Simple Summary Human papillomavirus (HPV) infection is a highly prevalent sexually transmitted disease globally. Although most HPV infections do not result in cancer, certain HPV strains are strongly associated with most cervical cancers, as well as with some cases of anogenital and oropharyngeal cancers. Epigenetic modifications have been revealed to impact the cellular pathways involved in the emergence of the neoplastic phenotype. The inherent reversibility and dynamic nature of epigenetic modifications render enzymes as epigenetic proper targets for the development of effective therapeutic strategies against HPV-induced tumors.Abstract Cervical cancer ranks as the fourth most prevalent cancer among women globally, with approximately 600,000 new cases being diagnosed each year. The principal driver of cervical cancer is the human papillomavirus (HPV), where viral oncoproteins E6 and E7 undertake the role of driving its carcinogenic potential. Despite extensive investigative efforts, numerous facets concerning HPV infection, replication, and pathogenesis remain shrouded in uncertainty. The virus operates through a variety of epigenetic mechanisms, and the epigenetic signature of HPV-related tumors is a major bottleneck in our understanding of the disease. Recent investigations have unveiled the capacity of viral oncoproteins to influence epigenetic changes within HPV-related tumors, and conversely, these tumors exert an influence on the surrounding epigenetic landscape. Given the escalating occurrence of HPV-triggered tumors and the deficiency of efficacious treatments, substantial challenges emerge. A promising avenue to address this challenge lies in epigenetic modulators. This review aggregates and dissects potential epigenetic modulators capable of combatting HPV-associated infections and diseases. By delving into these modulators, novel avenues for therapeutic interventions against HPV-linked cancers have come to the fore.

Epigenetic and Genetic Keys to Fight HPV-Related Cancers

Rinaldi, Luca;
2023-01-01

Abstract

Simple Summary Human papillomavirus (HPV) infection is a highly prevalent sexually transmitted disease globally. Although most HPV infections do not result in cancer, certain HPV strains are strongly associated with most cervical cancers, as well as with some cases of anogenital and oropharyngeal cancers. Epigenetic modifications have been revealed to impact the cellular pathways involved in the emergence of the neoplastic phenotype. The inherent reversibility and dynamic nature of epigenetic modifications render enzymes as epigenetic proper targets for the development of effective therapeutic strategies against HPV-induced tumors.Abstract Cervical cancer ranks as the fourth most prevalent cancer among women globally, with approximately 600,000 new cases being diagnosed each year. The principal driver of cervical cancer is the human papillomavirus (HPV), where viral oncoproteins E6 and E7 undertake the role of driving its carcinogenic potential. Despite extensive investigative efforts, numerous facets concerning HPV infection, replication, and pathogenesis remain shrouded in uncertainty. The virus operates through a variety of epigenetic mechanisms, and the epigenetic signature of HPV-related tumors is a major bottleneck in our understanding of the disease. Recent investigations have unveiled the capacity of viral oncoproteins to influence epigenetic changes within HPV-related tumors, and conversely, these tumors exert an influence on the surrounding epigenetic landscape. Given the escalating occurrence of HPV-triggered tumors and the deficiency of efficacious treatments, substantial challenges emerge. A promising avenue to address this challenge lies in epigenetic modulators. This review aggregates and dissects potential epigenetic modulators capable of combatting HPV-associated infections and diseases. By delving into these modulators, novel avenues for therapeutic interventions against HPV-linked cancers have come to the fore.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11695/127835
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