Genomic instability is one of the characteristics of cancer cells. It consists of alterations of genes during cell division. Cancer cases in patients can result from damage to multiple genes. These genes control cell division and tumor suppressor genes. The integrity of a genome is monitored by several mechanisms including DNA damage checkpoints, DNA repair machinery, and mitotic checkpoints within the cell. If there are defects in any one of these mechanisms the result is genomic instability. A few other things that can alter the regulation of the cell cycle are posttranslational modifications of histone tails, chromatin structure, and DNA methylation. This topic continues to be a debate about what exactly the driving force of the initiation …show more content…
Cellular integrity, in turn, prevents errors that arise from DNA replication, cellular metabolism, and carcinogenic exposure. These exposures consist of ultraviolet light, radiation, or damaging chemical substances. Many professionals believe that tumor initiation and following progression result from acquired genomic alteration within normal cells. The populations of tumor cells appear to be more unstable genetically than normal unaltered cells. Genomic instability causes individuals to maintain shorter cell cycles and also causes the bypassing of intracellular and immunological control systems. These factors give cancerous cells an advantage when it comes to growth and multiplying. There have been numerous research projects specifically dedicated to finding why this instability causes this in hopes of finding the underlying issues with cancer and stop it from being one of the leading causes of death. Genomic instability includes variations in small structures. These variations can include increased frequencies in mutations of base pairs, microsatellite instability, and changes in chromosome number or structure which are referred to as chromosome instability. The origins of these instabilities still remain a mystery but there are many educated hypotheses that try to explain why they all contribute to tumor initiation and