Advances in molecular mechanism of gastric cancer peritoneal metastasis

Table 2 Key genetic mutations and their signaling pathways in gastric cancer peritoneal metastasis

Gene	Alteration type	Affected pathway	Function	Clinical implication
CDH1	Deletion mutations	Cell adhesion and LGN	Randomization of cell division direction and increased invasiveness	Potential targeting direction for cell division
TP53	Deletion mutations	p53 signaling and apoptosis	Loss of cell cycle control and apoptosis	ctDNA TP53 mutation predicts poor response to chemotherapy
ARID1A	Deletion mutations	mTOR/SOX9	Enhanced migration and invasion	Potential target for mTOR inhibitors
NF2/RASA1	Deletion mutations	Wnt and YAP	Increased tumor stemness and metastatic capacity	Synthetic lethality with combined Bcl-2 and YAP inhibitors
ERBB2/ERBB3	Activating mutation	-	Enhanced TMB, CD8+ T cell infiltration, and TME immunological activity	Predict response to chemoimmunotherapy

This table summarizes the major genetic alterations implicated in gastric cancer peritoneal metastasis, their affected signaling pathways, functional consequences, and clinical implications. It highlights mutations that guide patient stratification, predict treatment response, or represent potential therapeutic targets. LGN: Leu-Gly-Asn repeat-enriched protein; ctDNA: Circulating tumor DNA; mTOR: Mammalian target of rapamycin; SOX9: SRY box 9; TMB: Tumor mutation burden.