ABSTRACT
Allografting represents the only therapeutic procedure capable of curing chronic myeloid leukaemia (CML). Unfortunately, the majority of CML patients do not have an HLA-matched sibling donor, and matched or partially matched unrelated donor transplants are still associated with a high transplant-related mortality within the first 100 days.1 For patients who do not have compatible donors and for older patients, therapy includes hydroxyurea, busulfan, and interferon- (IFN-). For patients who do not achieve haematologic and/or cytogenetic remission after IFN- therapy, alternative treatment strategies are needed. One option is offered by autologous stem cell transplantation. This procedure has been explored with in vitro and in vivo manipulation techniques for the treatment of late chronic-phase or more advanced-phase disease, and, more recently, upfront at diagnosis.2-6 Another approach has recently been proposed, using specific chemical inhibitors of ABL tyrosine kinase (see Chapter 32). In particular, preclinical studies with STI571 (Glivec; Gleevec) have demonstrated
significant haematologic responses at higher dose levels of the drug7,8 (see Chapter 34). In this chapter, we will focus on the results achieved with high-dose therapy followed by ‘rescue’ with mobilized haematopoietic progenitor cells (HPC).
