It is exactly a century since the gastric
hormone gastrin was first described as a blood-borne regulator of gastric acid secretion. The identities of the main active forms of the
hormone (the "classical
gastrins") and their cellular and molecular sites of action in regulating
acid secretion have all attracted sustained attention. However, recent work on
peptides derived from the
gastrin precursor that do not stimulate
acid secretion ("non-classical
gastrins"), together with studies on mice over-expressing the gene, or in which the
gastrin gene has been deleted, suggest hitherto unsuspected roles in regulating cell proliferation, migration, and differentiation. Moreover, microarray and proteomic studies have identified previously unsuspected target genes of the classical
gastrins. Some of the newer actions have implications for our understanding of the progression to
cancer in oesophagus, stomach, pancreas and colon, all of which have recently been linked in one way or another to dysfunctional signalling involving products of the
gastrin gene. The present review focuses on recent progress in understanding the biology of both classical and non-classical
gastrins.