Suppressor Protein p53 and Its Occurrence in Oral Tumours

Abstract

As summarised by Levine and Momand (1990), a cancer cell is the result of a multistep process in which multiple sequential mutations occur. In this process, two distinct categories can be discerned: the inappropriate activation of protooncogenes to become oncogenes and the inactivation of tumour suppressor genes, both of which may lead to disturbed cell proliferation and the development of tumours (Chang et al. 1993). One of the most intensely studied tumour suppressor genes is the p53 gene. The protein encoded by this gene appears to act as “the guardian of the genome” (Lane 1994) by blocking the division of cells that have sustained DNA damage, resulting in either a delay in progress through the cell cycle to permit repair or triggering cell death by apoptosis, thus eliminating abnormal cells that could lead to cancer (Levine et al. 1994). Moreover, p53 appears to play a role during embryogenesis, as mice lacking the p53 gene exhibited an increased incidence of neural tube defects (Sah et al. 1995) and an increased sensitivity to an environmental teratogen (Nicol et al. 1995).