Acta clinica Croatica, Vol. 44 No. 1, 2005.
Original scientific paper
Expression and Processing of Somatostatin in Developing Pancreas and Pancreatic Ductal Adenocarcinoma
D. Tamiolakis
C. Simopoulos
J. Venizelos
M. Lambropoulou
S. Nikolaidou
P. Tsikouras
G. Alexiadis
A. Tsalkidis
T. Jivannakis
N. Papadopoulos
Abstract
Somatostatin is a gastrointestinal peptide hormone that inhibits growth of pancreatic cancer as reported by an increasing body of evidence. Yet this is not always the case. To clarify the controversy we aimed to identify the expression of somatostatin in developing human embryonic pancreatic tissue and pancreatic adenocarcinoma given that somatostatin positive cells were shown either into primitive pancreatic ductal epithelium or into pancreatic carcinoma. Tissue sections representing pancreatic fetal specimens (n=15) and ductal pancreatic adenocarcinoma specimens (n=15) were assessed using immunohistochemical methods for somatostatin expression. Normal primitive exocrine ductal epithelium and endocrine epithelium showed a definite, statistically significant, higher expression of somatostatin over neoplastic pancreatic tissue of mixed (ductal-endocrine) and pure ductal type (p1=0.021, p2=0.001, p3<0.0001and p4=0.003 respectively) during the 8th to the 10th week. No statistically significantly different expression of somatostatin in the mantle zone of the islets over neoplastic tissue of mixed (p5=0.16) and pureductal type (p6=0.65), from the 13th to the 24th week was demonstrated. Pancreatic cancer cells can express somatostatin in a model that reproduces the normal expression of the peptide by d-cells during embryonal organogenesis. Therapy aimed at pancreatic cancer must be targeted to somatostatin and analogues as a potential adjuvant novel option.
Keywords
Pancreatic neoplasms - pathology, Pancreatic neoplasms - physiopathology, Pancreatic neoplasms - therapy; Gastrointestinal hormones - physiology; Somatostatin - physiology; Neoplasms metastasis - prevention control
Hrčak ID:
14231
URI
Publication date:
3.3.2005.
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