Etiology
The risk of gastric cancer has been associated with consumption of smoked and salted foods and lack of refrigeration.[8] The widespread use of refrigeration has been cited as a reason for the decrease in the incidence of gastric cancer in the US since 1930.
A number of studies have demonstrated an association between Helicobacter pylori and gastric cancer.[9][10][11][12]
Increased incidence of adenocarcinoma of the gastric cardia is believed, in part, to be attributable to increased obesity.[7]
Pathophysiology
Several events at the molecular level have been implicated in the development and progression of gastric cancers. Gastric cancer can involve loss of the tumor suppression gene, p53.[13] Several proto-oncogenes, such as ras, c-myc, and erbB2 (HER2), have been shown to be over-expressed in gastric cancers.[13] Helicobacter pylori has been associated with molecular events that could lead to gastric cancer, such as an increase in p53 mutations.[9]
The Cancer Genome Atlas (TCGA) Research Network has classified gastric cancer into four major genomic subtypes. These subtypes have distinct features and molecular alterations: 1) tumors that are positive for Epstein-Barr virus; 2) microsatellite unstable tumors; 3) genomically stable tumors; 4) chromosomal unstable tumors. This classification might be helpful to guide patient therapy in the future.[14]
Classification
Lauren classification[1]
Diffuse (occurs more often in young patients and has a worse prognosis than intestinal type)
Intestinal (frequently exophytic and ulcerated tumors and occurs in the proximal and distal stomach more often than diffuse type)
Japanese Endoscopy Society classification[2]
Type I: polypoid or mass-like tumors
Type II: flat, or either minimally elevated or depressed, tumors
Type III: tumors are associated with an ulcer
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