摘要
目的 探讨肺癌发生的分子生物学机制 ;方法 采用逆转录 -巢式聚合酶链反应 (reverse- tape polymerase chainreaction)的方法对 4 2例肺癌及 10例正常肺组织中的 FHIT(Fragile histidine triad)基因的缺失情况进行检测 ,并用 PCR技术检测了肺癌组织中人乳头状瘤病毒 (human papilloma virus,HPV)的 DNA片段 ;结果 6 6 .7% (2 8/ 4 3)肺癌组织中检测到 FHIT基因的缺失 ,而正常组织中未检测到 FHIT基因的缺失 ,二者差别有显著意义 (p<0 .0 1)。 4 2例肺癌组织中有 8例检测到 HPV的片段 ,阳性率为 19% (8/ 4 2 ) ,正常组织中未检测到 HPV的片段 ,且在 8例 HPV阳性的标本中均有 FHIT基因缺失。结论 FHIT基因的缺失在肺癌的发生中起一定的作用 ;可与肺癌的不同病理分型、分化程度及临床分期无关 ;但与吸烟有一定的相关性 ;同时 HPV的感染与肺癌的发生有一定关系 ,且与
Objective To investigate deletion of fragile histidine triad (FHIT) gene and human papillomavirus infections in lung cancer in order to study the molecular biology mechanism of lung cancer.Methods Forty-two lung cancer specimens and ten normal lung tissues were examined for abnormalities of FHIT gene by using RT-PCR and part of DNA in human papillomavirus (HPV) was examined by PCR.Results Aberrant transcripts of FHIT were found in twenty-eight of 42 (66.7%) cases of cancerous tissues while normal sized FHIT transcripts were detected in all 10 cases of normal lung tissues. The difference between these means a great deal (P<0.01) Eight out of 42 (19%) samples of lung cancer show infection of HPV, but in 10 normal lung tissues, no infection of HPV was found. In the above eight cases, deletion of FHIT was found.Conclusions These data indicate that (1) deletion of FHIT contributes to lung cancer. (2) deletion of FHIT has nothing to do with pathological types, clinical stages and degrees of differentiation, but has some connection with smoking. (3) HPV infection may cooperate with deletion of FHIT or effect separately in lung cancer.
出处
《临床肺科杂志》
2002年第4期3-5,共3页
Journal of Clinical Pulmonary Medicine
