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目的探讨脆性组氨酸三联体(FHIT)基因缺失与p53的过度表达和人乳头状瘤病毒16和(或)18(HPV16/18)感染在宫颈癌前病变(CIN)和宫颈癌(CC)发生发展中的作用和意义。方法采用免疫组化SP法检测52例CIN和69例CC中的FHIT基因和p53的表达,以原位杂交方法检测HPV16/18感染情况,并以18例正常宫颈组织作为对照。结果FHIT在正常宫颈组织(正常组)中呈阳性表达；FHIT在宫颈CIN组中的阴性率为30．8%,在CINⅢ期的表达,明显高于正常组和CINⅠ、Ⅱ期(P＜0．01)；在CC组中阴性率为66．7%(46/69),明显高于正常组和CIN组(P＜0．01),且随细胞分化的降低,FHIT阴性率上升。p53和HPV16/18在CC组的阳性率分别达56．5%(39/69)和84．1%(58/69),均高于CIN和正常组(P＜0．05),且CC组的p53阳性率随细胞分化的降低而升高(P＜0．01)。CIN和CC组的FHIT阳性和阴性者,p53阳性率差异均无统计学意义(P＞0．05),相关性分析也显示无相关关系；但两组FHIT阴性者的HPV16/18感染率明显高于FHIT正常表达者(P＜0．01),FHIT与HPV呈负相关关系。结论FHIT基因缺失与宫颈癌发生有关,它在CIN中的缺失可能可作为高危型CIN人群的筛选和宫颈癌早期诊断指标。CIN和CC中的FHIT缺失常与p53过度表达同时存在,但两者间无相关性。HPV16/18可能是引起FHIT和p53异常的共同原因。
Objective To investigate the relationship between the deletion of FHIT gene and the overexpression of p53 and the clinical significance of HPV16 / 18 (HPV16 / 18) infection in cervical precancerous lesions (CIN) and cervical cancer (CC) The development of the role and significance. Methods Immunohistochemical SP method was used to detect the expression of FHIT gene and p53 in 52 cases of CIN and 69 cases of CC. HPV16 / 18 infection was detected by in situ hybridization and 18 cases of normal cervical tissue were used as control. Results FHIT was positive in normal cervical tissue (normal group). The negative rate of FHIT in cervical CIN group was 30.8%. The expression of FHIT in CIN Ⅲ phase was significantly higher than that in normal group and CIN Ⅰ and Ⅱ .01). The negative rate in CC group was 66.7% (46/69), which was significantly higher than that in normal group and CIN group (P <0.01). The negative rate of FHIT increased with the decrease of cell differentiation. The positive rates of p53 and HPV16 / 18 in CC group were 56.5% (39/69) and 84.1% (58/69), respectively, which were higher than those in CIN and normal group (P <0.05) The positive rate of p53 increased with the decrease of cell differentiation (P <0.01). There were no significant differences in the positive rates of p53 between FHIT positive and negative patients in CIN and CC groups (P> 0.05), but no correlation was found between the positive rates of FHIT and negative in CIN and CC groups Which was higher than that of normal FHIT (P <0.01). There was a negative correlation between FHIT and HPV. Conclusion The deletion of FHIT gene is associated with the development of cervical cancer. The deletion of FHIT gene in CIN may be used as screening and early diagnosis of cervical cancer in high-risk CIN population. FHIT deletion in CIN and CC often coexist with p53 overexpression, but there is no correlation between the two. HPV16 / 18 may be the common cause of FHIT and p53 abnormalities.