Background: Gastric cancer (GC) is a deadly tumor with the fifth highest occurrence and highest global mortality rates. Owing to its heterogeneity, the underlying mechanism of GC remains unclear, and chemotherapy offers little benefit to individuals.
Aim: To investigate the clinical outcomes of TP53 and CDH1 mutations in GC.
Methods: In this study, 202 gastric adenocarcinoma tumor tissues and their corresponding normal tissues were collected. A total of 490 genes were identified using target capture. Through t-test and Wilcoxon rank-sum test, somatic mutations, microsatellite instability, and clinical statistics, including overall survival, were detected, compared, and calculated.
Results: The mutation rates of 32 genes, including TP53, SPEN, FAT1, and CDH1 exceeded 10%. TP53 mutations had a slightly lower overall occurrence rate (33%). The TP53 mutation rate was significantly higher in advanced stages (stage III/IV) than that in early stages (stage I/II) (P < 0.05). In contrast, CDH1 mutations were significantly associated with diffuse GC. TP53 is related to poor prognosis of advanced-stage tumors; nevertheless, CDH1 corresponds to a diffuse type of cancer. TP53 is exclusively mutated in CDH1 and is primarily affected by two distinct GC mechanisms.
Conclusion: Different somatic mutation patterns in TP53 and CDH1 indicate two major mechanisms of GC.
Keywords: CDH1 mutation; Clinical outcome; Diffuse gastric cancer; Gastric cancer; Somatic mutation; TP53 mutation.
©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.