Purpose: Epithelial cells exposed to carcinogens and genetic damage, once surpass reversible cell damage, either undergo apoptosis or transform into malignancy, chiefly oral squamous cell carcinoma (OSCC). Progressive accumulation of genetic errors in TP53 results in tumorigenesis. Inflammation is also a modulator in this process. The present study attempted to correlate the immunohistochemical expression of TP53 with increased aggressiveness of OSCC, to determine how these immune cells regulate the path of carcinogenesis and to define the role of inflammation in TP53 immunoexpression. Materials and Methods: Tissue sections from 24 biopsy-proven cases of OSCC were stained with anti-TP53 antibody. Five hundred neoplastic epithelial cells and inflammatory cells, each, were counted at invasive tumor front. Two hundred peritumoral neutrophils were counted based on nuclear lobes present. Results: The least TP53 expression was seen in well-differentiated OSCC (P < 0.001), whereas neutrophil count and plasma cell count were found to be least in well-differentiated OSCC (P < 0.001), whereas the number of lymphocytes and macrophages decreased with increased grading of OSCC (P < 0.001). Four- and five-lobed neutrophils were found to be highest in poorly differentiated OSCC (P < 0.001), whereas two-lobed neutrophil count was seen to be maximum in well-differentiated OSCC (P < 0.001). Conclusion: TP53 plays a significant role in the initiation and progression of OSCC. Inflammation plays a role of friend and a foe simultaneously, and little modification in the present treatment modalities for OSCC can bring a favorable change in the life of cancer survivors.
All Science Journal Classification (ASJC) codes
- Radiology Nuclear Medicine and imaging