中华肿瘤杂志
中華腫瘤雜誌
중화종류잡지
CHINESE JOURNAL OF ONCOLOGY
2001年
3期
220-223
,共4页
陆哲明%郭梅%李涛%柯杨%陈克能%邢海平%梅强%杨怀华
陸哲明%郭梅%李濤%柯楊%陳剋能%邢海平%梅彊%楊懷華
륙철명%곽매%리도%가양%진극능%형해평%매강%양부화
食管肿瘤%人乳头瘤病毒%p53基因%原位杂交%聚合酶链反应
食管腫瘤%人乳頭瘤病毒%p53基因%原位雜交%聚閤酶鏈反應
식관종류%인유두류병독%p53기인%원위잡교%취합매련반응
目的探讨食管癌高发区中人乳头瘤病毒(HPV)、爱泼斯坦-巴尔病毒(EBV)与食管癌发病的关系,并初步研究HPV感染与p53过表达之间的关系。方法设计了多对引物进行PCR、原位杂交及原位PCR、免疫组化,并对30例高发区食管癌进行检测。结果用PCR检出HPV-L1阳性率10.0%,HPV-16-E6阳性率60.0%,HPV-16-E7阳性率63.3%,HPV-18-E6及EBV的检出率分别为6.7%和0,p53蛋白的检出率为73.3%。用原位杂交和原位PCR检出HPV-16-E6阳性率均为53.3%。HPV-L1的低检出率及HPV-16-E6、HPV-16-E7基因的较高检出率可能提示,在肿瘤细胞中HPV常以部分丢失的形式整合,而E6、E7常在整合中保留。结论 HPV-16型可能与高发区食管癌发生密切相关,而HPV-18、EBV则关系不大。p53突变在食管癌的发病中起重要作用,但其与HPV感染之间的关系不大。
目的探討食管癌高髮區中人乳頭瘤病毒(HPV)、愛潑斯坦-巴爾病毒(EBV)與食管癌髮病的關繫,併初步研究HPV感染與p53過錶達之間的關繫。方法設計瞭多對引物進行PCR、原位雜交及原位PCR、免疫組化,併對30例高髮區食管癌進行檢測。結果用PCR檢齣HPV-L1暘性率10.0%,HPV-16-E6暘性率60.0%,HPV-16-E7暘性率63.3%,HPV-18-E6及EBV的檢齣率分彆為6.7%和0,p53蛋白的檢齣率為73.3%。用原位雜交和原位PCR檢齣HPV-16-E6暘性率均為53.3%。HPV-L1的低檢齣率及HPV-16-E6、HPV-16-E7基因的較高檢齣率可能提示,在腫瘤細胞中HPV常以部分丟失的形式整閤,而E6、E7常在整閤中保留。結論 HPV-16型可能與高髮區食管癌髮生密切相關,而HPV-18、EBV則關繫不大。p53突變在食管癌的髮病中起重要作用,但其與HPV感染之間的關繫不大。
목적탐토식관암고발구중인유두류병독(HPV)、애발사탄-파이병독(EBV)여식관암발병적관계,병초보연구HPV감염여p53과표체지간적관계。방법설계료다대인물진행PCR、원위잡교급원위PCR、면역조화,병대30례고발구식관암진행검측。결과용PCR검출HPV-L1양성솔10.0%,HPV-16-E6양성솔60.0%,HPV-16-E7양성솔63.3%,HPV-18-E6급EBV적검출솔분별위6.7%화0,p53단백적검출솔위73.3%。용원위잡교화원위PCR검출HPV-16-E6양성솔균위53.3%。HPV-L1적저검출솔급HPV-16-E6、HPV-16-E7기인적교고검출솔가능제시,재종류세포중HPV상이부분주실적형식정합,이E6、E7상재정합중보류。결론 HPV-16형가능여고발구식관암발생밀절상관,이HPV-18、EBV칙관계불대。p53돌변재식관암적발병중기중요작용,단기여HPV감염지간적관계불대。
Objective To investigate the association of HPV with the development of esophageal cancer(EC) in a high-incidence area of EC and to elucidate its correlation with p53 overexpression.Methods Thirty EC specimeas were collected from Anyang, Henan. Four pairs of primers were designed to perform in situ hybridization (ISH)and in situ PCR(ISPCR). Immunohistochemical staining was used to detect p53.Results HPV L1, HPV-16-E6 and HPV-16-E7 was detected in 10.0%,60.0% and 63.3% of the EC samples, respectively. The detection rate of HPV-18-E6 was low(6.7%) and no EBV was detected. Overexpression of p53 was identified in 73.3% EC. With ISH or ISPCR, HPV-16-E6 was positive in 53.3% of EC. Conclusion The low detection rate of HPV L1 and high detection rate of HPV-16-E6 and E7 genes suggest that HPV may be partially lost when inte-grating into tumor cell genome,while E6 and E7 genes are intact. The results support a role of HPV-16 in the pathogenesis of EC in high incidence area. Although p53 mutation takes an important part in tumor pathogenesis, it is not consistent with the HPV existence in the EC cells.