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目的研究子宫颈脱落细胞中人乳头瘤病毒(HPV)载量和人端粒酶RNA组分(hTERC)基因的表达与子宫颈上皮内瘤样病变(CIN)之间的关系。方法北京大学深圳医院子宫颈癌早诊早治中心诊断CINⅠ、CINⅡ/Ⅲ及浸润癌的患者分别为105例、59例、10例,并以51例非CIN(病理正常或炎症)者为对照。所有研究对象均取宫颈脱落细胞行HC-Ⅱ法高危型HPV(HR-HPV)和检测荧光原位杂交(FISH)法hTERC基因检测。结果 (1)根据组织学结果分为非CIN、CINⅠ、CINⅡ/Ⅲ和浸润癌组,各组HPV的阳性率分别为58.82%、67.62%、98.31%和100.00%,组间差异有统计学意义(P<0.01);非CIN、CINⅠ、CINⅡ/Ⅲ和浸润癌组病毒载量均值分别为135.67、345.04、535.08和612.62,CINⅡ/Ⅲ和浸润癌组的HPV病毒载量均值高于非CIN组(P<0.05)。随着病变程度加重,HPV阳性率和病毒载量均增加。(2)非CIN、CINⅠ、CINⅡ/Ⅲ和浸润癌组hTERC扩增率分别为3.92%、5.71%、57.63%和90.00%,各组间hTERC差异存在统计学意义(P<0.01);在CINⅡ/Ⅲ及浸润癌组hTERC扩增率显著增高,为非CIN和CINⅠ的10～15倍。各组hTERC扩增均数分别为6.50、9.00、17.81、36.50,扩增均数随病变加重明显升高,CINⅠ与非CIN组之间差异无统计学意义(P>0.05),其余各组间差异均有统计学意义(P<0.01)。CINⅡ/Ⅲ及浸润癌组hTERC扩增均数为非CIN和CINⅠ的2～4倍。(3)hTERC扩增在HPV阳性与阴性组分别为28.99%与3.57%,两组比较差异有统计学意义(P<0.01);非CIN组51例中,不伴有HPV感染的21例无hTERC扩增;CINⅠ与CINⅡ/Ⅲ组不伴HPV感染者各仅有1例hTERC扩增。结论 HPV载量和hTERC扩增均与CIN病变程度密切相关;hTERC扩增主要发生在HPV阳性病例,且与高度宫颈上皮内瘤变的关系更为密切,有望作为早期子宫颈癌及癌前病变的生物学标记物。
Objective To study the relationship between human papillomavirus (HPV) load and expression of human telomerase RNA (hTERC) gene and cervical intraepithelial neoplasia (CIN) in cervical exfoliated cells. Methods 105 cases, 59 cases and 10 cases of CINⅠ, CINⅡ / Ⅲ and invasive carcinoma were diagnosed respectively in the Center of Early Diagnosis and Treatment of Cervical Cancer in Peking University Shenzhen Hospital. Fifty-one patients with non-CIN (pathological or inflammatory) . All subjects were taken out of cervical exfoliated cells line HC-Ⅱ high-risk HPV (HR-HPV) and detection of fluorescence in situ hybridization (FISH) method hTERC gene detection. Results (1) The positive rate of HPV in each group was 58.82%, 67.62%, 98.31% and 100.00%, respectively, according to the histological findings, and the difference was statistically significant (P <0.01). The average viral load of non-CIN, CINⅠ, CINⅡ / Ⅲ and invasive cancer group were 135.67,345.04,535.08 and 612.62, respectively. The average value of HPV viral load in CINⅡ / Ⅲ and invasive cancer group was higher than that in non-CIN group (P <0.05). With the severity of the disease, HPV positive rate and viral load were increased. (2) The hTERC amplification rates of non-CIN, CINⅠ, CINⅡ / Ⅲand invasive carcinoma were 3.92%, 5.71%, 57.63% and 90.00%, respectively. There was significant difference in hTERC between the groups (P <0.01) / Ⅲ and invasive cancer group hTERC amplification was significantly higher, non-CIN and CIN Ⅰ 10 to 15 times. The average number of hTERC amplification in each group was 6.50,9.00,17.81,36.50, the average number of amplification increased significantly with pathological changes, the difference between CINⅠand non-CIN group was not statistically significant (P> 0.05) The differences were statistically significant (P <0.01). The average number of hTERC amplification in CINⅡ / Ⅲ and invasive carcinoma was 2 to 4 times higher than those in non-CIN and CINⅠ. (3) The hTERC amplification was 28.99% and 3.57% respectively in HPV positive and negative groups, the difference between the two groups was statistically significant (P <0.01). In non-CIN group, 21 cases without HPV infection hTERC amplification; only one case of hTERC amplification in CIN I and CIN II / III groups without HPV infection. Conclusion HPV load and hTERC amplification are closely related to the severity of CIN. HTERC amplification mainly occurs in HPV-positive cases and has a close relationship with high-grade cervical intraepithelial neoplasia. It is expected to serve as an early stage of cervical cancer and precancerous lesions Of biological markers.