Table 1. Intrinsic Subtypes.

	G-INT GC	G-DIF GC
Histology	Intestinal histology (91/133)	Diffuse histology (64/107)
Molecular alterations	Genes up-regulated were related to carbohydrate and protein metabolism (FUT2) and cell adhesion (LGALS4, CDH17)	Cell proliferation (AURKB) and fatty acid metabolism (ELOVL5) functional annotations were enriched
Treatment reaction	In vitro study, G-INT cell lines were sensitive to 5-FU and oxaliplatin	In vitro study, G-DIF cell lines were more sensitive to cisplatin
	Patients with G-INT tumors may derive benefit from adjuvant 5-FU-based therapy
Prognosis	Superior overall survival	Poor

G-INT: genomic intestinal; G-DIF: genomic diffuse; GC: gastric cancer; AURKB: aurora kinase B; CDH17: cadherin 17; ELOVL5: ELOVL family member 5; FUT2: fucosyltransferase 2; LGALS4: lectin; 5-FU: 5-fluorouracil.