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Overexpression of Fibroblast Growth Factor 8 Is a Predictor of Impaired Survival in Esophageal Squamous Cell Carcinoma and Correlates with ALK/EML4 Alteration. | LitMetric

AI Article Synopsis

  • Researchers investigated the prognostic significance of FGF8, ALK, and EML4 as biomarkers in esophageal squamous cell carcinoma (ESCC), focusing on patients who had surgery for the disease.
  • The study included 122 patients and utilized fluorescence in situ hybridization (FISH) and immunohistochemistry to analyze gene status and protein expression of FGF8, ALK, and EML4.
  • Results indicated that high levels of FGF8 overexpression predicted worse overall survival rates and showed a strong correlation with the alterations of ALK and EML4, suggesting FGF8 might be a target for future therapies.

Article Abstract

FGF8, ALK, and EML4 have been identified as promising biomarkers in a number of malignancies. The aim of this study was to examine the prognostic role of FGF8, ALK, and EML4 in esophageal squamous cell carcinoma (ESCC). Consecutive patients with ESCC who underwent upfront resection were included in this study. ALK and EML4 gene status was evaluated by fluorescence in situ hybridization (FISH) using a triple-color break-apart single-fusion probe and a probe against 2p11. FGF8, ALK, and EML4 protein expression was determined by immunohistochemistry. A total of 122 patients were included in this study. Multivariate analysis revealed that FGF8 overexpression is an independent negative prognostic factor for patients' overall survival (OS) ( = 0.04). Furthermore, a significant correlation between the expression of FGF8, and ALK ( = 0.04) and EML4 ( = 0.01) alteration was found. FGF8 overexpression is an adverse independent prognostic factor in patients with upfront resected ESCC. Furthermore, FGF8 expression significantly correlates with ALK and EML4 amplification and may therefore qualify as a future therapeutic target.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11545777PMC
http://dx.doi.org/10.3390/cancers16213624DOI Listing

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