Fig. 2. Runx1t1 loss reverses MYCN-mediated sustained hyperplasia and induces ganglia neurite extension.

a The percentage neuroblast hyperplasia scored from homozygous Th-MYCN (+/+) mice or littermate mice lacking the MYCN transgene (−/−), with either wild-type (+/+) or heterozygous loss (+/−) of Runx1t1. Scoring of N = 3–8 independent mice was performed for each genotype and timepoint. All data points were N = 3, except for +/+, +/+ week 1 and week 2 (N = 4); +/+, +/− day 0 (N = 8) and week 4 (N = 4); −/−, +/− day 0 (N = 6), week 1 (N = 4) and week 4 (N = 5). The graph is mean ± SEM. b Representative histology of RUNX1T1 staining in ganglia from mice homozygous for the Th-MYCN transgene, and either wild-type or heterozygous for Runx1t1 from day 0 and 4 weeks of age. Neuroblast hyperplasia is defined as ≥30 small round blue cells within a sympathetic ganglion⁹. Photos were taken at 600X magnification, and the scale bars represent 20 microns. c βIII-tubulin staining of sympathetic ganglia isolated from Th-MYCN mice. The percent coverage of neurites was calculated and the area under the curve determined for each ganglia. N = 4 (+/+, +/−) or 5 (−/−, +/+ and +/+, +/+), Graphs are Mean ± SEM, *p = 0.0181, ***p = 0.0007. Two-tailed unpaired t-test. d Heatmap displaying gene clustering following RNA-Seq analysis of ganglia dissected from two-week-old Th-MYCN mice with either homozygous or heterozygous Runx1t1, compared to fully developed murine neuroblastoma tumors. Source data are provided as a Source Data file.