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外阴鳞癌组织中HPV检测及FHIT基因杂合性缺失、微卫星不稳定性观察
引用本文:范余娟,蒙亚晴,杨开选,徐红.外阴鳞癌组织中HPV检测及FHIT基因杂合性缺失、微卫星不稳定性观察[J].山东医药,2012,52(2):21-23.
作者姓名:范余娟  蒙亚晴  杨开选  徐红
作者单位:1. 广西医科大学第一附属医院,南宁,530021
2. 四川大学华西第二医院
基金项目:广西自然科学基金资助项目
摘    要:目的 观察外阴鳞癌( VSCC)组织中HPV感染情况及脆性组氨酸三联体(FHIT)基因的杂合性缺失(LOH)、微卫星不稳定性(MSI),并探讨其意义.方法 选取VSCC组织24例、外阴尖锐湿疣(VCA)42例、正常外阴组织20例,用PCR法检测上述组织中的HPV6、11、16、18、31、33亚型,用PCR-单链构像多态性分析(PCR-SSCP)法检测FHIT基因D3S1300位点的LOH和MSI.结果 在正常外阴、VCA、VSCC组织中低危型HPV( HPV6/11)阳性分别为2、38、21例,高危型HPV(HPV16/18/31/33)阳性分别为0、13、10例;VCA、VSCC组织与正常外阴组织比较,P均<0.05.在正常外阴、VCA、VSCC组织中,FHIT基因D3S1300位点上LOH、MSI阳性分别为0、9、13例,VSCC与VCA、正常外阴组织比较,P均<0.05.VSCC组织中HR-HPV感染与FHIT基因D3 S1300位点LOH/MSI相关(r =0.438,P<0.05).结论 VSCC组织中存在较高的低危型、高危型HPV复合感染及FHIT基因LOH和(或)MSI;二者在VSCC的发生发展中发挥重要作用.

关 键 词:人乳头瘤病毒  脆性组氨酸三联体基因  杂合性缺失  微卫星不稳定性  外阴鳞癌  外阴尖锐湿疣

Observation of HPV infection and loss of heterozygosity, micro satellite instabilityon FHIT gene in vulvar squamous cell carcinoma tissue
FAN Yu-juan , MENG Ya-qing , YANG Kai-xuan , XU Hong.Observation of HPV infection and loss of heterozygosity, micro satellite instabilityon FHIT gene in vulvar squamous cell carcinoma tissue[J].Shandong Medical Journal,2012,52(2):21-23.
Authors:FAN Yu-juan  MENG Ya-qing  YANG Kai-xuan  XU Hong
Institution:1 First Affilicated Hospital,Guangxi Medical University,Nanning 530021,P.R.China)
Abstract:Objective To observe HPV infection and loss of heterozygosity(LOH),micro satellite instability(MSI) on FHIT gene in vulvar squamous cell carcinoma tissue,and explore its significance.Methods HPV DNA 6,11,16,18,31,33 were detected by PCR in VSCC(24 cases),VCA(42 cases) and normal vulva(20 cases).PCR-SSCP was used to detect the LOH,MSI for amplification with D3S1300 on FHIT gene.Results In normal vulva,VCA and VSCC groups,the number of patients with LR-HPV(HPV6/11) were 2,38 and 21 cases,and HR-HPV(HPV16,18,31,33) infection were 0,13 and 10 cases,there were statistics significant differences between normal vulva and VCA,normal vulva and VSCC(all P<0.05).In normal vulva,VCA and VSCC groups,the number of LOH andMSI positive on D3S1300 were 0,9,13 cases respectively,there were statistics significant differences between VSCC and VCA,VSCC and normal vulva(all P<0.05).HR-HPV infections were possibly relevant to the LOH and/or MSI on FHIT gene(the related coefficient was 0.438,P<0.05)in VSCC.Conclusion In VSCC,there are high LR-HPV and HR-HPV coinfection and high LOH,MSI on FHIT gene;both play important roles in the carcinogenesis of VSCC.
Keywords:human papillomavirus  fragile histidine triad gene  loss of haterozygosity  micro satellite intabihity  vulva squamous cell cancer  vulva condyloma acuminatum
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