Table 1.
Characteristics | EBV (9%) | MSI (22%) | CIN (50%) | GS (20%) | |
---|---|---|---|---|---|
Sex | Female | 5 (19%) | 36 (56%) | 50 (34%) | 22 (38%) |
Male | 21 (81%) | 28 (44%) | 97 (66%) | 36 (62%) | |
Lauren classification | Diffuse | 5 (19%) | 6 (9%) | 18 (12%) | 40 (69%) |
Intestinal | 15 (57%) | 48 (75%) | 118 (80%) | 15 (26%) | |
Mixed | 3 (11%) | 3 (5%) | 10 (7%) | 3 (5%) | |
not reported | 3 (11%) | 7 (11%) | 1 (1%) | 0 | |
Main actionable targets | PD-L1/2 expression JAK2 expression PIK3CA mutation |
Loss of HLA class 1 complexes PIK3CA mutation |
HER2 amplification EGFR amplification MET amplification CCNE1, CCND1, CDK6 amplification VEGFA amplification FGFR2 amplification |
VEGFA amplification FGFR2 amplification Cell adhesion pathwaysRHO-A? |
CCND1, cyclin D1; CCNE1, cyclin E1; CDK, cyclin dependent kinase; CIN, chromosomal instability; EBV, Epstein Barr virus; EGFR, epidermal growth factor receptor; FGFR, fibroblast growth factor receptor; GS, genomically stable; HER2, epidermal growth factor receptor 2; HLA, human leukocyte antigen; JAK, Janus kinase; MSI, microsatellite unstable; OGJ, oesophagogastric junction; PD-L, programmed death ligand; PIK3CA, phosphatidylinositol 4,5 bisphosphate 3 kinase, catalytic subunit α; MET: mesenchimal epithelial transition; VEGFA, vascular endothelial growth factor A.