Introduction: Oral cancer is a multistep process involving foul play of proto-oncogenes that induce cell proliferation, inactivation of tumor suppressor gene and cessation of programmed cell death. Among various proto-oncogenes, the nature and behavior of Bcl-2 and c-Myc in oral precancerous/cancerous lesions were obscured which require further assessment for better understanding of etiology, treatment and prognosis.
Aim: The aim of the study is to assess the expression of Bcl-2 and c-Myc in oral epithelial dysplasia and oral squamous cell carcinoma (OSCC).
Materials and methods: This retrospective study of 70 (oral dysplasia [30], OSCC [30] and normal gingiva [10]) is immunohistochemically assessed for Bcl-2 and c-Myc for distribution, intensity, percentage of positive cells, localization and immunoreactive scores using ImageJ software.
Results: Bcl-2 showed 60% and 37% positivity within dysplasia and OSCC, respectively (P = 0.03); c-Myc showed 87% and 90% positivity within dysplasia and OSCC, respectively. In OSCC, c-Myc showed moderate intensity (P = 0.04). Average percentage of positive cells expressing c-Myc and Bcl-2 increased proportionally within grades of dysplasia (P = 0.000 and P = 0.008, respectively), whereas in OSCC, only c-Myc showed significant expression (P = 0.021). Localization of c-Myc was seen in the nucleus among OSCC (P = 0.01). c-Myc and Bcl-2 showed moderate immunoreactivity in dysplasia (P = 0.005 and P = 0.013, respectively), whereas in OSCC, moderate immunoreactivity of c-Myc (P = 0.05) was observed.
Conclusion: Variable expression of c-Myc and Bcl-2 reveals that these proteins act in synergism in early phases of carcinogenesis, whereas in later stages, due to the diminished activity of Bcl-2, c-Myc interacts incoordination with other oncogenes contributing to tumor progression.
Keywords: Antiapoptotic protein; Bcl-2; c-Myc; dysplasia and oral squamous cell carcinoma; immunohistochemistry; nuclear transcription factor.