Figure 4.
Effects of COX-2 deficiency on HCD and KRASG12D/+ mediated pancreatic neoplastic development. (A) The ablation of COX-2 in HCD-fed KrasG12D/+ mice preserved pancreatic acinar cells, inhibited ductal-like cell formation, and reduced PanIN lesions. Seventy-five-day old male and female mice were induced by tamoxifen for the indicated gene expression or deletion in pancreatic acinar cells and subsequently treated with HCD or ND for 10 weeks. Paraffin sections of the pancreata from these mice were analyzed by H&E or IHC with antibodies against amylase, Mist1, CK19, or Muc5 (200× magnification). (B–E) Quantification of the stains in (A) with Fiji ImageJ software. NS, not significant. **, *** and ****, p-value < 0.01, 0.001 and 0.0001, respectively.