Mutated WT1, FLT3-ITD, and NUP98-NSD1 Fusion in Various Combinations Define a Poor Prognostic Group in Pediatric Acute Myeloid Leukemia

Figure 1

Study flowchart and patient characteristics. (a) Study flowchart outlining the process of patient recruitment in the data analysis. (b) WT1 mutations often co-occurred with FLT3-ITD and other genetic aberrations. AML-BFM, acute myeloid leukemia-Berlin-Frankfurt-Muenster; n, number; WT1, Wilms Tumor 1; FLT3-ITD, fms-related tyrosine kinase 3-internal tandem duplication; NPM1, nucleophosmin 1; NRAS, neuroblastoma RAS viral oncogene homolog; c-KIT, KIT proto-oncogene; CBF, core binding factor; MLL, rearrangements of MLL gene; NUP98-NSD1, Nucleoporin-Nuclear Receptor Binding SET Domain Protein 1 fusion gene; CN, cytogenetic-normal AML; AR, allelic ratio; CCR, continued complete remission; LFU, lost to followup; NR, non-response; PR, partial remission. CBF aberrations include translocation of chromosomes 8 and 21 and inversion or translocation of chromosome 16. Other cytogenetic aberrations such as trisomy 8, various chromosomal translocations, and complex karyotype alterations.