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目的 :探讨肺癌中 FHIT基因缺失与吸烟的关系。方法 :应用 RT- PCR及 DNA测序技术检测 2 1例肺鳞癌、10例肺腺癌中 FHIT基因缺失情况 ,应用 Fisher精确概率法统计 FHIT基因缺失与吸烟的相关性。结果 :31例肺癌中 ,吸烟组 FHIT基因缺失率为 6 6 .7% (12 / 18) ,显著高于非吸烟组 2 3.1% (3/ 13) ,(P=0 .0 2 )。 2 1例肺鳞癌中 ,吸烟组 FHIT基因缺失率为 73.3% (11/ 15 ) ,显著高于非吸烟组 16 .7% (1/ 6 ) ,(P=0 .0 2 9) ;而在 10例肺腺癌中 ,FHIT基因缺失率在吸烟组 (33.3% )与非吸烟组 (2 8.6 % )中差异不显著 (P=0 .70 8)。肺鳞癌组吸烟率 71.4%(15 / 2 1)显著高于肺腺癌组吸烟率 30 % (3/ 10 ) ,(P=0 .0 36 )。结论 :吸烟与肺鳞癌中较高的 FHIT基因缺失率相关 ,提示 FHIT基因是纸烟中致癌剂的靶分子。
Objective: To investigate the relationship between FHIT gene deletion and smoking in lung cancer. METHODS: RT-PCR and DNA sequencing were used to detect the deletion of FHIT gene in 21 cases of lung squamous cell carcinoma and 10 cases of lung adenocarcinoma. The Fisher exact probability method was used to count the correlation between FHIT gene deletion and smoking. RESULTS: Among 31 lung cancer patients, the FHIT gene deletion rate was 66.7% (12/18) in the smoking group, which was significantly higher than that in the non-smoking group (2 3.1%, 3/13) (P=0.02). In 21 lung squamous cell carcinomas, the FHIT gene deletion rate in the smoking group was 73.3% (11/15), which was significantly higher than that of the non-smoking group (16.7%) (1/6) (P=0.09); In 10 lung adenocarcinomas, the FHIT gene deletion rate was not significantly different between the smoking group (33.3%) and the non-smoking group (28.6%) (P=0.70 8). The smoking rate in lung squamous cell carcinoma group was 71.4% (15/21) significantly higher than that in lung adenocarcinoma group (30%) (P=0.036). Conclusion: Smoking is associated with a higher rate of FHIT gene deletion in lung squamous cell carcinoma, suggesting that FHIT gene is a target molecule for carcinogens in cigarette smoke.