Premium
Growth factor receptor expression in human gastroenteropancreatic neuroendocrine tumours
Author(s) -
Ulrich Wulbrand,
M. Wied,
P Zöfel,
Burkhard Göke,
R. Arnold,
Hans-Christoph Fehmann
Publication year - 1998
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1998.00397.x
Subject(s) - epidermal growth factor , biology , fibroblast growth factor receptor , growth factor receptor , growth factor , cancer research , transforming growth factor , fibroblast growth factor receptor 4 , growth factor receptor inhibitor , receptor , somatostatin receptor , somatostatin , endocrinology , medicine , receptor tyrosine kinase , epidermal growth factor receptor , fibroblast growth factor receptor 3 , tyrosine kinase , platelet derived growth factor receptor , receptor expression , fibroblast growth factor , genetics
Background Human gastroenteropancreatic neuroendocrine tumours are functionally and biologically heterogeneous, but their exact growth factor receptor expression pattern, important for onco‐ and carcinogenesis, remains unknown. Methods This study searched for the mRNA expression pattern of six tyrosine‐ and serine/threonine kinase receptors [hepatocyte growth factor (HGFR), fibroblast growth factor (FGFR), epidermal growth factor (EGFR), insulin‐like growth factor (IGF)‐1R, transforming growth factor (TGF)‐βR1, TGF‐βR2] together with the five somatostatin receptors in human gastroenteropancreatic neuroendocrine tumours (gastrinomas, insulinomas, tumours with carcinoid syndrome, functionally inactive neuroendocrine tumours) using reverse transcriptase‐polymerase chain reaction (RT‐PCR). Results EGF receptor was expressed almost exclusively in gastrinomas. Among the four tumour subtypes, expression frequencies of the somatostatin receptors 1 and 5, HGF‐, IGF‐1‐, TGF‐βR1, TGF‐βR2 and the EGF‐receptor varied significantly. Conclusions In spite of the common cellular origin of these tumours, differences in growth factor receptor expression suggest the existence of different pathways during tumour subtype development.