Benign vs malignant pancreatic lesions: Molecular insights to an ongoing debate

Table 1 Distinctive histologic features of pancreatic ductal adenocarcinoma and its benign mimics

PDAC	CP	AIP	PDP
Perineural invasion; perivascular invasion; naked glands in adipose tissue; desmoplasia; anisonucleosis (4:1 nuclear size variation)	Intact lobular architecture; fibrosis; secretory plugs	Type I: Dense lymphoplasmacytic infiltrate with an increased IgG4 expression; storiform fibrosis; obliterative phlebitis. Type II: Granulocytes in the ductal epithelium; absent IgG4 positive cells.	Duodenal wall thickening; brunner gland hyperplasia; smooth muscle hyperplasia; heterotopic pancreatic tissue

PDAC: Pancreatic ductal adenocarcinoma; CP: Chronic pancreatitis; AIP: Autoimmune pancreatitis; PDP: Paraduodenal pancreatitis.

Table 2 Summary of morphologic features and altered genes of pancreatic ductal adenocarcinoma subtypes

Subtype	Colloid	Medullary	Adenosquamous	Hepatoid	Signet ring cell
Morphologic features	More than 80% of extracellular mucin; focal signet-ring cells can be seen	Minimal glandular differentiation; syncytial growth pattern; abundant inflammatory infiltrate	More than 30% of squamous differentiation	More than 50% of hepatocellular differentiation	More than 80% of signet ring cell component
Altered genes	GNAS; ATM	MMR genes; POLE	SMAD4; CDKN2A	BAP1; Notch1	NA

MMR: Mismatch repair; NA: Not available.