ArticleOncology letters2020
Deregulation of cell adhesion molecules is associated with progression and poor outcomes in endometrial cancer: Analysis of The Cancer Genome Atlas data.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Identification of hub genes and pathways in Uterine corpus endometrial carcinoma (UCEC): A comprehensiveBiochemistry and biophysics reports · 2024Article
- It is time to implement molecular classification in endometrial cancer.Archives of gynecology and obstetrics · 2024Review
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- Curcumin Inhibits Vasculogenic MimicryCurrent cancer drug targets · 2024Article
- Comprehending the Proteomic Landscape of Ovarian Cancer: A Road to the Discovery of Disease Biomarkers.Proteomes · 2021Review
- Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell adhesion molecules (CAMs) determine the behavior of cancer cells during metastasis. Although some CAMs are dysregulated in certain types of cancer and are associated with cancer progression, to the best of our knowledge, a comprehensive study of CAMs has not been undertaken, particularly in endometrial cancer (EC). In the present study the expression of 225 CAMs in EC patients with various clinicopathological phenotypes were evaluated by statistical analysis using publicly available data from The Cancer Genome Atlas database. The Kaplan-Meier method, and univariate and multivariate Cox proportional hazards regression models were used for survival analyses. Among the differentially expressed CAMs that were associated with aggressive clinicopathological phenotypes, 10 CAM genes were independent prognostic factors compared with other clinicopathological prognostic factors, including stage, grade, age, lymph node status, peritoneal cytology and histological subtype. A total of six genes (L1 cell adhesion molecule, mucin 15, cell surface associated, cell adhesion associated, oncogene regulated, immunoglobulin superfamily member 9B, protocadherin 9 and protocadherin β1) were selected for integrative analysis. The six-gene signature was demonstrated to be an independent prognostic factor and could effectively stratify patients with different risks. Patients with more high-expression CAMs had a higher risk of poor overall survival (OS) rate. The mortality risk for patients with elevation of >4 CAMs was 11 times of that in those without elevation of these 6 CAMs. Similar results were obtained when relapse-free survival (RFS) time was used during the analysis. Prognostic reliability of the six-gene model was validated using data of an independent cohort from the International Cancer Genome Consortium. In conclusion, a combination of CAM alterations contributed to progression and aggressiveness of EC. The six-gene signature was effective for predicting worse OS and RFS in patients with EC and could be complementary to the present clinical prognostic criteria.
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