Keywords
cervical cáncer
epigenetics modification
How to Cite
Abstract
Cervical cancer is the fourth most common cause of death in women in the world according to World Cancer Report reports. Its pathophysiological is diverse although the main etiological agent is considered to be Human Papilloma Virus (VPH). Although VPH infection is identified as necessary for the development of CC, it is not sufficient for this. There are several hypotheses that attempt to explain the origin of the disease with the influence of the environment and the genetics and epigenetics of the individual. The article systematizes the relationship between VPH, epigenetic modifications, and cervical cancer from VPH infection. VPH infection in susceptible subjects causes changes in cellular epigenetic regulation mechanisms. The expression of viral oncogenic proteins enhances the mechanisms of uncontrolled cell proliferation and inhibits the apoptotic and control mechanisms of the cell cycle. The epigenetic landscape of the pathophysiology of VPH in cervical uterine cancer is promising and sees possible targets to direct treatment for infection and disease. However, some limitations such as the diversity of epigenetic mechanisms involved in VPH pathogenesis without being able to attribute the weight of each in the generation of carcinogenic transformation will be noted. Intermediaries in molecular signaling pathways that may be key in understanding pathogenesis are still unknown. Limitations of in vitro studies using transfected heterogeneous cell lines without achieving VPH infection should be addressed.
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