Is exocrine pancreatic cancer a hormone-dependent tumor? A study of the existence of sex hormone receptors in normal and neoplastic pancreas.
The 5-year survival rate of patients with exocrine pancreatic cancer after surgery is less than 5%, in patients treated with radical surgery, with or without adjuvant therapy. It has been well documented clinically and experimentally that sex hormones influence the physiology of the exocrine pancreas. Hormone manipulation inhibits the growth of human pancreatic cancer in nude mice. Several nonrandomized studies have suggested the efficacy of antihormone therapy in the treatment of advanced pancreatic cancer. However, the existence of sex hormone receptors in exocrine pancreatic cancer has been a matter of controversy. This study was designed to investigate the presence of sex hormone receptors (estrogens, progesterone and androgens in normal pancreas and exocrine pancreatic cancer, using two different methods: immunohistochemistry and enzyme immunoassay. Twenty-eight biopsies of normal pancreas and 15 biopsies of exocrine pancreatic cancer were studied. Estrogen receptors and progesterone receptors were measured by enzyme immunoassay, using specific monoclonal antibodies. Androgen receptors were determined by radioligand assay. Sixteen biopsies of normal pancreas and 12 biopsies of exocrine pancreatic cancer were studied by immunohistochemistry. In exocrine pancreatic cancer we could not detect estrogen receptors or progesterone receptors, either by enzyme immunoassay or immunohistochemistry. Androgen receptors were always negative (less than 2 fm/mg). In the normal pancreas, 5 out of 28 cases showed increased levels of progesterone receptors (greater than 10 fm/mg) as measured by enzyme immunoassay. Immunohistochemistry revealed progesterone receptors in the pancreatic islets of 16 normal pancreases studied. Nuclear staining was observed in more than 70% of the cells. Estrogen receptors were always negative by immunohistochemistry and enzyme immunoassay in the normal pancreas.2+n
Targarona
E M
EM
Department of Surgery, Hospital de Mutua de Terrassa, University of Barcelona, Spain.
Pons
M D
MD
Gonzalez
G
G
Boix
L
L
Marco
V
V
Marco
C
C
D000230:Adenocarcinoma / Q000737:chemistry*; D000368:Aged; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D007150:Immunohistochemistry; D008297:Male; D009376:Neoplasms, Hormone-Dependent; D010179:Pancreas / Q000737:chemistry*; D010190:Pancreatic Neoplasms / Q000737:chemistry*; D011869:Radioligand Assay; D011944:Receptors, Androgen / Q000032:analysis*; D011960:Receptors, Estrogen / Q000032:analysis*; D011980:Receptors, Progesterone / Q000032:analysis*
D011944:Receptors, Androgen; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone