ArticleOncology letters2025
Clinical importance of E-cadherin deficiency in resectable gastric cancer: A nested case-control study.
Article in Oncology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- JOSD1 stabilizes SULF1 to activate Wnt7B-FZD1 signaling in gastric cancer.Translational oncology · 2026Article
- KIRREL1 is a novel prognostic biomarker that promotes malignancy in gastric cancer via activation of the epithelial-mesenchymal transition pathway.Molecular genetics and genomics : MGG · 2026Article
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11 authors.
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Abstract
The prognosis of gastric cancer (GC) remains unsatisfactory despite advancements in diagnosis and treatment. Epithelial-mesenchymal transition-induced decreased cell-cell adhesion, often associated with E-cadherin deficiency, serves a crucial role in tumor invasion and metastasis. However, the relationship between E-cadherin deficiency and GC prognosis is unclear. The present study aimed to explore the association between E-cadherin deficiency and the prognosis of resectable GC. The nested case-control study involved prospective data collection and retrospective analysis. Between January 2013 and December 2022, a total of 1,574 patients treated for GC were eligible for prognostic analysis (104 in the E-cadherin deficiency group and 1,470 in the E-cadherin expression group). Logistic regression analysis was utilized to evaluate the univariate and multivariate associations between clinicopathological factors and E-cadherin deficiency. Propensity score matching analysis at a ratio of 1:4 was performed. Kaplan-Meier curves were employed to analyze the relationship between the prognosis of the E-cadherin deficiency group and the E-cadherin expression group. There were 104 cases of E-cadherin deficiency, accounting for an incidence of 6.6%. The results of the analysis revealed that a family history of GC [odds ratio (OR), 7.60; P<0.001], poorly differentiated tumors (OR, 8.67; P<0.001), perineural invasion (OR, 1.63; P=0.030) and elevated carcinoembryonic antigen (CEA) (OR, 1.83; P=0.034) were independent risk factors for E-cadherin deficiency in all enrolled patients. Following propensity score matching analysis, 86 cases in the E-cadherin deficiency group and 344 cases in the E-cadherin expression group were included. Survival analysis demonstrated no statistically significant difference in 5-year disease-free survival rates between the E-cadherin deficiency and expression groups (P=0.590). Similarly, the 5-year overall survival rates were comparable between the two groups (P=0.863). In summary, E-cadherin deficiency is associated with a family history of GC, poorly differentiated tumors, perineural invasion and elevated CEA levels. However, E-cadherin deficiency does not impact the prognosis of resectable GC.
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