DNA mutilation: A telltale sign of cancer inception

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.