In vivo mechanisms of resistance to cytarabine in acute myeloid leukaemia
作者： Carlos M. Galmarini , Xavier Thomas , Fabien Calvo , Philippe Rousselot , Muriel Rabilloud
DOI: 10.1046/J.1365-2141.2002.03538.X
关键词: Deoxycytidine kinase 、 DNA 、 Cytarabine 、 Topoisomerase 、 Reverse transcription polymerase chain reaction 、 DNA polymerase 、 Immunology 、 Leukemia 、 DNA polymerase I 、 Biology 、 Cancer research
摘要: Factors that reduce the intracellular concentration of triphosphorylated cytarabine (ara-CTP), active form (ara-C), may induce chemoresistance in acute myeloid leukaemia (AML) patients. These factors include reduced influx ara-C by hENT1 transporter, phosphorylation deoxycytidine kinase (dCK), and increased degradation high Km cytoplasmic 5'-nucleotidase (5NT) and/or cytidine deaminase (CDD). Increased levels DNA polymerase alpha (DNA POL) topoisomerase I (TOPO I) II II) have also been detected ara-C-resistant cell lines. To determine whether these are implicated clinical resistance, we analysed expression parameters at diagnosis, using reverse transcription chain reaction, blast cells 123 AML patients treated with ara-C. At hENT1, dCK, CDD, 5NT, TOPO I, II, POL MDR1 were expressed 83%, 22%, 7%, 37%, 59%, 39% 16% respectively. In univariate analysis, 5NT or diagnosis had significantly shorter disease-free survival (DFS). multivariate positivity deficiency related to a DFS. 5NT-positive blasts overall (OS). OS was positivity. results suggest POL, be resistance mechanisms
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