P-glycoprotein and multidrug resistance protein activities in relation to treatment outcome in acute myeloid leukemia

Clin Cancer Res. 2000 Aug;6(8):3205-14.

Abstract

Despite treatment with intensive chemotherapy, a considerable number of patients with acute myeloid leukemia (AML) die from their disease due to the occurrence of resistance. Overexpression of the transporter proteins P-glycoprotein (P-gp) and multidrug resistance protein (MRP) 1 has been identified as a major cause of cross-resistance to functionally and structurally unrelated drugs. In the present study, the functional activity of P-gp and MRP was determined in 104 de novo AML patients with a flow cytometric assay using rhodamine 123 (Rh123) in combination with PSC833 and carboxyfluorescein (CF) in combination with MK-571. The results were compared with clinical outcome and with known prognostic factors. The functional activity of P-gp and MRP, expressed as Rh123 efflux blocking by PSC833 and CF efflux blocking by MK-571, demonstrated a great variability in the AML patients. A strong negative correlation was observed between Rh123 efflux blocking by PSC833 and Rh123 accumulation (r(s) = -0.69, P < 0.001) and between CF efflux blocking by MK-571 and CF accumulation (r(s) = -0.59, P < 0.001). A low Rh123 accumulation and a high Rh123 efflux blocking by PSC833 were associated with a low complete remission (CR) rate after the first cycle of chemotherapy (P = 0.008 and P = 0.01, respectively). Patients with both low Rh123 and CF accumulation (n = 16) had the lowest CR rate (6%), whereas patients with both high Rh123 and CF accumulation (n = 11) had a CR rate of 73%. AML patients with French-American-British classification M1 or M2 showed a lower Rh123 accumulation than patients with French-American-British classification M4 or M5 (P = 0.02). No association was observed between the multidrug resistance parameters and overall survival of the AML patients. Risk group was the only predictive parameter for overall survival (P = 0.003).

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B, Member 1 / antagonists & inhibitors
  • ATP Binding Cassette Transporter, Subfamily B, Member 1 / metabolism*
  • ATP-Binding Cassette Transporters / antagonists & inhibitors
  • ATP-Binding Cassette Transporters / metabolism*
  • Adolescent
  • Adult
  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use
  • Cyclosporins / pharmacology
  • Drug Resistance, Multiple
  • Drug Resistance, Neoplasm
  • Female
  • Flow Cytometry
  • Fluoresceins / pharmacokinetics
  • Fluorescent Dyes / pharmacokinetics
  • Glutathione / metabolism
  • Humans
  • Leukemia, Myeloid / drug therapy*
  • Leukemia, Myeloid / metabolism*
  • Male
  • Middle Aged
  • Multidrug Resistance-Associated Proteins
  • Neoplasm Proteins / antagonists & inhibitors
  • Neoplasm Proteins / metabolism*
  • Propionates / pharmacology
  • Quinolines / pharmacology
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Randomized Controlled Trials as Topic
  • Reverse Transcriptase Polymerase Chain Reaction
  • Rhodamine 123 / pharmacokinetics
  • Survival Analysis
  • Treatment Outcome
  • Tumor Cells, Cultured

Substances

  • ATP Binding Cassette Transporter, Subfamily B, Member 1
  • ATP-Binding Cassette Transporters
  • Cyclosporins
  • Fluoresceins
  • Fluorescent Dyes
  • Multidrug Resistance-Associated Proteins
  • Neoplasm Proteins
  • Propionates
  • Quinolines
  • RNA, Messenger
  • Rhodamine 123
  • 6-carboxyfluorescein
  • verlukast
  • Glutathione
  • valspodar