Pancreatic acinar cell carcinoma: An analysis of cell lineage markers, p53 expression, and Ki-ras mutation

Anne Hoorens, Nicholas R. Lemoine, Elizabeth McLellan, Toshio Morohoshi, Terumi Kamisawa, Philipp U. Heitz, Bernhard Stamm, Josef Rüschoff, Bernd Wiedenmann, Günter Klöppel

Research output: Contribution to journalArticlepeer-review

168 Scopus citations


In a series of 22 pancreatic acinar cell carcinomas, including two acinar cystadenocarcinomas, cellular differentiation was analyzed by immunocytochemistry and electron microscopy. In addition, overexpression of p53 protein and Ki-ras codon 12 mutation was studied. Four of the 20 noncystic acinar cell carcinomas showed a pure acinar pattern, nine an acinar-solid, and seven a solid pattern. All tumors stained for at least 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 tumors expressed neuroendocrine markers (synaptophysin, eight of 22; chromogranin 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 demonstrated in one tumor. Electron microscopy revealed zymogen granules (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 carcinomas show obvious capacity to differentiate into several directions, but nevertheless constitute an entity different from ductal adenocarcinomas or endocrine tumors.

Original languageEnglish
Pages (from-to)685-698
Number of pages14
JournalAmerican Journal of Pathology
Issue number3
StatePublished - Sep 1993
Externally publishedYes


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