ABSTRACT
DNA damage is a discrepancy in its chemical structure precipitated by a multitude of factors. Most DNA damages can be repaired efficiently through diverse restorative mechanisms subjective to the type of damage. DNA-damaging agents elicit a medley of cellular retorts like cell cycle arrest, followed by DNA repair mechanisms or apoptosis. An unrepaired DNA damage in a nonreplicating cell does not generally engender mutations but a similar scenario in replicating cell routes to permanent modification of genetic material shrugging to carcinogenesis. DNA mutilation can be allied to disarray in bases, debasement of backbone, or crosslinks. Base damages or backbone damages like single-strand and double-strand DNA breaks are usually produced by reactive oxygen species and ionizing radiation. This substantial DNA damage has broadly been considered to be caused by various exogenous and endogenous agents with variable rates of causality and decrees of risk, sourcing toward cancer or other diseases, necessitating furtherance in diagnostics at sequential points. The purpose of this article is to review in detail the various types of DNA damages, their contributory factors, and recent developments in their identification.
ABSTRACT
Background and Aim: USP22 is a positive regulator in tumor growth, its depletion leads to cell cycle arrest at G1 phase. USP22 over expression was positively correlated with proteins involved in proliferation and negatively correlated with tumor suppressor protein tumor supprn. Ki-67 expression is associated with USP22 over expression in oral squamous cell carcinoma (OSCC) and also in cervical and prostate cancers. The aim of this study is to evaluate the expression of USP22 and Ki-67 in OSCC by using an immunohistochemical staining procedure. Materials and Methods: Immunohistochemistry was used to determine the expression of USP22 protein in 50 archival tissue blocks of histopathologically diagnosed OSCC and 15 normal oral mucosa tissue blocks. The histopathological correlation of USP22 with Ki-67 was done. Results: Expression of USP22 and Ki-67 was seen in the nuclei of epithelial cells. Statistical analysis of the mean expression of USP22 in OSCC and normal tissue showed a significant difference (P = 0.000000119). A significant difference was also observed in Ki-67 between OSCC and normal tissue (P = 0.00000086). Correlation test showed a weak correlation (R = 0.19) between USP22 and Ki-67 expression of group 1. Similarly, a weak correlation (R = 0.51) was observed in group 2. Conclusion: A statistically significant difference in the expression of USP22 and Ki-67 was observed between normal mucosa and OSCC. It can be used in early diagnosis of OSCC but its use as a prognostic indicator is questionable and should be exemplified with a larger study sample.
