Gastrin is trophic for normal gastric and colonic mucosa. We examined the potential trophic effects of chronic
gastrin administration on the growth of mouse
colon adenocarcinoma (MC-26). Thirty-three mice bearing transplantable MC-26
colon cancers were treated with varying doses (125, 250, or 500 micrograms/kg/day) of
pentagastrin. Significant increases in
tumor weight and
DNA content were observed. Fundic mucosal weight and
DNA content in these mice showed a dose-related trophic response. The weight of control fundic mucosa was 10 mg and rose to 20, 45, and 65 mg with increasing doses of
gastrin. The
DNA content of control fundic mucosa was 155 micrograms and rose to 220, 340, and 480 micrograms as the dose of
gastrin was increased.
Pentagastrin stimulated growth of the MC-26
colon cancer, but the threshold for
gastrin-stimulated
tumor growth was different from that of normal mucosal growth. The hyperplastic response of the fundic mucosa was increased by increasing
gastrin doses; whereas,
colon cancer hyperplasia was maximal at the lowest dose tested (125 micrograms/kg/day) and did not increase further with increasing doses of
hormone. Mice bearing
gastrin-stimulated
tumors died at a significantly greater rate than did mice with untreated
tumors (80% of control mice and none of the treated mice were alive at day 55). The effects of
gastrin treatment on the growth of MC-26
colon cancer persist
after treatment is discontinued; mice with
tumors that were treated with
gastrin for either 7 or 14 days and in which the treatment was stopped were all dead by 35 or 28 days, respectively, after the end of treatment.