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Table 2 Summary of clinically relevant and actionable genomic alterations and molecular subtypes of GC

From: Genomic alterations and molecular subtypes of gastric cancers in Asians

Subgroup Key mutations Key CNV events Drugs in development
MSI KRAS, PIK3CA (H1047R), PTEN, mTOR, ARID1A Very few alterations MEK-ERK and PI3K-mTOR pathway inhibitors, immunotherapies
MSS/EMT PIK3CA, RhoA CCNE1 PI3K-mTOR, CDK2, and ROCK inhibitors
MSS/TP53 TP53 CCND1, CCNE1, ERBB2, EGFR, KRAS, MYC RTK-focused agents, MEK-ERK, CDK4/6, and CDK2 inhibitors
MSS/TP53+ ARID1A, PIK3CA (E542/545K) CCNE1, KRAS MEK-ERK, CDK2, and PI3K-mTOR pathway inhibitors
  1. CNV copy number variation, KRAS kirsten rat sarcoma viral oncogene homolog, PIK3CA phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha, PTEN phosphatase and tensin homolog, mTOR mechanistic target of rapamycin, ARID1A AT-rich interactive domain 1A, MEK mitogen-activated protein kinase kinase, ERK extracellular signal-regulated kinase, PI3K phosphoinositide 3 kinase, RhoA Ras homolog family member A, CCNE1 cyclin E1, CDK cyclin-dependent kinase, ROCK Rho-associated protein kinase, CCND1 cyclin D1, ERBB2 Erb-B2 receptor tyrosine kinase 2, EGFR epidermal growth factor receptor, MYC v-Myc avian myelocytomatosis viral oncogene homolog, RTK receptor tyrosine kinase. Other abbreviations as in Table 1