中华实验和临床病毒学杂志
中華實驗和臨床病毒學雜誌
중화실험화림상병독학잡지
Chinese Journal of Experimental and Clinical Virology
2015年
5期
417-420
,共4页
任婕%张其柱%杨英捷%訾聃%周建奖%谭玉洁
任婕%張其柱%楊英捷%訾聃%週建獎%譚玉潔
임첩%장기주%양영첩%자담%주건장%담옥길
乳头状瘤病毒,人%基因型%变异(遗传学)%宫颈疾病
乳頭狀瘤病毒,人%基因型%變異(遺傳學)%宮頸疾病
유두상류병독,인%기인형%변이(유전학)%궁경질병
Papillomavirus,human virus%Genotype%Mutation (genetics)%Cervical disease
目的 检测HPV16 E6/E7基因变异在对照组、CIN及宫颈癌中的发生情况,探讨变异体与宫颈病变的相关性.方法 用核酸分子快速导流杂交基因分型技术进行HPV感染分型检测,PCR扩增HPV16 E6/E7基因,对基因进行切胶纯化后,双向测序.结果 DNA序列总变异发生率为76.5%(62/81),氨基酸总变异率为66.7%(54/81);E6、E7基因变异率均高于原型.E6/E7变异检出率在浸润癌组和对照组之间、癌前病变组和对照组之间进行比较,差异均有统计学意义(P<0.05).氨基酸序列E6-D32E(T96A)和E7-M28V(A82G)+ L94P(T281C)位点突变同时伴随存在,同变异体D32E/M28V+ L94P最为常见,检出率为35.8% (29/81),变异检出率在浸润癌组和对照组、癌前病变组和对照组之间进行比较,差异也有统计学意义(P<0.05).在浸润癌组与癌前病变组之间对同变异体D32E/M28V+ L94P进行分析,发现同变异体虽比原形增多,但在两组之间无统计学差异(P>0.05).结论 HPV16 E6/E7基因的变异体D32E/M28V+ L94P与宫颈浸润癌及癌前病变有关.HPV16 E6/E7基因变异体D32E/M28V+ L94P的致癌性在宫颈浸润癌及癌前病变中没有程度上的差异.
目的 檢測HPV16 E6/E7基因變異在對照組、CIN及宮頸癌中的髮生情況,探討變異體與宮頸病變的相關性.方法 用覈痠分子快速導流雜交基因分型技術進行HPV感染分型檢測,PCR擴增HPV16 E6/E7基因,對基因進行切膠純化後,雙嚮測序.結果 DNA序列總變異髮生率為76.5%(62/81),氨基痠總變異率為66.7%(54/81);E6、E7基因變異率均高于原型.E6/E7變異檢齣率在浸潤癌組和對照組之間、癌前病變組和對照組之間進行比較,差異均有統計學意義(P<0.05).氨基痠序列E6-D32E(T96A)和E7-M28V(A82G)+ L94P(T281C)位點突變同時伴隨存在,同變異體D32E/M28V+ L94P最為常見,檢齣率為35.8% (29/81),變異檢齣率在浸潤癌組和對照組、癌前病變組和對照組之間進行比較,差異也有統計學意義(P<0.05).在浸潤癌組與癌前病變組之間對同變異體D32E/M28V+ L94P進行分析,髮現同變異體雖比原形增多,但在兩組之間無統計學差異(P>0.05).結論 HPV16 E6/E7基因的變異體D32E/M28V+ L94P與宮頸浸潤癌及癌前病變有關.HPV16 E6/E7基因變異體D32E/M28V+ L94P的緻癌性在宮頸浸潤癌及癌前病變中沒有程度上的差異.
목적 검측HPV16 E6/E7기인변이재대조조、CIN급궁경암중적발생정황,탐토변이체여궁경병변적상관성.방법 용핵산분자쾌속도류잡교기인분형기술진행HPV감염분형검측,PCR확증HPV16 E6/E7기인,대기인진행절효순화후,쌍향측서.결과 DNA서렬총변이발생솔위76.5%(62/81),안기산총변이솔위66.7%(54/81);E6、E7기인변이솔균고우원형.E6/E7변이검출솔재침윤암조화대조조지간、암전병변조화대조조지간진행비교,차이균유통계학의의(P<0.05).안기산서렬E6-D32E(T96A)화E7-M28V(A82G)+ L94P(T281C)위점돌변동시반수존재,동변이체D32E/M28V+ L94P최위상견,검출솔위35.8% (29/81),변이검출솔재침윤암조화대조조、암전병변조화대조조지간진행비교,차이야유통계학의의(P<0.05).재침윤암조여암전병변조지간대동변이체D32E/M28V+ L94P진행분석,발현동변이체수비원형증다,단재량조지간무통계학차이(P>0.05).결론 HPV16 E6/E7기인적변이체D32E/M28V+ L94P여궁경침윤암급암전병변유관.HPV16 E6/E7기인변이체D32E/M28V+ L94P적치암성재궁경침윤암급암전병변중몰유정도상적차이.
Objective This study aimed to determine the distribution of HPV-16 E6/E7 genetic variation in patients with invasive cervical cancer or pre-cancer and normal person.Methods HPV infection was detected through flow-through hybridization and gene chip techniques to determine the prevalence of HPV 16 E6/E7 genetic variation.HPV16 E6/E7 gene was amplified by PCR,and the gene was purified by gel and then sequenced bi-directional.Results The rates of DNA sequence mutation and amino acid mutation were 76.5% (62/81) and 66.7% (54/81),respectively.Both E6 and E7 genes showed higher mutation rate than their prototypes.The prevalence of E6/E7 mutation significantly differed between the cervical cancer and the controls (P < 0.05) and also between the cervical precancer and the controls (P < 0.05).Mutations were simultaneously detected at the E6-D32E (T96A) and E7-M28V (A82G)/L94P (T281C) sites of the amino acid sequence.The most common genetic variation was D32E/M28V/L94P,which accounted for 35.8% of the cases (29/81).D32E/M28V/L94P mutation was higher in the cervical cancer and pre-cancer compared with the controls (P < 0.05).D32E/M28V/L94P mutation was higher in the cervical cancer and pre-cancer compared with the prototype,but there were no difference between the cervical cancer and the cervical pre-cancer(P > 0.05).Conclusions HPV-16 E6/E7 genetic variations,such as D32E/M28V/L94P,was associated with cervical cancer or pre-cancer.HPV-16 E6/E7 genetic variations has no difference in the degree of cancer igenesis in the cervical cancer and pre-cancer.