Publication at Second Faculty of Medicine |
2013
Abstract
Pediatric acute myeloid leukemia (AML) is a heterogeneous malignant disease, characterized by abnormal proliferation and impaired differentiation of myeloid cells. Acquired cytogenetic aberrations such as t(8;21)(q22;q22)/AML-ETO, inv(16)(p13q22)/CBFβ-MYH11, t(15;17)(q22;q21)/PML-RARα, rearrangements involving MLL and molecular aberrations in genes such as FLT3, NPM1, CEBPA and WT1 are involved in AML pathogenesis and are prognostic factors for treatment outcome.