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This failure may be attributed to lack of control of confounding factors, such as H. pylori in the control groups. A recent study, in which H. pylori infection was controlled for, showed that hypergastrinemia is associated with a 3.3-fold increase in the relative risk of developing colorectal cancer (17) . It is conceivable, therefore, that hypergastrinemia may promote progression through the adenoma-carcinoma sequence. This hypothesis is strengthened by the preliminary findings of Smith and Watson (18) that human adenomas of all sizes and grades express an isoform of the cholecystokinin B/gastrin receptor.
Thus, the aim of the present study was to evaluate the effect of serum hypergastrinemia induced by omeprazole, a proton pump inhibitor that increases serum gastrin levels 2–4-fold (11 , 12 , 19) , on colonic neoplastic progression in the multiple intestinal neoplasia APCMin-/+ mouse model of APC.

| MATERIALS AND METHODS | Top
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
| APCMin-/+ Mice.
APC-/+ mice were bred within the Cancer Studies Unit at the University of Nottingham under Home Office Project License No. PPL 4011454. Heterozygous male APCMin-/+ mice were bred with wild-type C57/Bl6 female mice. The offspring were characterized for the Min genotype by PCR as described previously (20) .
Entry of Mice into Therapeutic Studies.
After results from the PCR analysis were