The Role of CCK in Tumor Growth

Abstract

Cancers of the gastrointestinal tract, particularly those of colonic, pancreatic, and gastric origin, are major causes of disability and death in the Western world. There has been little progress in our understanding of the causes and progression of these diseases in spite of remarkable advances in the area of tumor biology. One such advance is the realization that “growth factors” may modulate the proliferative rates of malignant neoplasms. Peptides such as epidermal growth factor, the transforming growth factors, and several others may affect tumor growth through direct actions on tumor cell receptors, receptors may be “overexpressed” in tumor cells, and these factors may even be synthesized and released by tumor cells to initiate autocrine growth stimulation. It is also possible that other substances, such as gastrointestinal hormones, may modulate cancer cell growth rates. This idea comes from the well-known trophic effects of gastrointestinal peptide hormones on various target tissues, and the possibility that malignant cells originating from these tissues may retain specific hormonal receptors that still influence proliferation. CCK is a potent growth stimulant of the normal exocrine pancreas [1], and many studies have used this background as an impetus to determine whether CCK also affects pancreatic cancer growth. Several reviews are available on the topic of gastrointestinal hormones and their potential role in pancreatic and other gastrointestinal cancers [2–6]