Fig. 3From: Combined Dusp4 and p53 loss with Dbf4 amplification drives tumorigenesis via cell cycle restriction and replication stress escape in breast cancerDusp4 loss potentiates tumorigenesis in cooperation with p53 loss and MYC overexpression. A Tumor formation and growth rate of orthotopically transplanted PMECs bearing Dusp4 loss, Trp53 loss, and/or MYC amplification. Dusp4-competent and excised comparator cell lines in each case were transplanted into opposite mammary fat pads (n = 5 mice/group). Dusp4FLOX Trp53Δex5 and Dusp4NULL Trp53Δex7 derivatives were lost early in development due to contamination and thus are not isogenic with one another, but bear similar functional genomic modifications. B Example images of nu/nu mice bearing Dusp4-competent and excised comparator cell line inoculations in opposing mammary fat pads. C Representative images of H&E histology of tumors derived from Dusp4NULL Trp53Δ MYCAMP cells with adenosquamous or squamous differentiation. KP: keratin pearls. D Multiplexed immunofluorescence for basal (Krt5) and luminal (Krt8/18) keratins in tumors arising from Dusp4NULL Trp53Δ MYCAMP cells, with an associated normal duct as a control for staining. KP: keratin pearlsBack to article page