肺癌患者K-ras、FHIT基因异常与吸烟关系

Abstract

Objective To study the relationship between the abnormal of proto-oncogene K-ras gene and Fragile Histidine Triad (FHIT) gene with cigarette smoking in lung cancer tissue. To reveal the target of smoking in lung cancer. Methods Polyanerase chain reaction plus restriction fragment length polymorphism (PCR-RFLP) were used to detect the mutation of K-ras gene and reverse transcription polymerase chain reaction (RT-PCR) method was used to detect the abnormal transcription of FHIT gene in 80 cases lung cancer tissue and 20 cases of normal control lung tissue. Analyze the relationship between cigarette smoking with K-ras mutation and the abnormal transcription of FHIT gene. Results K-ras mutation rate in lung cancer tissue was 52.58%. The abnormal transcription rate of FHIT gene was 71.25%. Statistical significant difference was found compared to normal control lung tissue. K-ras mutation rate and FHIT gene abnormal transcription rate of cigarette smoking group was higher than that of no smoking groups in lung cancer patients (P＜0.05). BI of lung cancer patient was related to K-ras mutation and FHIT gene abnormal transcription. Pearson coefficient of continency is 0.337 and 0.399 respective. K-ras gene mutation had close correlatetion with cigarette smoking in lung adenocarcinoma. FHIT gene abnormal transcription had close correlatetion with cigarette smoking in lung squamous cell carcinoma and small cell lung cancer. No relevance was found between K-ras mutation rate and FHIT gene abnormal transcription rate in lung cancer, but significant difference was found between them. Conclusion The mutation of K-ras gene and the abnormal transcription of FHIT gene have close correlatetion with tumorigenic development of lung cancer. K-ras and FHlT became the molecule target of smoke cancerigenic. Cigarette smoking is an important factor that causes K-ras gene mutation in lung adenocarcinoma and FHIT gene abnormal transcription in lung squamous cell carcinoma and small cell lung cancer.