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The clone designated HL-60/MX2 was approximately 35 fold less sensitive to mitoxantrone than the HL-60 parental cells.
HL-60/MX2 cells display atypical multidrug resistance (MDR) with the absence of P-glycoprotein overexpression and altered topoisomerase II catalytic activity and reduced levels of topoisomerase II alpha and beta proteins.
HL-60/MX2 cells are cross-resistant to etoposide, teniposide, bisantrene, dactinomycin, 4'-(9-acridinylamino)methane- sulfon-m-anisidide, and the anthracyclines daunorubicin and doxorubicin but retain sensitivity to the Vinca alkaloids vincristine and vinblastine, melphalan, mitomycin C and cisplatin.
Resistance to mitoxantrone is stable for up to six months.
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Harker WG, et al. Multidrug resistance in mitoxantrone-selected HL-60 leukemia cells in the absence of P-glycoprotein overexpression. Cancer Res. 49: 4542-4549, 1989. PubMed: 2568172
Harker WG, et al. Mitoxantrone resistance in HL-60 leukemia cells: reduced nuclear topoisomerase II catalytic activity and drug-induced DNA cleavage in association with reduced expression of the topoisomerase II beta isoform. Biochemistry 30: 9953-9961, 1991. PubMed: 1655025