Gastric Cancer: Molecular Pathology State

Despite the progressive decrease observed in the past fifty years, gastric cancer (GC) is the fourth of the world rankings incidence of various types of cancer and is the second as a cause of cancer-related death. There is distinct geographical variation in gastric cancer incidence with the highest rates reported from Japan, Korea and Eastern Asia. Other high incidence areas are Eastern Europe and parts of Latin America, while Western Europe, Africa, Australia and the US generally have low incidence rates. In the last decade there has been a downward trend in the incidence and mortality from this cancer. The reasons are to be found in the improvement of food both as regards its preservation procedures and the variability in the diet and for the decrease of infection by Helicobacter pylori (H. pylori). H. pylori infection is strongly associated with risk for stomach cancer. Likely, this association is supported by the strong link between this bacterium infections and precancerous lesions, including chronic atrophic gastritis and dysplasia. The development of gastric cancer is characterized by multistage process in which several alterations of genetic and epigenetic nature accumulate. These alterations are mainly related to abnormalities of growth factors and receptors, DNA mismatch repair genes, angiogenic factors, transcription factors, adaptor proteins, cell cycle regulators, and many other macromolecular cell components. All these abnormalities identify from one side the molecular and biological aspect of gastric cancer cells and from the other might suggest possible strategies for therapeutic intervention.