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Association of Cellular Cannibalism with Immunohistochemical Expression of CD31, CD68 and BCL2 in Oral Squamous Cell Carcinoma: An Observational Study. | LitMetric

Association of Cellular Cannibalism with Immunohistochemical Expression of CD31, CD68 and BCL2 in Oral Squamous Cell Carcinoma: An Observational Study.

J Maxillofac Oral Surg

Department of Oral Pathology and Microbiology, Post Graduate Institute of Dental Sciences (PGIDS), Pt. Bhagwat Dayal Sharma University of Health Sciences, Rohtak, Haryana 124001 India.

Published: August 2024

Objective: Cellular cannibalism (CC) is a prime metabolic event to determine the aggressive potential of oral squamous cell carcinoma (OSCC). However, the etiology and mechanism behind this degradation are still ambiguous. The aim of the study was to explore the etiopathogenetic mechanism behind CC, along with its association with degree of differentiation, angiogenic, phagocytic and antiapoptotic activity in OSCC.

Design: Seventy-three tissue sections of various histological grades of OSCC were retrieved from departmental archives and scanned for cannibalistic cells. Immunohistochemical analysis using CD31, CD68, and BCL2 was performed. The data obtained were analyzed using Chi-square, Spearman's correlation test and multiple regression analysis ( < 0.05).

Results: CCs were present significantly in various grades of OSCC ( < 0.00). Immunohistochemical analysis revealed a significant difference in CD68, BCL2 ( < 0.05 in both), and CD31 ( < 0.001) expression with CC. The internalized cells showed positivity for CD68 and negativity for BCL2. Regression analysis revealed that tumor grade, CD31 and BCL2 immunoreactivity were significant predictors of frequency of CC.

Conclusion: The association of CC with degree of differentiation, CD31, CD68, and BCL2 expression could predict the biological behavior of OSCC and might serve as a promising histopathological parameter in future.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303648PMC
http://dx.doi.org/10.1007/s12663-024-02217-1DOI Listing

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