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Altered influence of CCK-B/gastrin receptors on HDC expression in ECL cells after neoplastic transformation.

Journal article
Authors Lars Kölby
Bo Wängberg
Håkan Ahlman
I M Modlin
E Theodorsson
Ola Nilsson
Published in Regulatory peptides
Volume 85
Issue 2-3
Pages 115-23
ISSN 0167-0115
Publication year 1999
Published at Institute of Surgical Sciences, Department of Surgery
Pages 115-23
Language en
Keywords Animals, Benzodiazepines, pharmacology, Carcinoid Tumor, genetics, metabolism, pathology, Cell Transformation, Neoplastic, Enterochromaffin Cells, metabolism, Gastric Mucosa, metabolism, Gastrins, blood, Gene Expression, Histamine H2 Antagonists, pharmacology, Histidine Decarboxylase, genetics, Hormone Antagonists, pharmacology, Humans, Muridae, RNA, Messenger, genetics, metabolism, RNA, Neoplasm, genetics, metabolism, Receptors, Cholecystokinin, metabolism, Stomach Neoplasms, genetics, metabolism, pathology, Triazoles, pharmacology
Subject categories Cancer and Oncology


Gastrin is one of the main factors controlling enterochromaffin-like (ECL) cell endocrine function and growth. Long-standing hypergastrinemia may give rise to ECL cell carcinoids in the gastric corpus in man and in experimental models. We have analysed the expression and function of CCK-B/gastrin receptors in normal ECL cells and in ECL cell tumours (gastric carcinoids) of the African rodent Mastomys natalensis. Hypergastrinemia induced by short-term (5 days) histamine2-receptor blockade (loxtidine) resulted in increased histidine decarboxylase (HDC) mRNA expression in the gastric oxyntic mucosa. This increase was significantly and dose-dependently reversed by selective CCK-B/gastrin receptor blockade (YM022). Long-term (12 months) hypergastrinemia, induced by histamine2-receptor blockade, gave rise to ECL cell carcinoids in the gastric oxyntic mucosa. CCK-B/gastrin receptor mRNA was only slightly elevated while HDC mRNA expression was eight-fold elevated in ECL cell carcinoids and was not influenced by CCK-B/gastrin receptor blockade. Thus CCK-B/gastrin receptor blockade of hypergastrinemic animals reduces the HDC mRNA expression in normal mucosa but not in ECL cell carcinoids. These results demonstrate that HDC mRNA expression in neoplastic ECL cells is not controlled by CCK-B/gastrin receptors.

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