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. Author manuscript; available in PMC: 2015 Jan 1.
Published in final edited form as: Toxicol Pathol. 2013 Oct 31;42(1):217–228. doi: 10.1177/0192623313508250

Figure 1. Pancreatic cancer progression in human and mouse.

Figure 1

Top: schematic representation of normal exocrine pancreas cells, transitioning from left to right into increasingly dysplastic PanIN and PDAC. In addition to visible abnormalities including papillary morphology, loss of polarity, nuclear atypia, intraluminal budding and stromal invasion (see Table 1 for additional details), PanIN-PDAC progression is associated with increasing accumulation of genetic lesions including activation of KRAS and loss of tumor suppressor genes including CDKN2A, TP53, SMAD4 and BRCA2. Bottom: H&E-stained sections of mouse pancreata of indicated genotypes, illustrating normal acinar (ac) and duct (du) cells as well as an early-stage PanIN lesion and advanced PDAC.