Published online Feb 27, 2024. doi: 10.4240/wjgs.v16.i2.276
Peer-review started: December 10, 2023
First decision: December 18, 2023
Revised: December 26, 2023
Accepted: January 30, 2024
Article in press: January 30, 2024
Published online: February 27, 2024
Processing time: 77 Days and 13.8 Hours
In this editorial we comment on an article published in a recent issue of the World J Gastrointest Surg. A common gene mutation in gastric cancer (GC) is the TP53 mutation. As a tumor suppressor gene, TP53 is implicated in more than half of all tumor occurrences. TP53 gene mutations in GC tissue may be related with clinical pathological aspects. The TP53 mutation arose late in the progression of GC and aided in the final switch to malignancy. CDH1 encodes E-cadherin, which is involved in cell-to-cell adhesion, epithelial structure maintenance, cell polarity, differentiation, and intracellular signaling pathway modulation. CDH1 mutations and functional loss can result in diffuse GC, and CDH1 mutations can serve as independent prognostic indicators for poor prognosis. GC patients can benefit from genetic counseling and testing for CDH1 mutations. Demethylation therapy may assist to postpone the onset and progression of GC. The investigation of TP53 and CDH1 gene mutations in GC allows for the investigation of the relationship between these two gene mutations, as well as providing some basis for evaluating the prognosis of GC patients.
Core Tip: The separation of TP53 and CDH1 mutations in gastric cancer (GC) demonstrates their separate processes. Mutations in TP53 are linked to advanced-stage cancers and a poor prognosis, whereas CDH1 mutations are linked to widespread GC. This work emphasizes the variability of GC and sheds light on prospective targeted therapeutics based on distinct mutation patterns. Understanding the mutational landscape of TP53 and CDH1 can help to develop tailored therapy strategies for GC patients.
