Abstract
Background and aim Colorectal cancer (CRC) is a heterogeneous disease, with a diverse immune cell infiltrate. Interferon-stimulating gene 15 (ISG-15) is a type I interferon-regulated gene that is secreted by diverse inflammatory cells. The aim of this work was to evaluate the role of ISG-15 in CRC and to correlate its expression with clinicopathological data and patient survival. Materials and methods This retrospective case–control study included 87 chemo-naive CRC cases, 12 adenomas, and 59 non-neoplastic colonic tissue cases from Egyptian patients; all cases were stained for ISG-15 antibody. Results The present study showed that high expression of ISG-15 was correlated with malignant transformation in colorectal tissues, as higher epithelial H-score of ISG-15 was significantly associated with malignant group in comparison with non-neoplastic group (P=0.004). Epithelial overexpression of ISG-15 in CRC was significantly associated with smaller tumor size (P=0.023 and 0.011). Stromal overexpression of ISG-15 in CRC was significantly associated well-differentiated tumors (P=0.026). Moreover, ISG-15 overexpression in epithelium and stroma was associated with long survival period in CRC (P=0.02 and 0.001, respectively). More importantly, ISG-15 expression, either epithelial or stromal, was an independent prognostic factor in CRC. Conclusion High expression of ISG-15 correlates with malignant transformation in colorectal tissues, as ISG-15 is overexpressed in CRC in comparison with non-neoplastic and is associated with factors of good prognosis. In CRC, ISG-15 overexpression is associated with longer overall survival. Epithelial ISG-15 expression is the most independent prognostic factor in CRC.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.