Title : Paclitaxel sensitivity correlates with p53 status and DNA fragmentation, but not G2/M accumulation.

Pub. Date : 1999 Jul 15

PMID : 10421546






7 Functional Relationships(s)
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1 Paclitaxel sensitivity correlates with p53 status and DNA fragmentation, but not G2/M accumulation. Paclitaxel tumor protein p53 Homo sapiens
2 Although initial studies demonstrated that various DNA-damaging agents can induce p53, more recent studies have also shown p53 induction following nonDNA-damaging agents, including paclitaxel. Paclitaxel tumor protein p53 Homo sapiens
3 RESULTS: A 4-fold increase in paclitaxel sensitivity was observed among RKO cells deficient in p53 function compared with wild-type RKO cells (IC 50: 4 nM, 1 nM, 1nM for RKO, RKO.p53.13, RC 10.3, respectively). Paclitaxel tumor protein p53 Homo sapiens
4 RESULTS: A 4-fold increase in paclitaxel sensitivity was observed among RKO cells deficient in p53 function compared with wild-type RKO cells (IC 50: 4 nM, 1 nM, 1nM for RKO, RKO.p53.13, RC 10.3, respectively). Paclitaxel tumor protein p53 Homo sapiens
5 The increased cytotoxic effect in RKO cells with inactive p53 correlated with an increased propensity towards micronucleation and DNA fragmentation following paclitaxel treatment. Paclitaxel tumor protein p53 Homo sapiens
6 CONCLUSIONS: RKO cells lacking functional p53 demonstrate significantly enhanced sensitivity to paclitaxel compared with that of wild-type RKO cells. Paclitaxel tumor protein p53 Homo sapiens
7 Although previous published reports of enhanced paclitaxel sensitivity in p53-deficient cells correlated this finding with increased G2/M arrest, we did not observe any significant correlation between paclitaxel-induced cell kill and the degree of mitotic arrest. Paclitaxel tumor protein p53 Homo sapiens