Relevant variants at BC for 39 patients. (A) Variants at BC. Recurrent CNVs are shown except for immunoglobulin and T-cell receptor deletions. (B) Overlap of variant type per patient at BC. (C) The percentage frequency of each mutated gene or locus is indicated above each column and calculated relative to the number of patients who underwent a particular form of sequencing or treatment (eg, the frequency of ABL1 mutations is calculated for the 33 patients who had received TKIs at the time of sequencing). Recurrent CNVs are graphed, except immunoglobulin and T-cell receptor deletions. IKZF1 and RUNX1 fusions and deletions are grouped with the other variants in these genes. The non–Ph-associated fusions are shown if 1 of the fusion partners was a known cancer gene. (D) Pairwise cooccurrence of variant types and genes. All genes that were mutated in ≥3 patients are included. The width of the ribbon correlates with the relative frequency of cooccurring mutated genes/variant type. Variants are arranged in clockwise order of frequency. Fusions where 1 of the partners was a cancer gene are grouped (fusions), except for MLL fusions (MLL-X). MLL fusions were the most frequent fusions and had few cooccurring variants, whereas ABL1 KD mutations and RUNX1 and IKZF1 variants had multiple cooccurring variants. The novel recurrently mutated gene SETD1B is shown for all patients with variants in this gene to show cooccurrence, although the variant was below the level of detection in 1 patient at BC. (E) The same plot is shown where the colors indicate cooccurring variants associated with myeloid BC (MBC) in red and LBC in blue, which reveals that cancer gene–associated fusions were rare in LBC, as were ASXL1 variants. The Ph-associated fusions were more frequently linked with LBC.