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. 2026 Jan 21;123(4):e2511733123. doi: 10.1073/pnas.2511733123

Fig. 5.

The figure shows C29h treatment scheme, H and E and I H C of pancreata, quantification of A D M and PanINs, and acinar-identity genes m R N As.

C29h inhibits PDAC development in KrasG12D/PEC/IkkαΔPEC mice. (A) C29h treatment scheme. (B) H&E and IHC of untreated and C29h-treated pancreata with quantification. (Scale bars, 50 µm and 100 µm.) (Amylase). CD8+ T cell density normalized to tissue area (cells/mm2) and averaged per tumor. Mean ± SD (n = 3 to 6 tumors). Unpaired two-tailed t tests and Mann–Whitney test (NQO1); P < 0.05, *P < 0.01, **P < 0.001. (C and D) Quantification of ADM and PanINs (C) and acinar-identity genes mRNAs (D) in KrasG12D/PEC/IkkαΔPEC pancreata ± C29h. Mean ± SEM (lesion counts, n = 56 to 77 fields) or mean ± SD (mRNA, n = 4 to 6). Kruskal–Wallis with Dunn’s test (C); multiple unpaired t tests, Holm–Šídák method (D); *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; ns-not significant. (E) NQO1 mRNA (Left) and protein (Right) in the same pancreata; ERK1/2, loading control. Mean ± SD (n = 4 to 6). Unpaired two-tailed t tests; P < 0.05. (F) Indicated mRNAs in above pancreata. Mean ± SD or ± SEM (Cxcl12) (n = 4 to 7). Unpaired two-tailed t tests; P < 0.05, *P < 0.01.