FIGURE 1. Endogenous Myc function is required for formation and maintenance of early-stage Kras-induced lung hyperplasias/adenomas.
From the following article:
Modelling Myc inhibition as a cancer therapy
Laura Soucek, Jonathan Whitfield, Carla P. Martins, Andrew J. Finch, Daniel J. Murphy, Nicole M. Sodir, Anthony N. Karnezis, Lamorna Brown Swigart, Sergio Nasi & Gerard I. Evan
Nature 455, 679-683(2 October 2008)
doi:10.1038/nature07260
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.
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