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Immunohistochemical expression of tumor necrosis factor-like weak inducer of apoptosis and fibroblast growth factor-inducible immediate early response protein 14 in oral squamous cell carcinoma and its implications.
Journal of Investigative and Clinical Dentistry 2019 September 22
AIM: To study the expression of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and fibroblast growth factor-inducible immediate early response protein 14 (Fn14) in oral squamous cell carcinoma (OSCC), to elucidate the possible role of TWEAK-Fn14 in OSCC development.
METHODS: Immunohistochemistry for TWEAK-Fn14 was performed on 61 oral mucosal samples: healthy oral mucosa (HOM; N = 15); oral dysplastic lesions (ODL; N = 15); and OSCC (N = 31). Extent of staining (ES) and immunoreactive score (IRS) were assessed. The data was statistically analyzed.
RESULTS: All OSCC expressed TWEAK, and the Fn14 expression was noted in 90% of OSCC. A significant difference in the TWEAK and Fn14 expression was noted among the groups. ES and IRS of TWEAK-Fn14 significantly increased in OSCC compared with ODL and HOM. ES of TWEAK was significantly higher than Fn14 in all 3 groups. ES of TWEAK-Fn14 was significantly higher at the invasive tumor front (ITF) than in the whole tumor. TWEAK-Fn14 showed a significant association with clinicopathological parameters of prognostic significance.
CONCLUSION: Findings suggest that TWEAK and Fn14 may participate in the growth and progression of OSCC. Increased expression of TWEAK-Fn14 at the ITF may facilitate increased proliferation, altered differentiation and invasion.
METHODS: Immunohistochemistry for TWEAK-Fn14 was performed on 61 oral mucosal samples: healthy oral mucosa (HOM; N = 15); oral dysplastic lesions (ODL; N = 15); and OSCC (N = 31). Extent of staining (ES) and immunoreactive score (IRS) were assessed. The data was statistically analyzed.
RESULTS: All OSCC expressed TWEAK, and the Fn14 expression was noted in 90% of OSCC. A significant difference in the TWEAK and Fn14 expression was noted among the groups. ES and IRS of TWEAK-Fn14 significantly increased in OSCC compared with ODL and HOM. ES of TWEAK was significantly higher than Fn14 in all 3 groups. ES of TWEAK-Fn14 was significantly higher at the invasive tumor front (ITF) than in the whole tumor. TWEAK-Fn14 showed a significant association with clinicopathological parameters of prognostic significance.
CONCLUSION: Findings suggest that TWEAK and Fn14 may participate in the growth and progression of OSCC. Increased expression of TWEAK-Fn14 at the ITF may facilitate increased proliferation, altered differentiation and invasion.
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