Fig. 4: Loss of Arrdc3 markedly accelerated MYC-driven lymphomagenesis in mice.

A Offspring of inter-crosses between Arrdc3^+/− and Eμ-Myc^T/+;Arrdc3^+/− mice do not obey Mendelian ratios post-birth (X² = 122.11, df = 5, p < 0.05 (p < 1 × 10⁻¹⁵)). By contrast, E14.5 foetuses generated from such inter-crosses were seen to obey Mendelian ratios (X² = 4.95, df = 5, p > 0.05 (p = 0.422)). Expected numbers are marked with a red E. B Kaplan–Meier survival curve of Eμ-Myc^T/+;Arrdc3^+/+ mice (median survival = 91 days), Eμ-Myc^T/+;Arrdc3^+/− mice (median survival = 77 days), and only one Eμ-Myc^T/+;Arrdc3^−/− mouse that survived the developmental perinatal lethality. The absence of one allele of Arrdc3 slightly, but not significantly, accelerated lymphoma development in Eμ-Myc mice (Mantel-Cox test, df = 1, p > 0.05 (p = 0.0686)). C Kaplan–Meier lymphoma-free survival curve of lethally irradiated recipient mice that had been transplanted with Eμ-Myc^T/+;Arrdc3^+/+ or Eμ-Myc^T/+;Arrdc3^−/− foetal liver cells. We observed a statistically significant acceleration of lymphoma development in mice that had been transplanted with Eμ-Myc^T/+;Arrdc3^−/− foetal liver cells (median survival = 67 days) compared to control mice that had been transplanted with Eμ-Myc^T/+;Arrdc3^+/+ foetal liver cells (median survival = 210 days) (Mantel-Cox test, df = 1, X² = 13.22, p < 0.001 (p = 0.000276)).