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. Author manuscript; available in PMC: 2015 Jun 30.
Published in final edited form as: Nature. 2008 Aug 17;455(7213):679–683. doi: 10.1038/nature07260

Figure 1. Endogenous Myc function is required for formation and maintenance of early-stage Kras-induced lung hyperplasias/adenomas.

Figure 1

a, Representative haematoxylin-and-eosin-stained sections of lungs from CMVrtTA single transgenic mice (CMVrtTA+doxycycline), untreated Kras;TRE-Omomyc;CMVrtTA triple transgenic mice (Kras;TRE-Omomyc; CMVrtTA − doxycycline) and doxycycline-treated LSL-Kras;TRE-Omomyc;CMVrtTA triple transgenic mice (Kras;TRE-Omomyc;CMVrtTA+doxycycline), 4 weeks after infection with adenoviral Cre. Hyperplastic lesions are indicated by black arrowheads. b, Graphical representation of total BADJ cells scored as proliferating (Ki67-positive). Error bars represent standard deviation derived from approximately 100 BADJs per mouse. At least three mice were used per series. c, Myc inhibition triggers regression of early-stage lung adenomas. Haematoxylin and eosin staining of lungs from mice treated or not with doxycycline for 1 week, starting 6 weeks after Cre-recombinase-expressing adenovirus infection, is shown. A small adenoma is indicated by black arrowheads. d, TUNEL staining reveals positive cells in Omomyc and Ras co-expressing samples (Kras;TRE-Omomyc;CMVrtTA+doxycycline), but not in untreated or single transgenic controls (Kras;TRE-Omomyc;CMVrtTA −doxycycline and CMVrtTA +doxycycline). Higher magnification of positive cells is shown in the insert on the right.