Figure 6.

Dependency on Myc is Rapidly Acquired by Lung Adenocarcinomas

(A) Representative immunostaining for Ki67, CD206, TUNEL (white arrows), and CD31 in adenocarcinomas at indicated time points following Myc activation for 7 days (7d tam) and subsequent de-activation (7d tam, then 7d off) compared to KRas^G12D-only (control). The tumor edges boxed in the top panels are shown enlarged below. Scale bars apply across each row.

(B) Quantification of histological changes in Ki67, CD206, TUNEL, CD3, and NKp46 in lung tumors after short term (7d tam) Myc-activation and subsequent Myc de-activation for 3 and 7 days (3d, 7d off) compared to KRas^G12D-only control (7d oil).

(C) Fold change in tumor cell proliferation (Ki67) and death (TUNEL) in mice treated with oil (control) or with tamoxifen for 7 days followed by tamoxifen withdrawal for 3 or 7 days. Individual and average values of tumor cell death and proliferation are displayed in (B).

(D) Representative H&E staining of part of and whole lung lobes together with corresponding quantification of total tumor burden (left y axis) and tumor multiplicity (right y axis) in lungs of mice treated with tamoxifen for 7 days followed by Myc de-activation for either 7 days or 4 weeks (7d, 4w off) and compared to KRas^G12D-only control (7d oil). T = tumor.

Quantification graphs: FoV = field of view. (B): n = 25 individual tumors (small symbols) from 5 mice (large symbols) per time point. (D) Each individual data point represents a single mouse (n = 8 mice per group). Box and whisker graphs represent tumor multiplicity of 8 mice per group. Error bars represent the median with interquartile range (Ki67, CD206, TUNEL, CD3) or mean ± SD (NKp46). p values are based on Student’s t test (Ki67, CD206, TUNEL, CD3) or two-way ANOVA (NKp46). NS = non-significant; ^∗p < 0.05, ^∗∗p < 0.01, ^∗∗∗p < 0.001, ^∗∗∗∗p < 0.0001.

See also Figure S1.