We therefore investigated whether serum gastrin or CCK concentrations at baseline were associated with the incidence of gastric non-cardia adenocarcinomas (GNCA), oesophagogastric junctional adenocarcinomas (EGJA) or gastric carcinoid tumours over 24 years of follow-up in a study nested within the all-male Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study of Finnish smokers.
Despite the absence of CCK receptors from many gastrointestinal adenocarcinomas, evidence from animal models and from tumour cell lines in vitro suggests that the CCK-2 receptor may contribute to the development of esophageal and gastric adenocarcinomas, and further experimental work in these areas is clearly warranted.
Although CCK has been shown to promote the growth of human adenocarcinoma cell lines, its role in the growth of human pancreatic adenocarcinomas in vivo is less clear.
This study examined the temporal expression of CCK receptors in human fetal, postnatal, and adult pancreas to determine whether the appearance of CCK-A receptors in pancreatic adenocarcinomas reflected oncofetal antigen or pancreatic neoantigen expression.
The cell line will be useful in further studies on the mechanism(s) by which CCK stimulates growth of certain human pancreatic adenocarcinomas and normal human pancreatic exocrine tissue.