Recent research suggests that over expression of P-glycoprotein is involved in the resistance of some malignancies to structurally unrelated cytotoxic agents (Pastan & Gottesman, 1987; Kaye & Kerr 1991). It is postulated that P-glycoprotein decreases intracellular concentrations of cytotoxic agents by promoting their active efflux across the cell membrane (Musto et al. 1991). Modulating agents such as cyclosporin A and its analogues, (Sonneveld & Nooter 1990), verapamil, quinidine, the newer cephalosporines and torenifene have been put forward to inhibit resistance, by inhibiting active drug efflux. We report a case of acute myeloid leukaemia which was resistant to standard induction therapy. In vitro tests showed cyclosporin A to increase the sensitivity of the patient's myeloblasts to daunorubicin by threefold. Remission was successfully induced when cyclosporin A was combined with daunorubicin, cytosine, arabinoside and etoposide.
[1]
D. Kerr,et al.
Multidrug resistance: clinical relevance in haematological malignancies.
,
1991,
Blood reviews.
[2]
P. Musto,et al.
High risk of early resistant relapse for leukaemic patients with presence of multidrug resistance associated P‐glycoprotein positive cells in complete remission
,
1991,
British journal of haematology.
[3]
P. Sonneveld,et al.
Reversal of drug‐resistance by cyclosporin‐A in a patient with acute myelocytic leukaemia
,
1990,
British journal of haematology.
[4]
N. Fox,et al.
Chemosensitivity testing of fresh leukaemia cells using the MTT colorimetric assay
,
1989,
British journal of haematology.
[5]
I. Pastan,et al.
Multiple-drug resistance in human cancer.
,
1987,
The New England journal of medicine.