An association between elevated serum gastrin levels and the presence of human colorectal cancer has been reported, and gastrin has been shown to stimulate the growth of experimentally induced colon neoplasia.
Although trophic actions of gastrin on the gastric mucosa have been well-established, the effect of G17 amide, progastrin and intermediates to colon neoplasia in humans is controversial.
The short isoform of the CCK-B was detected in 80% of the normal colon tissues, 76.5% of the colon tumors, 100% of the metastasis samples and 75% of the colonic cell lines; whereas the long isoform, which is presumably more strongly activated by gastrin, was expressed in 50% of the normal colon samples, 23% of the colon tumors, 43% of the hepatic metastases and 1 cell line (Sk-Co15).