宫颈癌前病变与宫颈鳞癌组织中Foxp3的表达及临床意义

目的 观察宫颈鳞癌及癌前病变组织中Foxp3的表达情况.方法 采用免疫组化检测浸润性宫颈鳞癌(FIGOⅠ期或ⅡA期,共20例)、宫颈上皮内瘤样病变(CIN1、CIN2、CIN3各20例)、宫颈HPV感染(20例)及正常宫颈(20例)组织中Foxp3的表达情况.结果 浸润性宫颈鳞癌与CIN3患者宫颈组织中Foxp3表达明...     

宫颈癌中抑癌基因FHIT表达与HPV16基因状态

目的:探讨抑癌基因FHIT表达及人乳头瘤病毒16(HPV16)的基因型整合状态在宫颈癌发生发展中的作用及相关性。方法:选取柳州市人民医院2013年6月至2014年12月收治的42例宫颈癌、55例宫颈上皮内瘤样病变(CIN)和20例宫颈正常组织的患者,免疫组化法检测宫颈组织中FHIT蛋白表达;多重PCR法检测HPV16 E2/E7表达。结果:FHIT蛋白的总阳性表达率为57.26%(67/117),正常宫颈组织、CINⅠ、CINⅡ、CINⅢ和宫颈癌中FHIT蛋白阳性率分别为85.00%、80.00%、75.00%、60.00%和26.19%。随着宫颈病变加重,FHIT蛋白阳性表达率下降,组间差异有统计学意义(χ~2=7.335;P=0.003)。117例单纯HPV16阳性标本HPV16总整合率为81.20%,正常宫颈组织、CINⅠ、CINⅡ、CINⅢ和宫颈癌中整合率分别为60.00%、66.67%、75.00%、95.00%和92.86%;随病变加重,整合率增强,组间差异有统计学意义(χ~2=5.713,P=0.003);FHIT蛋白阳性表达在不同HPV16整合时不同,差异有统计学意义(χ~2=11.989,P=0.000)。结论:HPV16基因整合可能通过诱导FHIT基因低表达从而促使宫颈癌发生发展。     

FHIT基因、HPV16E6的表达与宫颈鳞癌发病的相关性研究

目的：探讨抑癌基因脆性组氨酸三联（fragile histine triad,FHIT）基因、人乳头瘤病毒16E6（HPV16E6）蛋白在宫颈鳞癌中的表达及其相互关系。方法：应用免疫组织化学链霉菌抗生物素蛋白-过氧化物酶连接（SP）法观察40例宫颈鳞癌、30例宫颈上皮内瘤样病变（CIN）和30例正常宫颈组织中FHIT基因、HPV16E6的表达。结果：FHIT基因在正常宫颈组织、CIN和宫颈鳞癌组织中的阳性表达率分别为96.7%,66.7%和30.0%,各组间阳性等级表达比较差异有统计学意义（χ2=43.595,P〈0.001）。FHIT基因阳性表达在宫颈鳞癌病理分级、临床分期中的比较,差异无统计学意义（χ2分别为3.378和3.315,均P〉0.05）。HPV16E6在正常宫颈组织、CIN和宫颈鳞癌组织中的阳性表达率分别为13.3%,53.3%和82.5%,各组间阳性等级表达比较差异有统计学意义（χ2=32.538,P〈0.001）。HPV16E6蛋白阳性表达在宫颈鳞癌病理分级、临床分期中的比较,差异无统计学意义（χ2分别为0.231和1.399,均P〉0.05）。结论：宫颈鳞癌中FHIT基因表达减少或缺失,以及HPV16E6的高检出率,提示二者在宫颈鳞癌的发生发展中起重要作用,可能是宫颈鳞癌发病机制之一。通过对FHIT基因和HPV16E6蛋白的致病机制以及相互影响的研究,有助于揭示宫颈癌发病机制,二者有可能用于临床宫颈癌诊断、预防和基因治疗。     

HPV16基因整合与FHIT蛋白缺失在宫颈癌变中的作用

目的 探讨HPV16的基因型整合状态及FHIT基因缺失在宫颈癌发生发展中的作用及相关性。方法选取44例宫颈癌、58例宫颈上皮内瘤样病变(CIN)和20例宫颈正常组织的患者,免疫组化检测宫颈FHIT蛋白的表达;并用多重PCR法检测HPV16 E2/E7表达。结果 122例单一HPV16阳性标本HPV16总整合率为78.69%,在正常宫颈组织、CIN1、CIN2、CIN3和宫颈癌中整合率分别为60.00%、66.67%、75.00%、86.96%和88.63%,随病变加重,整合率增强,组间差异有统计学意义(P0.05);FHIT蛋白的总缺失率为43.44%,FHIT蛋白在正常宫颈组织、CIN1、CIN2、CIN3和宫颈癌中的缺失率分别为15.00%、20.00%、25.00%、43.48%和72.73%。FHIT蛋白的缺失率,随病变加重,缺失率增高,组间差异有统计学意义(P0.05)。FHIT蛋白缺失在不同HPV16整合时不同,差异有统计学意义(P0.05)。结论 HPV16基因整合和FHIT蛋白缺失在宫颈癌的发生、发展中起重要作用,HPV16基因整合可能通过诱导FHIT基因低表达从而促使宫颈癌发生发展。     

宫颈癌及其癌前病变组织中FHIT蛋白异常表达与HPV16E6、HPV16E7蛋白表达的相关性

目的 探讨宫颈癌中三联脆组(FHIT)蛋白表达与HPV16 E6、E7蛋白表达的相关性.方法 采用免疫组化SP法对四川大学华西第二医院1999年1月至2003年2月的15例正常宫颈、25例宫颈上皮内瘤变(CIN)以及61例浸润性宫颈鳞癌组织标本进行FHIT蛋白、HPV16E6、HPV16 E7蛋白表达的检测.结果 (1)在正常宫颈上皮、CINI～II、CINⅢ及浸润性宫颈鳞癌中,FHIT 蛋白阳性表达率分别为100%(15/15)、71.43%(10/14)、36.36%(4/11)、14.75%(9/61),P＜0.05;HPV16E6蛋白阳性表达率分剐为0(0/15)、7.14%(1/14)、36.36%(4/11)、59.02%(36/61),P＜0.05;HPV16E7蛋白阳性表达率分别为20.00%(3/15)、42.86%(6/14)、63.64%(7/11)、57.38%(35/61),P＞0.05.(2) 宫颈病变组织中FHIT蛋白的阳性表达与HPV16E6蛋白阳性表达呈负相关(P＜0.0l,r=-0.449),与HPV16E7蛋白表达无相关性(P＞0.05).结论 宫颈癌中FHIT 蛋白的异常表达与HPV16 E6蛋白表达有关,FHIT蛋白和HPV16E6蛋白的联合检测可能可作为宫颈癌前病变转归的指标.     

子宫颈癌组织中水通道蛋白8和bcl-2蛋白的表达及其相关性

目的 探讨水通道蛋白(AQP)8、bcl-2蛋白在宫颈癌组织中的表达及其相关性.方法 采用免疫组化Envision二步法检测AQP8和bcl-2蛋白在74例宫颈癌(其中鳞癌46例、腺癌28例)、34例宫颈上皮内瘤变(CIN)和15例正常宫颈组织中的表达情况,并分析两者的相关性.结果 AQP8和bcl-2蛋白主要在CIN异型细胞和宫颈癌细胞的细胞质内表达,AQP8蛋白在宫颈鳞癌、腺癌、CIN和正常宫颈组织中的阳性表达率分别为98%、61%、71%和53%,鳞癌高于腺癌、CIN和正常宫颈组织,差异有统计学意义(P＜0.01);腺癌与CIN、正常宫颈组织比较,CIN与正常宫颈组织比较,差异均无统计学意义(P＞0.05).bcl-2蛋白在宫颈鳞癌、腺癌、CIN和正常宫颈组织中的阳性表达率分别为74%、71%、53%和20%,鳞癌与腺癌组织比较,差异无统计学意义(P＞0.05);鳞癌、腺癌高于CIN、正常宫颈组织,CIN也高于正常宫颈组织,差异均有统计学意义(P＜0.01).AQP8和bcl-2蛋白在宫颈癌组织中的表达呈明显正相关(rs=0.463,P=0.000).结论 AQP8和bcl-2蛋白在宫颈癌组织中的表达呈明显正相关,AQP8蛋白表达上调可能与宫颈癌的发生、发展有一定的关系.     

p16~(INK4A)蛋白及HPV感染与宫颈上皮内瘤变和宫颈鳞癌的关系研究

目的:通过检测慢性宫颈炎(chronic cervicitis)、宫颈上皮内瘤变(cervical intraepithelial neoplasia,CIN)及宫颈鳞癌(squamous carcinoma of the cervix,SCC)组织中p16INK4A蛋白表达与人乳头瘤病毒(human papillomavirus,HPV)感染的状况,探讨p16INK4A蛋白和HPV感染与宫颈鳞癌发生发展的关系。方法:采用免疫组化PV-9000方法检测114例宫颈组织标本的p16INK4A表达,用核酸分子快速导流杂交基因芯片技术(HybriMax)检测21种HPV DNA。结果:(1)慢性宫颈炎、CINⅠ、CINⅡ、CINⅢ、SCC组织中p16INK4A蛋白表达阳性率分别为0%、45.83%、72.73%、84.00%、91.30%,随着宫颈病变程度加重,p16INK4A蛋白表达阳性率逐渐增高,表达强度增加,差异有统计学意义(P<0.05)。(2)慢性宫颈炎、CINI、CINⅡ、CINⅢ、SCC中HPV感染阳性率分别为20.00%、37.50%、54.55%、56.00%、73.91%,HPV感染在不同宫颈病变组织中差异有统计学意义(P<0.05)。随宫颈病变程度加重,HPV阳性率呈递增趋势,不同病变组织中位于前3位的HPV感染型别分别为:CINⅠ组,HPV16、18、58;CINⅡ～Ⅲ组,HPV16、33、52;宫颈鳞癌组,HPV16、18,52。(3)相关分析结果显示,病变组织中p16INK4A蛋白表达与HPV感染呈正相关(r=0.268,P<0.05)。结论:p16INK4A蛋白表达与宫颈病变程度有关,p16INK4A可能参与了HPV相关的宫颈癌发生。二者联合检测对宫颈癌筛查和预防具有重要意义。     

半乳糖凝集素-1蛋白在宫颈病变组织中的表达及其与高危型人乳头瘤病毒的关系

目的:探讨半乳糖凝集素-1(Galectin-1)蛋白在宫颈上皮内瘤变(CIN)及宫颈癌中的表达及其与高危型人乳头瘤病毒(HR-HPV)的关系。方法:用免疫组织化学法检测宫颈癌(54例)、CINⅠ(10例)、CINⅡ(20例)、CINⅢ(25例)和正常宫颈组织(20例)中Galectin-1蛋白的表达,用第二代杂交捕获法(HC-Ⅱ)检测HR-HPV感染情况,分析Galectin-1与CIN及HR-HPV的关系。结果:Galectin-1蛋白在正常宫颈、CINⅠ、CINⅡ、CINⅢ和宫颈癌组织中的阳性表达率分别为5.0%、20.0%、40.0%、56.0%、48.1%,随着CIN病变程度的加重,Galectin-1蛋白阳性表达逐渐增强;宫颈癌和CINⅡ、CINⅢ的Galectin-1蛋白阳性表达率明显高于正常宫颈组织和CINⅠ(P<0.01),宫颈癌与CINⅡ、CINⅢ间比较、差异无统计学意义(P>0.05)。宫颈癌中Galectin-1蛋白阳性表达在有否淋巴结转移、组织学分级、临床分期和有否HR-HPV的感染中比较,差异有统计学意义(P<0.05,P<0.01),在不同组织学类型中比较,差异无统计学意义(P>0.05)。结论:Galectin-1蛋白表达增强与宫颈病变的进展有一定关系,HR-HPV可能通过诱导宫颈上皮高表达Galectin-1而促使宫颈癌发生、发展。     

SHP-2在宫颈病变组织中的表达及其与HPV感染的关系

目的研究SHP-2在宫颈病变组织中的表达及其与HPV感染的关系。方法选取2013年1月~12月在我院妇产科住院治疗的70例宫颈鳞癌患者(宫颈癌组)、50例宫颈上皮内肿瘤患者(CIN组)及20例宫颈正常患者(正常组),取宫颈组织,采用免疫组化染色检测宫颈组织中SHP-2的表达。结果宫颈癌组SHP-2的表达明显高于正常组,差异有统计学意义(P0.05);宫颈癌组SHP-2的表达明显高于CIN组,差异有统计学意义(P0.05);CIN组与正常组SHP-2表达水平比较,差异无统计学意义(P0.05);HPV16/18在正常组的感染率为15.0%,在CIN组的感染率为74.0%,在宫颈癌组的感染率为82.9%,差异有统计学意义(P0.05);采用Spearman相关分析,结果证实HPV感染和SHP-2在宫颈癌组织中的表达有相关性差异有统计学意义(r=0.331,P0.05)。结论 SHP-2在宫颈癌患者组织中高表达,HPV感染与宫颈癌发生有关,在宫颈癌组织中HPV感染与SHP-2的表达存在相关性。     

宫颈上皮内瘤变及早期宫颈癌组织中P16、HPV L-1壳蛋白的表达及与HR-HPV载量相关性研究

目的:探讨宫颈上皮内瘤变(CIN)及早期宫颈癌组织中P16、HPV L-1壳蛋白的表达及与高危型人乳头瘤病毒(HR-HPV)载量的相关性。方法:分别采用免疫组化法和第二代杂交捕获法(hybrid captureⅡ,HC-2)检测26例慢性宫颈炎组织、83例低度鳞状上皮内病变(LSIL)(CINⅠ83例)、109例高度鳞状上皮内病变(HSIL)(CINⅡ49例,CINⅢ60例)、11例早期宫颈鳞癌组织中P16蛋白、HPV L-1壳蛋白的表达及HR-HPV载量,并分析其相关性。结果:1在宫颈癌前病变中随病变级别增高,HR-HPV阳性率增加,差异有统计学意义(P0.01)。各组织学分级中病毒载量分布差异有统计学意义,HSIL(44.95%)及早期宫颈癌组织(63.64%)中皆以低病毒载量(1~100 RLU/CO)为主。从慢性宫颈炎、LSIL、HSIL到早期宫颈癌,P16蛋白阳性表达率分别为11.54%(3/26),55.42%(46/83),85.32%(93/109),100.00%(11/11),差异有统计学意义(P0.01);L-1壳蛋白阳性率分别为15.38%(4/26),28.92%(24/83),14.68%(16/109),0.00%(0/11),差异有统计学意义(P0.05)。2229例宫颈组织中,随HPV载量增加,P16蛋白表达增强;L-1壳蛋白阳性表达率增加,差异有统计学意义(P0.01)。3在慢性宫颈炎组中,P16蛋白阳性表达与HPV载量呈正相关(r=0.491,P0.05)。在LSIL组中,P16蛋白与HPV载量(r=0.459,P0.01)及L1壳蛋白表达(r=0.297,P0.01)皆呈正相关。4在HSIL及早期宫颈癌组中,P16蛋白、L-1壳蛋白表达与HPV载量三者之间无明显相关性(P0.05)。结论:P16、HPV L-1壳蛋白异常表达是宫颈癌前病变发生发展的早期分子事件,对判断CINⅠ有参考价值,可能比HR-HPV载量更具有预测价值。     

宫颈癌及上皮内瘤变人乳头瘤病毒基因型的检测

目的:了解宫颈癌及上皮内瘤变人乳头瘤病毒(HPV)的感染率及其基因型的分布。方法:用PCR-RFLP法检测239例宫颈癌及上皮内瘤变患者HPV感染并进行分型。先用PGMY09/11共同引物扩增生殖道粘膜型HPV L1区的高度保守区,然后联合使用RsaⅠ、MseⅠ、PstⅠ和HaeⅢ4个限制性内切酶对阳性PCR产物进行酶切,利用不同的酶切片段鉴定HPV的基因型。结果:在239例宫颈癌及上皮内瘤变患者中共检出205例(85·8%)HPV感染,其中宫颈上皮内瘤变Ⅰ级(CINⅠ)、宫颈上皮内瘤变Ⅱ~Ⅲ级(CINⅡ~Ⅲ)和宫颈癌中HPV感染率分别是66·7%,89·9%和98·3%,差异有统计学意义(P<0·001)。在宫颈癌及上皮内瘤变中共检出22型HPV,其中主要基因型及其感染率分别是HPV16(45·6%)、58(12·1%)和52(6·3%)。结论:宫颈癌及上皮内瘤变中HPV感染的基因型至少可达22型,其中以HPV16、58和52为最常见。     

FHIT在宫颈癌及宫颈上皮内瘤变的表达及意义

目的:探讨在宫颈癌和宫颈上皮内瘤变(cervical intraepithelial neoplasia,CIN)发生中脆性组氨酸三联体(fragile histid ine triad,FHIT)基因表达异常的作用及与HPV感染的关系。方法:用免疫组化法检测67例宫颈癌、42例CINⅢ和35例正常宫颈上皮组织的FHIT的表达。用PCR法检测宫颈癌石蜡组织中的HPV DNA,并用直接测序法或反向核酸杂交法对HPV分型。结果:正常宫颈组织中FHIT基因表达下调率为8.6%,CINⅢ组为28.57%,宫颈癌组为46.27%,差异均有统计学意义(P<0.05)。CINⅢ组FHIT蛋白表达下调率虽比宫颈癌组为低,但组间无统计学差异(P=0.66)。67例宫颈癌病例中,高危型HPV感染阳性者的FHIT表达下降或缺失占55.32%,明显高于无高危型HPV感染者(20%)(P<0.05)。宫颈癌患者的年龄、临床分期、肿瘤组织学分级、肿瘤浸润深度和淋巴结转移与FHIT蛋白表达均无明显相关(P>0.05)。FHIT表达下调或缺失31例宫颈癌患者的5年生存率为77.1%,FHIT正常表达36例的5年生存率为79.3%(P>0.05)。结论:FHIT在宫颈癌及CINⅢ中的表达明显下调,可能与HPV感染协同在宫颈癌的发生中起了重要作用。而FHIT在宫颈癌发展中的作用及与预后的关系,有待大样本的进一步研究。     

High-risk human papillomavirus DNA testing and high-grade cervical intraepithelial lesions

OBJECTIVE: To explore the role of high-risk human papillomavirus (HPV) DNA testing in the improvement of the recognition of cervical cancer and precancerous lesions in women with abnormal cervical cytology. METHODS: A total of 2152 women with abnormal cervical cytology were submitted to both HPV DNA testing and biopsy guided by colposcopy and the results were correlated. RESULTS: Positive rate of high-risk HPV DNA in groups of atypical squamous cells of undetermined significance (ASC-US), atypical squamous cells, cannot exclude high-grade (ASC-H), low-grade squamous intraepithelial lesions and high-grade squamous intraepithelial lesions was 53.7, 53.2, 84.6 and 93.0%, respectively. In each group, the detection rate of grade 2,3 cervical intraepithelial neoplasia (CIN 2,3) or cervical cancer in patients with positive HPV DNA was significantly higher than that with negative HPV DNA (P<0.05). In ASC-US group, the negative predictive value of high-risk HPV DNA testing for detection of CIN 2,3 and cervical cancer was 99.8% and the sensitivity 98%. CONCLUSION: HPV DNA testing is a useful indicator in the management of patients with ASC-US and plays an important role in the evaluation of risk for CIN 2,3 and cervical cancer.     

Association between cervical schistosomiasis and cervical cancer. A report of 2 cases

BACKGROUND: HPV is now considered the most important risk factor for the development of cervical intraepithelial neoplasia (CIN) and cancer. Although CIN and cancer have been previously reported in association with cervical schistosomiasis, those reports failed to control for the potential coexistence of high-risk HPV. CASES: Two women, 1 with high grade CIN and 1 with invasive cervical cancer, were negative for high-risk HPV subtypes. Evidence of cervical and systemic schistosomal infestation was evident in both cases. CONCLUSION: In support of prior published studies, cervical schistosomiasis seems to be a possible risk factor for the development of CIN and cancer. As populations around the world migrate, North American colposcopists need to become aware of this association.     

宫颈病变中HPV16感染状况、微卫星不稳定性及错配修复基因表达的研究

目的通过检测HPV16、微卫星不稳定性（microsatellitein stability,MSI）和错配修复基因（hMLH1、hMSH2）的表达,探讨三者在宫颈病变进展中的作用及意义。方法将宫颈病变组织分为宫颈炎、宫颈上皮内瘤变（cervicalintraepithelialneoplasia,CIN）CIN1、CIN2～CIN3、宫颈癌4组。用PCR方法检测HPV16感染状况,用聚合酶链-单链构象多态性分析方法检测宫颈组织中MSI的表达,采用免疫组织化学SP法来检测宫颈组织中的hMLH1和hMSH2的表达,并分析三者的相关性。结果CIN120例中25.0%（5/20）检测到HPV16,CIN2～CIN331中54.8%（17/31）检测到HPV16,二者比较χ2=4.413,P=0.034;宫颈癌中各期HPV16感染比较,差异均无统计学意义。选取的三个微卫星位点D3S2832E、RH91127和SHGC-56838均在宫颈炎中未检测到MSI,在CIN和宫颈癌中均检测到MSI的存在。但总体的表达率较低,最高只有46.7%。错配修复基因的低表达检测结果和MSI的检测结果一致,唯一不同的是前者的总体表达率较高,最高的低表达率为80%;宫颈病变中MSI与错配修复基因（本文即hMLH1、hMSH2）蛋白低表达及HPV16为正相关。结论HPV16的感染导致错配修复基因的低表达,进一步引起微卫星不稳定性,可能是宫颈癌发生、发展的重要机制,HPV16、微卫星不稳定性和错配修复基因有望作为宫颈癌高危人群的检测指标。     

High risk HPV and p53 protein expression in cervical intraepithelial neoplasia.

INTRODUCTION: Cervical intraepithelial lesions due to HPV infection are common in Brazil. An understanding of the mechanisms of the interaction between HPV and host factors is still incomplete. In spite of the high incidence of cervical cancer in Brazil, such studies with Brazilian patients are scarce. The purpose of this study was to correlate the presence of high-risk types of HPV and expression of p53 protein, grade of cervical lesion, age, high-risk sexual behaviors and smoking. It was also intended to establish whether p53 expression might be useful as a marker for CIN progression. METHODS: HPV detection was performed on paraffin sections using biotin-labeled probes by in situ hybridization. p53 protein expression was evaluated by immunohistochemistry. RESULTS: Seventy-eight patients with cervical dysplasia were included in the study. CIN 1 was diagnosed in 38 cases, and CIN 2+3 in 40 cases. High-risk HPV was detected in 42 patients. No correlation was found between the grade of cervical lesion or the presence of HPV and smoking, and high-risk sexual behavior. Expression of p53 was significantly higher in CIN 1, as compared with CIN 2+3, but did not correlate with HPV status. CONCLUSION: Higher expression of p53 protein in early lesions supports the hypothesis of a partially protective role of the wild-type p53 in early stages of cervical lesions.     

HER-2 codon 655 polymorphism in cervical carcinogenesis

HER-2 codon 655 polymorphism together with human papillomavirus (HPV) types were examined in a total of 279 cervical smear samples. Forty-nine patients with high-grade squamous intraepithelial lesion had higher frequency of high-risk HPV than 167 patients with low-grade squamous intraepithelial lesion and 63 controls. There was no statistical difference in the frequencies of HER-2 Ile/Ile, Ile/Val, and Val/Val genotypes between squamous intraepithelial lesions (SILs) and controls. When the Ile/Ile genotype was compared to the Ile/Val + Val/Val genotypes, there was also no statistical difference in the genotype prevalence between SILs and controls either in 91 or 188 patients with or without high-risk HPV, respectively. These results suggest that the HER-2 polymorphism at codon 655 in cervical cell samples is unlikely to be associated with HPV status and the onset of cervical cancer in a Japanese population.     

Secondary prevention of cervical cancer

Cervical cancer affects women in their reproductive ages. Screening is an important secondary prevention strategy. The long process of carcinogenic transformation from human papillomavirus (HPV) infection to invasive cancer provides ample opportunities to detect the disease at a stage when treatment is highly effective. Suitable screening tests are cytology, visual inspection after acetic acid application and HPV detection tests. Evidence of effectiveness of the tests to reduce cervical cancer mortality and the cost-effectiveness of screening programs have been demonstrated. Cervical intraepithelial neoplasia grade 2 and grade 3 are the high-grade cervical cancer precursors and need to be treated. Treatment is safe and effective with ablative or excisional techniques. The World Health Organization recommends screening women at least once in a lifetime between 30 and 49 years of age and ensuring effective treatment of the detected abnormalities. Combination of HPV vaccination and population-based screening will be instrumental in eliminating cervical cancer.     

HPV L1壳蛋白联合HR-HPV分型、TCT检测对宫颈癌前病变及宫颈癌的诊断价值分析#br#

Objective? To explore the diagnostic value of human papilloma virus L1 (HPV L1) capsid protein combined with high-risk HPV (HR-HPV) typing and thinprep cytology test (TCT) for cervical precancerous lesions and cervical cancer. Methods?1 094 women who received cervical cancer screening were selected as the research subjects, and were grouped based on histopathological results. The expression level of HPV L1 capsid protein, and positive rates of HR-HPV and TCT were compared between the groups. Results?There was a significant difference between TCT positive rate and HR-HPV positive rate (P<0.05). Histopathological examination found 179 normal cases or cases only with inflammation (control group), 26 cases of CIN gradeⅠ (CIN1 group), 44 cases of CIN gradeⅡ (CIN2 group), 40 cases of CIN gradeⅢ (CIN3 group) and 21 cases of cervical cancer (cervical cancer group). The positive rates of TCT and HR-HPV in cervical cancer group were the highest, and the expression level of HPV L1 capsid protein was the lowest (P<0.05). The AUC values of HPV L1 capsid protein combined with HPV typing and TCT to diagnose cervical precancerous lesions and cervical cancer were 0.897 and 0.804, respectively (P<0.05). Conclusion?HPV L1 capsid protein, HPV typing and TCT are of clinical value in the diagnosis of cervical precancerous lesions and cervical cancer.