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Keywords:

  • hepatoid carcinoma;
  • ductal carcinoma;
  • islet cell carcinoma;
  • hepatocellular differentiation;
  • α-fetoprotein;
  • transdifferentiation

Common embryologic foregut derivation of the pancreas and liver and cellular phenotypic transformation (i.e., hepatocytic transdifferentiation of pancreatic cells) may explain the phenomenon of hepatoid carcinoma of the pancreas.

Abstract

BACKGROUND

The majority of primary extrahepatic neoplasms exhibiting features of hepatocellular carcinoma in terms of morphology, immunohistochemistry, and behavior have been described in the stomach. To the authors' knowledge only a few cases have involved other organ sites. They frequently are associated with other histologic type tumors such as adenocarcinoma, and portend an aggressive behavior.

METHODS

Two examples of hepatoid carcinoma arising from the pancreas are reported in the current study.

RESULTS

One case was a malignant islet cell tumor with a full-blown clinical syndrome of glucagon overproduction, histologic evidence of hepatocytic differentiation, bile production, and α-fetoprotein (AFP) positivity. The second tumor was a ductal carcinoma showing periodic acid–Schiff positive and diastase-resistant hyaline globules, AFP production, and ultrastructural resemblance to hepatocytic cells.

CONCLUSIONS

The rare observation of cellular phenotypic transformation that corresponds with the process of hepatocytic transdifferentiation of pancreatic cells demonstrated in animal models and the common embryologic foregut derivation of the pancreas and liver also may explain the phenomenon of pancreatic hepatoid carcinoma. Cancer 2000;88:1582–9. © 2000 American Cancer Society.