ArticleMedical science monitor : international medical journal of experimental and clinical research2019
The Prognostic Role of Expression of Nectin-4 in Esophageal Cancer.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Prognostic value of nectin-4 in human cancers: A meta-analysis.Frontiers in oncology · 2023Pooled it
- Nectin-4 expression in clear cell renal cell carcinoma.Scientific reports · 2026Article
- Preclinical Theranostic Study ofACS omega · 2026Article
- Nectin-4 expression patterns and therapeutics in oncology.Cancer letters · 2025Review
- Nectin4-targeted molecular imaging in solid tumors: Current status and future perspectives.View (Beijing, China) · 2025Article
- Assessing the expression of Nectin-4 in solid tumors by immunohistochemistry - what do we know?Histology and histopathology · 2025Review
- The Significance of Nectin Family Proteins in Various Cancerogenous Processes.International journal of molecular sciences · 2025Review
- Article
- Expression patterns of TROP2 and Nectin-4 in oropharyngeal squamous cell carcinoma in relation to HPV status: potential biomarkers for targeted therapy.Therapeutic advances in medical oncology · 2025Article
- Therapeutic prospects of nectin-4 in cancer: applications and value.Frontiers in oncology · 2024Review
- Review
- Nectins and Nectin-like Molecules in Colorectal Cancer: Role in Diagnostics, Prognostic Values, and Emerging Treatment Options: A Literature Review.Diagnostics (Basel, Switzerland) · 2022Review
- Article
- Article
- Expression of nectin-4 in papillary renal cell carcinoma.Discover oncology · 2022Article
- Nectin-4 promotes osteosarcoma progression and metastasis through activating PI3K/AKT/NF-κB signaling by down-regulation of miR-520c-3p.Cancer cell international · 2022Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Nectin-4 is overexpressed in several human malignant tumors. This study aimed to investigate the expression of Nectin-4 in esophageal cancer tissues compared with adjacent normal esophageal tissue and its association with clinicopathological parameters and prognosis. MATERIAL AND METHODS Nectin-4 expression in esophageal cancer tissues was compared with adjacent normal esophageal tissue from 94 patients using immunohistochemistry, Western blot, and quantitative reverse transcription-polymerase chain reaction (RT-qPCR). The chi-squared (χ²) test and Fisher's exact test compared categorical variables. The log-rank test and Kaplan-Meier survival analysis assessed the relationship between Nectin-4 expression and overall survival (OS). Univariate and multivariate Cox proportional risk models compared Nectin-4 expression, patient prognosis, and clinicopathological parameters. RESULTS Nectin-4 expression was significantly increased in esophageal cancer tissue compared with normal tissue (P<0.001), tumor size ≥4.5 cm, and tumor invasion in T3/T4 compared with T1/T2 stage. Kaplan-Meier survival analysis showed that the OS of patients with increased Nectin-4 expression was significantly reduced compared with patients with low levels of Nectin-4 expression. Patient prognosis in men was less than women, tumor diameter ≥4.5 cm, lymph node involvement, and depth of invasion were associated with poor prognosis. Independent prognostic factors were Nectin-4 expression, lymph node involvement, and depth of invasion. CONCLUSIONS In patients with esophageal cancer, the expression levels of Nectin-4, lymph node involvement, and depth of tumor invasion were independent prognostic factors. Further studies should be performed to evaluate the diagnostic and prognostic roles of Nectin-4 and its potential role as a therapeutic target.
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