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. 2022 Jan 10;13:156. doi: 10.1038/s41467-021-27088-9

Fig. 4. In vivo PGRN blockade suppresses tumor initiation and progression in mouse PDAC.

Fig. 4

a mIF staining and quantification of PGRN+ tumor cells (PGRN+PanCK+) in the pancreas of wild-type mice and CKP mice with preneoplasia (4 weeks), early (6 weeks) and advanced (>8 weeks) PDAC. Filled arrowheads indicate PGRN+ tumor cells; Hollow arrowheads indicate PGRN+ macrophages. b Timeline for treatment of CKP mice with mouse isotype (mIg) or anti-PGRN antibody (PAb), 50 mg/kg. c Representative pictures of tumors and spleens from mIg-treated (mIg, n = 10), PGRN Ab-treated (PAb, n = 8), and untreated (ctrl, n = 5) CKP mice. d Weight of pancreas of CKP mice upon dissection. One-way ANOVA, Kruskal–Wallis test. e PGRN blockade suppresses tumorigenesis in CKP mice. Left panel: H&E staining of pancreas and spleens of CKP mice. Non-tumorous pancreatic tissues are highlighted by black lines. Right panel: IHC staining of panCK in the CKP pancreata. f The percentage of PanCK+ cells in the whole pancreata was quantified by Definiens software. One-way ANOVA, Kruskal–Wallis test. IHC staining of (g) PGRN and (h) pan-macrophage marker F4/80, M2 marker MRC1, M1 markers pSTAT1 and iNOS in CKP tumors treated with or without PGRN Ab (PAb) or mIg (50 mg/kg). The lower panels show the percentage of respective positive cells in the whole tumorous tissues as quantified by Definiens software. ctrl: n = 5; mIg: n = 10; PAb: n = 8. Mean + or ± SD is shown. One-way ANOVA, Kruskal–Wallis test. Scale bar unit: μm.