Deregulated Myc Cooperates Oncogenically with KRasG12D at All Stages of Lung Adenoma Evolution, Related to Figure 1
(A) Representative H&E staining of lung sections harvested at 6, 12 and 18 weeks after AdV-Cre inhalation, without (oil control) or with (+ tamoxifen) Myc co-activation for the final 6 weeks, as indicated. Groups I, II and III refer to the three different experimental protocols depicted in Figure S1A. Scale bars apply to each column of panels.
(B) Quantification of tumor burden in lungs of mice from Groups I, II and III, as described above. Each individual data point represents a single mouse. Group I: n = 6 mice. Group II: n = 10 mice. Group III: n = 9 (oil) and 10 (Tam) mice.
(C) Kaplan-Meier survival plot of KRasG12D-driven tumor-bearing mice (12 weeks post KRasG12D activation) then treated for 6 weeks with either oil (control) or Tamoxifen to activate Myc. n = 10 (oil) and 14 (Tam) mice.
(D) Representative H&E staining of lung sections comparing the tumorigenic impact of Myc alone (left), KRasG12D alone (middle) and Myc and KRasG12D together (right). AdV-Cre was administered by inhalation to each of the depicted genotypes (mentioned below the panels) and lungs harvested 12 weeks later. Left - Myc alone, activated for final 6 weeks; middle - KRasG12D alone (oil control), right – KRasG12D plus Myc co-activated for final 6 weeks (tamoxifen treatment). Scale bars apply to each row of panels.
Error bars represent the median with interquartile range. P values are based on Student’s t test (B) or Log-rank test (C). ∗p < 0.05, ∗∗∗∗p < 0.0001.