Journal
GASTROENTEROLOGY
Volume 119, Issue 1, Pages 162-171Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1053/gast.2000.8527
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Funding
- NCI NIH HHS [CA60087, CA72992] Funding Source: Medline
- NIDDK NIH HHS [DK52778] Funding Source: Medline
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Background & Aims: Processing intermediates of preprogastrin (gly-gastrin and progastrin), termed nonamidated gastrins, are mitogenic for several cell types including colonic epithelial cells. However, presently it is not known if nonamidated gastrins play a role in colon carcinogenesis and if the effects are similar to those of amidated gastrins, Methods: Colon carcinogenesis in response to azoxymethane (AOM) was examined in transgenic mice overexpressing either progastrin (hGAS) or amidated gastrin (INS-GAS), compared with that in wild-type (WT) mice. Results: In AOM-treated groups, the total number of tumors per colon was significantly higher in hGAS (4.8 +/- 0.34) than INS-GAS (3.0 +/- 0.16) and WT (2.7 +/- 0.35) mice. Total numbers of adenocarcinomas and adenomas per animal colon were also significantly higher in hGAS than INS-GAS and WT mice. The size of the tumors was greater in hGAS mice, resulting in a significantly higher tumor burden per mouse in the hGAS mice than INS-GAS and WT mice. Although >90% of the tumors were located in the distal half of the colon in INS-GAS and WT mice, a significant number (42%) were present at the proximal end of the colon in hGAS mice. Conclusions: The results suggest that the risk for developing colon carcinomas and adenomas in response to AOM is significantly increased in mice expressing high levels of progastrin, but not amidated gastrins.
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