生物化学与生物物理进展
生物化學與生物物理進展
생물화학여생물물리진전
PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS
2001年
2期
214-217
,共4页
李惠芳%常艳丽%李娜%杨苏敏%贾宗智
李惠芳%常豔麗%李娜%楊囌敏%賈宗智
리혜방%상염려%리나%양소민%가종지
宫颈肿瘤%基因突变%P53%人乳头状瘤病毒%免疫组化%PCR%单链构象多态性
宮頸腫瘤%基因突變%P53%人乳頭狀瘤病毒%免疫組化%PCR%單鏈構象多態性
궁경종류%기인돌변%P53%인유두상류병독%면역조화%PCR%단련구상다태성
cervical carcinoma%gene mutation%P53%human papillomavirus%immunohistochemistry%PCR%SSCP
利用免疫组化、聚合酶链反应(PCR)、单链构象多态性(SSCP)分析等方法, 对49例同一标本宫颈癌组织中p53蛋白、P53外显子7～8变异、HPV6、11、16、18-DN A进行检测,以探讨它们在宫颈癌形成中的作用、相互关系和临床意义.结果表明: a.P5 3基因外显子7～8突变率14.29％、p53蛋白阳性率48.98％、HPV-DNA阳性率87.76％.b.P53基因突变不一定伴有p53蛋白阳性,但P53基因突变而p53蛋白阴性的标 本必是HPV-DNA阳性;91.67％的p53蛋白阳性标本具有HPV-DNA阳性.c.HPV16-DNA阳 性率显著高于HPV6、11、18-DNA阳性率.证明：宫颈癌的发生主要与HPV16感染有关,其 次是P53基因突变所致;p53蛋白阳性由HPV感染和/或P53基因突变所致.
利用免疫組化、聚閤酶鏈反應(PCR)、單鏈構象多態性(SSCP)分析等方法, 對49例同一標本宮頸癌組織中p53蛋白、P53外顯子7～8變異、HPV6、11、16、18-DN A進行檢測,以探討它們在宮頸癌形成中的作用、相互關繫和臨床意義.結果錶明: a.P5 3基因外顯子7～8突變率14.29％、p53蛋白暘性率48.98％、HPV-DNA暘性率87.76％.b.P53基因突變不一定伴有p53蛋白暘性,但P53基因突變而p53蛋白陰性的標 本必是HPV-DNA暘性;91.67％的p53蛋白暘性標本具有HPV-DNA暘性.c.HPV16-DNA暘 性率顯著高于HPV6、11、18-DNA暘性率.證明：宮頸癌的髮生主要與HPV16感染有關,其 次是P53基因突變所緻;p53蛋白暘性由HPV感染和/或P53基因突變所緻.
이용면역조화、취합매련반응(PCR)、단련구상다태성(SSCP)분석등방법, 대49례동일표본궁경암조직중p53단백、P53외현자7～8변이、HPV6、11、16、18-DN A진행검측,이탐토타문재궁경암형성중적작용、상호관계화림상의의.결과표명: a.P5 3기인외현자7～8돌변솔14.29％、p53단백양성솔48.98％、HPV-DNA양성솔87.76％.b.P53기인돌변불일정반유p53단백양성,단P53기인돌변이p53단백음성적표 본필시HPV-DNA양성;91.67％적p53단백양성표본구유HPV-DNA양성.c.HPV16-DNA양 성솔현저고우HPV6、11、18-DNA양성솔.증명：궁경암적발생주요여HPV16감염유관,기 차시P53기인돌변소치;p53단백양성유HPV감염화/혹P53기인돌변소치.
P53 gene (exon7～8) mutatins and p53 proteins and HPV 6，11，16，18-DNA were examined in 49 cervical carcinoma by immunohistochemistry, polymerase chain reaction (PCR) and single strand conformation polymorphism (SSCP) in order to investigate their role and mutual relation and clinical significance in the onco genesis of cervical carcinoma. The results showed that first, p53 proteins posit ive rate was 48.98％, and not outstandingly related to the differentiation and the invasive degree of cervical carcinoma(P＞0.05); the defects of P53 gene (exon7～8) were not found but P53 (exon7～8) mutations were detected in 7 of 49(14.29％) cervical carcinoma; then, HPV16-DNA positive rate was much higher than HPV6,11,18-DNA positive rate respectively(P＜0.001),and the different HPV-DNA was simultaneously tested in one cerv ical carcinoma; last, not all cases of P53 mutations had p53 proteins posi tive, but the cases of P53 mutations and p53 proteins negative certainly had HPV infections, and HPV positive cases were much more than its negative one in the cases of p53 proteins positive(P＜0.001). These results proved that the oncogenesis of cervical carcinoma is mainly associated with HPV16 infections, and second related to P53 (exon7～8) mutations. p53 proteins positive results from P53 mutations or/and HPV infections in cervical carc inoma.
