癌变·畸变·突变 ›› 2009, Vol. 21 ›› Issue (4): 291-294.doi: 10.3969/j.issn.1004-616x.2009.04.010

• 论著 • 上一篇    下一篇

FHIT和p16基因甲基化与肺癌的发生

亢春彦1;肖 红1;吴逸明2;   

  1. 1.河南职工医学院病理学教研室, 河南 郑州 450003;2.郑州大学公共卫生学院劳动卫生
  • 收稿日期:2008-12-22 修回日期:2009-04-22 出版日期:2009-07-30 发布日期:2009-07-30
  • 通讯作者: 吴逸明

Relationship between Methylation of FHIT and p16 Genes and Lung Cancer

KANG Chun-yan1;XIAO Hong1;WU Yi-ming2;   

  1. 1. Department of Pathology; Henan Medical College for Staff and Workers; Zhengzhou 450003; 2. Occupational Health and Toxicology; College of Public Health; Zhengzhou University, Zhengzhou 450052; Henan; China
  • Received:2008-12-22 Revised:2009-04-22 Online:2009-07-30 Published:2009-07-30
  • Contact: WU Yi-ming

摘要: 背景与目的: 探讨FHIT和p16基因甲基化与肺癌发生之间的关系。 材料与方法: 采用甲基化特异性PCR检测59例原发性肺癌组织,相对应的32例正常组织及11例支气管鳞状化生组织中FHIT基因、p16基因启动子区CpG岛甲基化状况。 结果: 肺癌组织和正常肺组织中的FHIT基因甲基化率分别为37.3%(22/59)、0.0%(0/32);两组间的差异有统计学意义(P<0.01);支气管鳞状化生组织FHIT基因甲基化阳性率为18.1%(2/11)。肺癌组织和正常肺组织中的p16基因甲基化率分别为50.8%(30/59)、0.0%(0/32);两组间的差异具有统计学意义(P<0.01);支气管鳞状化生组织p16基因甲基化阳性率为18.1%(2/11)。肺癌患者吸烟组中FHIT、p16基因甲基化联合检测的阳性率为90.6%(29/32),与非吸烟组(33.3%;9/27)相比较,其差异具有统计学意义(P<0.05)。 结论: FHIT基因和p16基因启动子区甲基化可能与肺癌的发生有关。

关键词: FHIT基因, p16基因, 甲基化, 肺癌, 甲基化特异性聚合酶链技术

Abstract: BACKGROUND AND AIM: To illustrate the relationship between the methylation of FHIT and p16 genes and the development of lung cancer. MATERIALS AND METHODS: Methylation of the promoters of FHIT gene and p16 gene was evaluated by methylation-specific PCR in 59 lung cancer tissues; 32 adjacent non-carcinoma tissues and 11 bronchal epithelial squamous tissues. RESULTS: FHIT methylation in lung cancer tissue samples; adjacent non-carcinoma tissue samples were 37.3%(22/59) and 0%(0/32)respectively; with significant difference(P<0.01). Methylation was found in 2 of 11 (18.1%) bronchal epithelial squamous samples. p16 methylation of lung cancer tissue samples; adjacent non-carcinoma tissue samples were 50.8%(30/59)and 0.0%(0/32)respectively; showing a significant difference(P<0.01); Methylation was found in 2(18.1%)of 11 bronchal epithelial squamous samples. FHIT/p16 combined detection of methylation found many more positive tissues in smoking patients than the single gene. There was a significant difference between smokers and non-smokers(P<0.05). CONCLUSION: The 5'- CpG island methylation of FHIT and p16 was frequent in lung cancer and may be an early event in lung carcinogenesis.

Key words: FHIT gene, p16 gene, methylation, lung cancer, methylation-specific PCR

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