Fig. 1 | Nature Communications

Fig. 1

From: In vivo reprogramming drives Kras-induced cancer development

Fig. 1

Kras/p53 compound mutations are insufficient for PDAC development. a A schematic illustration of the genetic construct to activate HA-KrasG12D in the pancreas. b Representative histology and immunostaining for HA-KrasG12D. Scale bars, 50 μm. c Genetic strategy to study the influence of somatic activation of Kras and p53 mutations in the pancreas. d Southern blotting of LSL-KrasG12D and LSL-p53R172H allele. ESCs containing Pdx1 ires-Cre, LSL-KrasG12D and LSL-p53R172H alleles were used as control. Note that majority of two LoxP alleles are converted into one LoxP allele in the pancreas of KPC mouse (Cont control, Panc pancreas). e Immunostaining for pERK and Ki67 in the pancreas of 6-week-old wild-type mice, KC mice, and KPC mice. KPC mice at 8 weeks of age showed a focal PDAC area with pERK staining (bottom). Scale bars: HE and pERK (low magnification) staining, 200 μm; pERK (high magnification) staining, 50 μm; and Ki67 staining, 100 μm

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