Cervical cancer and XRCC1 gene polymorphisms
Objective: To undertake a literature review on the development of cervical cancer, emphasizing epidemiological data, human papillomavirus (HPV) infection in carcinogenesis, and the role of the XRCC1 gene in DNA repair, in order to provide valuable information for the medical and scientific community. The goal is to provide a valuable resource for clinical practice. Bibliographic Review: Cervical cancer ranks as the fourth most common malignancy worldwide. Despite known environmental, behavioral, and genetic risk factors, their management remains inadequate. Persistent infection with oncogenic HPV is a well-established risk factor; however, not all infected individuals develop cervical cancer, suggesting the involvement of additional mechanisms. Among these, polymorphisms in the XRCC1 gene have gained attention. XRCC1 encodes a scaffold protein essential for DNA repair coordination and cell cycle regulation. Three main XRCC1 polymorphisms—Arg194Trp, Arg280His, and Arg399Gln—are associated with impaired DNA repair, genomic instability, and increased cervical cancer susceptibility. Final Considerations: A deeper understanding of the genetic and cellular mechanisms underlying cervical cancer may facilitate the development of targeted medical interventions for women, contributing to improved quality of life reduced mortality.
Authors
- Ivan Barbosa Barros
- Andréia Michelle Alves Cunha de Alcântara
- Karla Simone Costa de Souza (ORCID: https://orcid.org/0000-0002-8541-1444)
- Maria de Mascena Diniz Maia (ORCID: https://orcid.org/0000-0001-5893-455X)
- Ivan de Alcântara Barbosa Barros
- Paulo Roberto Eleutério de Souza (ORCID: https://orcid.org/0000-0002-9186-9849)
- Islla Raquel Medeiros da Silva (ORCID: https://orcid.org/0009-0002-5203-6032)
Publication Details
- Journal
- Revista Eletrônica Acervo Saúde
- Published
- 2025-05-30
- DOI
- https://doi.org/10.25248/reas.e20401.2025
- Primary Topic
- Molecular Biology Techniques and Applications
- Type
- article
- Field-Weighted Citation Impact
- 0.00