Fig. 1: Pediatric t-MN (n = 44) is mainly driven by KMT2A fusions.
From: Selective pressures of platinum compounds shape the evolution of therapy-related myeloid neoplasms
a A table depicting the different first diagnoses of t-MN patients and the treatment categories that each patient received. ALL: acute lymphoblastic leukemia; AML: acute myeloid leukemia; bT: beta-thalassemia; FA: Fanconi anemia; MDS: myelodysplastic syndrome; NB: neuroblastoma; NGB: neuroganglioblastoma; OS: osteosarcoma; SCT: allogenic stem cell transplantation; TLBL: T-cell lymphoblastic lymphoma; TOPi: topoisomerase inhibitors. The country in which the sample was collected is indicated in the left side of the table. b Per-patient timelines depicting the latency time between the first diagnosis and the t-MN diagnosis. Rows per patient match with (a). c Distribution of latency times in years. d Circos plot of the structural variants (n = 72) in t-MN patients that involved at least one cancer gene. e Oncoprint depicting the clonal driver events that were present in t-MN samples. The bar plots on top represent the number of driving events present in each sample. Small drivers are only included if they occurred in more than one patient. CN-LOH: copy neutral loss of heterozygosity. f Circos plot depicting the copy number profiles of all t-MN samples. Source data are provided as a Source Data file.
