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Clinicopathological Significance of Cell Adhesion Molecule 4 Expression in Gallbladder Cancer and Its Prognostic Role. | LitMetric

AI Article Synopsis

  • CADM4 is identified as a tumor-suppressor candidate that is involved in cell interactions, and its role in gallbladder cancer (GBC) was evaluated in this study.
  • Low levels of CADM4 expression were linked to more advanced stages of cancer and worse prognosis, indicating its potential significance in the aggressiveness of GBC.
  • The findings suggest that CADM4 expression may serve as an important prognostic marker for patient outcomes in gallbladder cancer.

Article Abstract

Cell adhesion molecule 4 (CADM4) is involved in intercellular interactions and is a tumor-suppressor candidate. The role of CADM4 in gallbladder cancer (GBC) has not been reported. Therefore, the clinicopathological significance and prognostic value of CADM4 expression in GBC were evaluated in the present study. Immunohistochemistry (IHC) was performed on 100 GBC tissues to assess CADM4 expression at the protein level. The association between CADM4 expression and the clinicopathological characteristics of GBC was analyzed, and the prognostic significance of CADM4 expression was evaluated. Low CADM4 expression was significantly associated with advanced T category ( = 0.010) and high AJCC stage ( = 0.019). In a survival analysis, low CADM4 expression was associated with shorter overall survival (OS; = 0.001) and recurrence-free survival (RFS; = 0.018). In univariate analyses, low CADM4 expression was associated with shorter OS ( = 0.002) and RFS ( = 0.023). In multivariate analyses, low CADM4 expression was an independent prognostic factor of OS ( = 0.013). Low CADM4 expression was associated with tumor invasiveness and poor clinical outcomes in patients with GBC. CADM4 may play an important role in cancer progression and patient survival and can be used as a potential prognostic marker of GBC.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10138777PMC
http://dx.doi.org/10.3390/ijms24086898DOI Listing

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