Abstract
Children with Down syndrome (DS) have an increased risk of developing acute myeloid and B-cell precursor acute lymphoblastic leukemia (BCP-ALL).1 The prognosis of DS ALL is at best similar and often inferior to that of sporadic ALL (non-DS) patients.2, 3 DS ALL is characterized by unique biological features when compared with non-DS ALL. For instance, DS ALL has a lower frequency of the favorable genetic abnormalities t(12;21)(p13;q22) (ETV6–RUNX1) and the unfavorable t(9;22)(q34;q11) (BCR-ABL1),3, 4 but a higher frequency of JAK2 mutations and CRLF2 rearrangements.5, 6 Using genome-wide screening techniques, several (novel) genomic aberrations involved in the pathogenesis of (non-) DS ALL were identified.7, 8 The potential prognostic impact of most of these novel aberrations and whether these patients may benefit from specific therapies targeted to these unique genetic features needs to be investigated further.
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