A personalized approach to gastroesophageal cancer begins with the understanding that this is not one disease, but several related yet distinct entities. These may share molecular characteristics, but have a separate underlying epidemiology, etiology and clinical behavior. Distal or antral true ‘gastric’ cancers are more prevalent in Asia, are associated with high salt diet and Helicobacter pylori infection leading to chronic atrophic gastritis and intestinal metaplasia . By contrast, proximal tumors affecting the gastroesophageal junction and lower esophagus are more common in western populations and are associated with obesity, reflux esophagitis and the precursor lesion of Barrett’s esophagus . Diffuse gastric cancer is a unique malignancy with no known epidemiological risk factors (with the exception in rare cases of hereditary CDH1 mutation), no precursor lesion and an almost completely distinct pattern of clinical behavior and molecular biology to both distal and proximal intestinal-type cancers [1,2].
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