Extended Data Fig. 5: KrasG12D/+-max models display rapid oncogenic growth after injury.
From: Injury prevents Ras mutant cell expansion in mosaic skin
a) Quantification of the initial percent tdTomato+ area in the first revisit of KrasG12D/+-mosaic in uninjured (n = 4 mice) and injured (n = 5 mice) conditions and KrasG12D/+-max in injured (n = 3 mice) condition. At least three independent areas of approximately 300 μm2 were analysed for each mouse (Methods). Data are represented as means and standard deviations. b, c) Histopathologic examination via H&E staining of uninjured and injured ear skin within 2 weeks PWI. n = 4 KrasG12D/+-mosaic, n = 5 KrasG12D/+-max. b) KrasG12D/+-mosaic (left) in uninjured ear skin with normal epithelium, dermis and cartilage and injured ear (right) showing mixed inflammatory cell infiltrate and increased number of fibroblasts consistent with early scar tissue. c) KrasG12D/+-max uninjured ear (right) showing normal epithelial thickness and architecture. This is in comparison to the injured ear (left) showing significant expansion of the epithelial layer with hypergranulosis, focal parakeratosis alternative to the compact hyperkeratin. Focal cytologic atypia is present. Scale bars indicated on the figure. Magnified insets of the epidermis in the lower left corner of each image. d) Macroscopic image of the aberrant growth around the wound of the KrasG12D/+-max model in contrast to the normal epithelium of the KrasG12V/+-mosaic model.
