Abstract
Acute myeloid leukemia (AML) is a cancer of the blood and bone marrow characterized by uncontrolled proliferation of hematopoietic precursor cells with impaired hematopoiesis leading to neutropenia, anemia and thrombo cytopenia. AML is the second most common pediatric leukemia and has the worst prognosis of all major childhood cancers, more than one third of leukemia deaths occuring in children and adolescents are due to AML. Approximately 850 cases of pediatric AML are diagnosed each year in the USA. According to the NCI’s SEER Cancer Statistics Review, it is estimated that 12,330 men and women will be diagnosed with AML with approximately 8950 deaths in 2010. Most of the improvements in outcome of AML within the last few decades have been attributed to enrolling pediatric patients in clinical trials, use of intensive chemotherapies and improved supportive care. Despite treatment advances in the past decade, AML survival remains poor and treatmentrelated adverse events remain signif icant. One of the challenges facing clinicians is the development of resistance to chemotherapeutic drugs and treatmentrelated mortality. The majority of the clinical AML trials include intensive chemotherapy with or without subsequent stem cell transplantation. Cytarabine (araC) has been the backbone of AML chemotherapy for several decades and is normally used in combination with anthracyclines such as daunorubicin. For the last 40 years the standard of care for induction treatment has included a combination of 7 days of araC and 3 days of daunorubicin. At plasma concentrations of 0.5–1 μM, uptake transporter human equilibrative nucleoside transporter (hENT1) is crucial for araC uptake into the cell [1]. Once inside the cell, araC is activated by multiple
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