非小细胞肺癌中脆性组氨酸三联体基因异常的探讨

The Study on Abnormalities of FHIT Gene in Non-small Cell Lung Cancer

  • 摘要: 目的:探讨脆性组氨酸三联体(FHIT)基因在非小细胞肺癌(NSCLC)中作用机制及其与临床病理间的关系。方法:通过PCR-变性聚丙烯酰胺凝胶电泳-硝酸银染色方法检测40例非小细胞肺癌及其癌旁肺组织与FHIT基因紧密连锁的D3S1300位点杂合性缺失(LOH), 并比较其与各临床病理的关系。结果:1)FHIT基因在肺癌组和对照组杂合性缺失的发生率分别为70.0%和0, 两组比较有显著性差异(P<0.001)。2)发生FHIT基因杂合性缺失的28例肺鳞癌患者中23例(82.1%)有吸烟史;发生FHIT基因杂合性缺失的12例肺腺癌患者中7例(58.3%)有吸烟史。FHIT基因杂合性缺失与吸烟因素及肺癌组织类型具有相关性(P<0.05)。3)FHIT基因杂合性缺失的发生率与年龄、性别、临床分期、淋巴结转移等临床病理间无明显相关性。结论:非小细胞肺癌FHIT基因杂合性缺失与吸烟因素密切相关, 提示FHIT基因可能是烟中致癌物的靶分子。

     

    Abstract: Objective:To study the mechanism and effect of FHIT gene in non-small cell Lung can-cer and to investigate the relationships between FHIT and the clinical data, such as age, gender, smoking, histological type, clinical stage and lympho node metastasis. Methods: Forty cases of NSCLC and normal tissues LOH (loss of heterozygote) of FHIT gene were deteited by PCR-electrophoresis (de-natured polyacrylamide gel)-silver staining and significance of FHIT transformation in NSCLC occur-rence was discussed. Results: The consequence showed that about 70.0% (28/40)displayed LOH in NSCLC group and this was significantly higher compared to the control group (0/40). We also found that 23 cases (82.1%) were the smokers in 28 cases with lung squamous cancer, and 7 (58.3%) were the smokers in 12 cases with lung adenoid cancer. The rate of the smoking patients with lung squamous cancer was higher than those of lung adenoid cancer patients. We also found FHIT gene LOH was related to smoking and histological type, but it was not related to other clinical data. Conclusion: LOH of FHIT gene plays a very important role in carcinogenesis in NSCLC. Smoking is relevant to deficiency rate of the lung squamous cancer and it suggests that the FHIT gene is the carcinogenic target molecule in the cigarette

     

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