Methods: In vitro cellular drug resistance to the cytarabine(Ara- C), daunorubicin(DNR), homoharringtonine(HHT), amsacrine(AMSA) and mitoxantrone(MTZ) was investigated using MTT assay.
Results: There is no significant difference of p170 expression and in vitro cellular drug resistance between the groups of patients with AML at diagnosis(138 cases), refractory(8 cases), relapse(14 cases), CML blastic phase(8 cases), and secondary to MDS(8 cases).
Objective: To investigate the correlation between cellular drug resistance in vitro and P170 expression and specific cytogenetic aberrations in patients with acute myeloid leukemia(AML).
Conclusion: There is no correlation between in vitro cellular drug resistance , p170 expression level and clinical phase in patients with AML, p170 expression level and some cytogenetic subgroup display specific drug- resistance profiles.
RESULTS: Expression of drug resistance related protein was lower in Saos2 cell line than that in U2OS cells. Chemotherapy sensitivity on adriamycin(ADM),cisplatinum(DDP),fluorouracilum(5-Fu),mitomycin(MMC),dacarbazine(DTIC),vincristine(VCR) was higher in Saos2 than those in U2OS cells.
PGP-mediated cellular drug resistance may thus be circumvented in leukemic blasts by application of chemosensitizers or, potentially, alternative anthracyclines.
The study of cellular drug resistance has been stimulated by the development of short-term 'total cell kill' assays, such as the MTT assay, for use on patient samples.
As far as MDR contributes to the overall cellular drug resistance of solid tumours with hypoxic and acidic microenvironments, PSC 833 holds the greatest promise for clinical reversal of unresponsiveness to the respective group of chemotherapeutics.
Conclusions: This study suggests that GJIC plays a role in cellular drug resistance, and highlights the potential use of GJIC modulators in combination with chemotherapy.