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Risk of progression of early cervical lesions is associated with integration and persistence of HPV-16 and expression of E6, Ki-67, and telomerase
BACKGROUND: Low-grade squamous intraepithelial lesions (LSIL) are the earliest lesions of the uterine cervix, the persistence and integration of high-risk human papillomavirus (HR-HPV) as type 16, which promotes the development of more aggressive lesions. AIM: To select more aggressive lesions with...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Medknow Publications & Media Pvt Ltd
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945621/ https://www.ncbi.nlm.nih.gov/pubmed/24648664 http://dx.doi.org/10.4103/0970-9371.126644 |
Sumario: | BACKGROUND: Low-grade squamous intraepithelial lesions (LSIL) are the earliest lesions of the uterine cervix, the persistence and integration of high-risk human papillomavirus (HR-HPV) as type 16, which promotes the development of more aggressive lesions. AIM: To select more aggressive lesions with tendency to progress to invasive cervical cancer. MATERIALS AND METHODS: A total of 75 cytological specimens in liquid base (Liqui-PREP) were analyzed: 25 specimens were with no signs of SIL (NSIL) and without HPV; 25 NSIL with HPV-16, and 25 with both LSIL and HPV-16. The expression of Ki-67, telomerase, and viral E6 was evaluated by immunocytochemistry; and the detection of viral DNA was done by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLPs) for genotyping or sequencing of HPV-16. The physical state of HPV-16 was evaluated by in situ hybridization with amplification with tyramide. RESULTS: Of the total group, 58.6% had LSIL associated with persistence and of these 59.3% was associated with integrated state of HPV as intense expression of E6, Ki-67 (P = 0.013, P = 0.055) has except for the expression of telomerase present a non-significant association (P<0.341). CONCLUSIONS: Overexpression of E6 and Ki-67 is associated with the integration of HPV-16, favoring viral persistence, and increasing the risk of progression in women with NSIL and LSIL. |
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