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Squamous intraepithelial lesions (SIL) and cervical cancer are primary due to suboptimal immune response against human papillomavirus (HPV). The FASL/FAS system is a trigger of extrinsic pathway apoptosis. The distribution of polymorphisms rs1800682 (-670 A > G) FAS and rs763110 (-844C > T) FASL was studied in cervical smears from 372 females (182 with stable or regressed low-grade SIL (LSIL) (groupI) and a group of 190 high-grade SIL (HSIL) (groupII). No significant differences were observed for rs1800682 in FAS between the study groups. In contrast, rs763110 CC genotype of FASL was found in 35.7% of group I females, and in 50.5% of group II (p = 0.0027; OR = 1.83 (95% CI = 1.21-2.79)). When only females infected with high-risk HPV were analysed, these differences were even higher (p = 0.0024; OR = 2.21 (95% CI = 1.30-3.75)). CC genotype in FASL seems to be associated with increased risk of LSIL to HSIL progression suggesting a role in HPV tolerance, persistent infection, and HSIL development. Copyright © 2021 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.

Citation

Vicente Santaclara, Daniel Torres-Moreno, Carmen M Bernal-Mañas, María Alejandra Isaac, Sebastián Ortiz-Reina, Pablo Conesa-Zamora. Relationship between polymorphisms in the FAS/FASL death receptor system and progression of low-grade precursor lesions infected with high-risk human papilloma virus. Human immunology. 2021 Sep;82(9):621-624

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PMID: 34127318

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