Skip to main content
Fig. 3 | Breast Cancer Research

Fig. 3

From: Combined Dusp4 and p53 loss with Dbf4 amplification drives tumorigenesis via cell cycle restriction and replication stress escape in breast cancer

Fig. 3

Dusp4 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 pearls

Back to article page