflux, mediated by ATP-binding cassette (ABC) transporters such as P-glycoprotein (P-gp) (ABCB1) and BCRP (ABCG2) (22). Moreover, a small molecule inhibitor that is equipotent against 2 essential mitotic kinases may reduce the potential for resistance driven by target-modifying mutations (23,24).…”
Section: Introductionmentioning
confidence: 99%