Skip to main content
. 2021 Mar 29;22(5):e51573. doi: 10.15252/embr.202051573

Figure 4. Mice lacking PRSS35 are more sensitive to wound‐ and chemically‐induced carcinogenesis.

Figure 4

  • A
    Incidence of wound‐induced papilloma formation in InvEE PRSS35+/+ (WT; n = 8) and InvEE PRSS35−/− (PRSS35 KO; n = 10) mice at site of wounding. (*P = 0.0218; Gehan–Breslow–Wilcoxon test).
  • B
    H&E‐stained skin sections of wound‐induced papillomas of InvEE PRSS35+/+ and InvEE PRSS35−/− mice. Scale bars: 100 µm.
  • C, D
    Incidence of papilloma formation (ns: non‐significant; Gehan–Breslow–Wilcoxon test) (C) and number of tumours per mouse (D) in wild‐type (WT, n = 17) and PRSS35 KO (n = 22) mice treated with DMBA‐TPA (*P = 0.0171; Wilcoxon matched‐paired rank test). Data represent means ± SEM.
  • E
    Representative pictures of the back skin of WT and PRSS35 KO mice undergoing the DMBA‐TPA treatment at week 15 and week 20 after the start of TPA treatment. White arrows indicate tumours. Scale bar: 1 cm.
  • F
    Tumour size at week 20 after the start of TPA treatment. The biggest tumour of each mouse was measured (WT; n = 8; KO; n = 14; ns: Mann–Whitney test). Data represent means ± SEM.