Helicobacter pylori, infecting more than 50% of the world population, results in
gastritis, usually located in the
antral portion of the stomach, accompanied by hypergastrinemia, the key factor in gastric and colorectal
carcinogenesis. Excessive mucosal cell proliferation for many years may eventually result in gastric
atrophy, cell mutation and transformation of gastric mucosal cells into
gastrin-producing cells, which also express
gastrin receptors serving to stimulate cell proliferation and
tumor growth. These processes may be completed by the expression of
cyclooxygenase-2 (COX-2) as an
inflammation enzyme to release excessive amounts of
PGE(2), leading to further proliferation, reduction in apoptosis, angiogenesis and
tumor growth. H. pylori eradication results in complete regression of
MALT lymphoma and subsequent normalisation of excessive
gastrin release and COX-2 expression. Reduction of
gastrin by active immunisation (
gastrimmune), blocking of
gastrin receptors with specific blockers and suppression of COX-2 might be helpful in inhibiting
tumor growth and invasion.