Cholecystokinin and Pancreatic Cancer

Abstract

Administration of the enterohormone cholecystokinin to animals stimulates growth of the pancreas. This hormone further promotes carcinogenesis and tumor growth of the pancreas. Stimulation of endogenous cholecystokinin secretion through the induction of deficiency of intraintestinal proteases and bile salts by trypsin-inhibiting nutrients, bile salt-binding drugs, or surgical intervention is also capable of stimulating growth and tumour development in the rat. In man, factors suggested to increase the risk of pancreatic cancer, such as a high-fat and high-protein diet or gastrectomy, are known to stimulate plasma cholecystokinin secretion. Receptors for cholecystokinin have been demonstrated on human pancreatic adenocarcinomas, and cholecystokinin has been demonstrated to enhance the growth of xenografted pancreatic cancer. The recently developed cholecystokinin receptor antagonists inhibit not only pancreatic growth but also pancreatic carcinogenesis in animals. These new drugs may be valuable new tools for inhibiting pancreatic cancer growth in humans.

Key Words:

• Carcinogenesis
• cholecystokinin
• cholecystokinin receptor antagonist
• pancreas
• pancreatic cancer