Fig. 2: Fusion landscape in childhood cancers.

a Cohort composition. We analyzed 2638 leukemia (blue), 1459 brain tumors (yellow), and 1093 solid tumors (magenta), totaling 5190 childhood cancer patients. Percent patient tumors with oncogenic fusion detected are indicated with gray rings. b–d Spectrum of neo-splicing (b), neo-translational (c) and chimeric exon (d) fusions. e–g Spectrum of canonical fusions in leukemia (e), brain tumor (f) and solid tumor (g). In panels b–g, bars are color-coded according to tumor types in panel a. Distribution of DNA breakpoints (light blue dots) for oncogenic fusions is uniformly distributed in corresponding intronic regions for EWSR1-FLI1 (h) and CBFB-MYH11 (i), but not for TCF3-PBX1 (j). P values (and Q values after Bonferroni correction for multiple testing) of the uniformity test (two-sided Kolmogorov–Smirnov test; see Methods) are indicated along with sample size in panels h–j. k Prevalence of oncogenic fusions (y-axis) demonstrates a weak but marginally significant (P = 0.058) association with gene length (x-axis) in leukemia. l Statistically significant (P = 0.002) association between prevalence and gene length when the analysis is conditional on KMT2A-rearranged leukemia. Linear model, P value and R² value are indicated for panels k–l. Source data are provided accordingly as files a–g, h–j and k–l in Source Data file.