Cellular markers in the gastric precancerous process

gastric cancer is one disease or, as emphasized by Fenoglio-Preiser and colleagues, whether there are distinct and different pathways to a malignant gastric neoplasm.3 To simplify matters, cardia cancers will not be discussed as they do not appear to be linked to H. pylori.In addition, the tubular, papillary and mucinous types (WHO classification) of gastric cancer will be considered as synonymous with the intestinal type of cancer (of the Lauren classification) and the signet ring and undifferentiated cancers (WHO classification) will be considered to correspond to the diffuse type of tumour (Lauren).Many of the important molecular changes described in carcinogenesis, including gastric carcinogenesis, were originally defined as being due to a loss of function of a tumour suppressor gene or gain of function of an oncogene.This separation is somewhat artificial as we learn more about the physiological functions of these genes in controlling the cell cycle and in mediating cell-cell and cell-matrix interactions.Thus, many of the mutations described in gastric carcinogenesis affect genes known to alter proliferation and apoptosis and probably occur early in carcinogenesis.In contrast, decreased cell-cell or cell-matrix interactions, which occur later in solid tumourigenesis, are more common in diffuse than intestinal gastric cancers and may relate more to the tendency to produce metastasis than to the initial transformation process.