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1.1 Myelogenous leukemia and the need for novel drug targets The successful treatment of myelogenous leukemia depends upon the continuing coordinate efforts of the medical and research communities and patients to understand the complex nature of leukemia development and progression, and to battle drug resistant cells. Novel drug therapies, like Imatinib, have been developed which target the mutant BCR-ABL (Breakpoint Cluster Region-Abelson Kinase) protein, and have significantly changed the treatment regimens for chronic myelogenous leukemia (CML). However, while Imatinib is frequently effective against the majority of the leukemic cells, and patients often undergo remission after treatment, these patients also relapse due to a leukemic drug-resistant population (Schemionek et al., 2010). In comparison to CML, the treatment for acute myelogenous leukemia (AML) is predominantly induction therapy using strong anti-mitotic agents, followed by consolidation therapy to kill residual diseased cells (Venditti et al., 2000). These therapies are not specifically targeted to mutated proteins in the cells, and therefore can be more toxic to the patient's normal cells. Researchers have attempted to target mutated proteins in AML. However, unlike BCR-ABL, targeting FLT3-ITD (FMS-like tyrosine kinase 3-Internal Tandem Duplication) and FLT3-TKD (FMS-like tyrosine kinase 3Tyrosine Kinase Domain) mutations have not been as successful as CML-Imatinib therapy (Kindler et al., 2010). Therefore, challenges facing patients with AML remain significant, and drug-resistant relapses remain a threat.

Novel Targets in Myelogenous Leukemia: The Id Family of Proteins