Progesterone receptor immunoreactivity in pancreatic endocrine tumors. An immunocytochemical study of 156 neuroendocrine tumors of the pancreas, gastrointestinal and respiratory tracts, and skin.
BACKGROUND
The immunoreactivity for progesterone receptors (PR) of the majority of endocrine cells of the human pancreas has prompted the authors to investigate if PR expression is maintained in pancreatic endocrine tumors and is correlated with the main clinicopathologic features of these neoplasms. Furthermore, the study has been extended to other neuroendocrine cells and tumors to determine whether PR immunoreactivity is a common feature of neuroendocrine cells and tumors other than those of the pancreas.


METHODS
One hundred fifty six neuroendocrine tumors of the pancreas, gastrointestinal and respiratory tracts, and skin were immunostained for PR with three different monoclonal antibodies and for estrogen receptors (ER). Additional immunostainings for general neuroendocrine markers and for pancreatic hormones were performed in selected cases.


RESULTS
Nuclear immunoreactivity for PR has been documented in the neoplastic cells of 56 (58.33%) of 96 pancreatic endocrine tumors. PR immunoreactivity was not influenced by the sex and age of the patients or the occurrence of a clinical syndrome related to inappropriate hormone secretion. Tumors synthesizing pancreatic polypeptide, glucagon, and insulin expressed PR in higher percentages (80%, 75%, and 66%, respectively) than those producing other pancreatic hormones or those that were not functioning. Irrespective of the functionally different tumor types, PR immunoreactivity showed a significant correlation (P = 0.0003) with the absence of metastases and the lack of tumor invasion of neighboring organs or of large vessels. As opposed to normal and neoplastic islet cells, the neuroendocrine cells and tumors of the gastrointestinal tract, respiratory tract, and skin did not show any PR immunoreactivity, with the single exception of a typical carcinoid tumor of the lung. ER were not identified in any pancreatic or extrapancreatic neuroendocrine cells or tumors.


CONCLUSIONS
Nuclear PR are immunocytochemically detectable in most pancreatic endocrine tumors and are correlated significantly to the absence of pathologic evidence for malignancy. Conversely, PR expression has not been found in normal and neoplastic endocrine cells and tumors investigated.
Viale
G
G
Department of Pathology, University of Milan School of Medicine, Italy.
Doglioni
C
C
Gambacorta
M
M
Zamboni
G
G
Coggi
G
G
Bordi
C
C
D007516:Adenoma, Islet Cell / Q000737:chemistry*; D000293:Adolescent; D000328:Adult; D000368:Aged; D053379:Chromogranin A; D002864:Chromogranins / Q000032:analysis; D005260:Female; D005753:Gastric Mucosa / Q000737:chemistry; D005770:Gastrointestinal Neoplasms / Q000737:chemistry*; D005934:Glucagon / Q000032:analysis; D006801:Humans; D007124:Immunoenzyme Techniques; D007328:Insulin / Q000032:analysis; D007413:Intestinal Mucosa / Q000737:chemistry; D007515:Islets of Langerhans / Q000737:chemistry; D008168:Lung / Q000737:chemistry; D008175:Lung Neoplasms / Q000737:chemistry*; D008297:Male; D008875:Middle Aged; D009092:Mucous Membrane / Q000737:chemistry; D010190:Pancreatic Neoplasms / Q000737:chemistry*; D010191:Pancreatic Polypeptide / Q000032:analysis; D011960:Receptors, Estrogen / Q000032:analysis; D011980:Receptors, Progesterone / Q000032:analysis*; D012878:Skin Neoplasms / Q000737:chemistry*; D013004:Somatostatin / Q000032:analysis; D016708:Synaptophysin / Q000032:analysis
D053379:Chromogranin A; D002864:Chromogranins; D007328:Insulin; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016708:Synaptophysin; D013004:Somatostatin; D010191:Pancreatic Polypeptide; D005934:Glucagon