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The Clinical and Cellular Pharmacology Of Vincristine, Corticosteroids, l‐Asparaginase, Anthracyclines and Cyclophosphamide In Relation To Childhood Acute Lymphoblastic Leukaemia

Recently, slow early response to remission induction therapy has been recognized as a poor prognostic factor for childhood acute lymphoblastic leukaemia (ALL) (Reiter et al, 1994; Nachman et al, 1997). Indeed, augmentation of post-remission induction therapy has been shown to improve the outcome for such cases (Nachman et al, 1998). The potential importance of primary drug resistance, as measured by the methylthiazol tetrazoliumbromide (MTT) assay, has been investigated as a determinant of potential response to remission induction therapy and overall prognosis (Pieters et al, 1991; Kaspers et al, 1997). Moreover, an association between the delivered drug dose of vincristine, l-asparaginase and anthracycline has been described for children with higher risk ALL (Gaynon et al, 1991). However, there have been no studies of the importance of the clinical and cellular pharmacology of the antileukaemic agents that form the mainstay of remission induction and intensification/consolidation therapy for childhood ALL. The purpose of this review will be to discuss the possible optimization of vincristine, corticosteroids, l-asparaginase, anthracyclines and cyclophosphamide in the therapy of childhood ALL. For this, the discussion will focus on the known mechanisms of cytotoxicity of these agents in vitro, their activity as single agents and studies of the clinical and cellular pharmacology of these agents in the therapy of childhood ALL.