Vega-Peña Arianna, Illades-Aguiar Berenice, Flores-Alfaro Eugenia, López-Bayghen Esther, Leyva-Vázquez Marco Antonio, Castañeda-Saucedo Eduardo, Alarcón-Romero Luz Del Carmen
Laboratory for Research in Cytopathology and Histoquemical, Guerrero, México.
Laboratory for Molecular Biomedicine, Guerrero, México.
J Cytol. 2013 Oct;30(4):226-32. doi: 10.4103/0970-9371.126644.
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.
To select more aggressive lesions with tendency to progress to invasive cervical cancer.
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.
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).
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.
低度鳞状上皮内病变（LSIL）是子宫颈最早出现的病变，高危型人乳头瘤病毒（HR-HPV）16型的持续感染和整合会促进更具侵袭性病变的发展。
筛选出更具侵袭性且有进展为浸润性宫颈癌倾向的病变。
共分析了75份液基（Liqui-PREP）细胞学标本：25份标本无鳞状上皮内病变（NSIL）迹象且无HPV感染；25份NSIL伴有HPV-16感染；25份伴有LSIL和HPV-16感染。通过免疫细胞化学评估Ki-67、端粒酶和病毒E6的表达；通过聚合酶链反应（PCR）和限制性片段长度多态性（RFLP）进行HPV-16基因分型或测序以检测病毒DNA。通过酪胺信号放大原位杂交评估HPV-16的物理状态。
在整个研究组中，58.6%的患者存在与持续性感染相关的LSIL，其中59.3%与HPV的整合状态相关，表现为E6、Ki-67的强表达（P = 0.013，P = 0.055），除端粒酶表达外无显著相关性（P<0.341）。
E6和Ki-67的过表达与HPV-16的整合相关，有利于病毒持续感染，并增加NSIL和LSIL女性患者病情进展的风险。
