PANCREATIC ACINAR CELL-CARCINOMA - AN ANALYSIS OF CELL LINEAGE MARKERS, P53 EXPRESSION, AND KI-RAS MUTATION

In a series of 22 pancreatic acinar cell carcinomas, including two aci nar cystadenocarcinomas, cellular differentiation was analyzed by immu nocytochemistry and electron microscopy. In addition, overexpression o f p53 protein and Ki-ras codon 12 mutation was studied. Four of the 20 noncystic acinar cell carcinomas showed a pure acinar pattern, nine a n acinar-solid, and seven a solid pattern. All tumors stained for at l east one of the following pancreatic acinar markers: trypsin (21 of 22 ), lipase (19 of 22), chymotrypsin (13 of 22), phospholipase A2 (nine of 22), and pancreatic stone protein (19 of 22). One-third of the tumo rs expressed neuroendocrine markers (synaptophysin, eight of 22; chrom ogranin A, six of 21) and duct cell markers (CA19.9, nine of 21; B72.3 , six of 21). Cellular coexpression of trypsin and synaptophysin was d emonstrated in one tumor. Electron microscopy revealed zymogen granule s (nine of nine). In only one of 16 tumors a Ki-ras mutation at codon 12 was found, whereas in none of 19 tumors could overexpression of p53 protein be demonstrated. The results suggest that acinar cell carcino mas show obvious capacity to differentiate into several directions, bu t nevertheless constitute an entity different from ductal adenocarcino mas or endocrine tumors.