论文部分内容阅读
目的 :研究非小细胞肺癌 (NSCLC)不同来源与病理分期类型的组织标本中P16基因表达的相互关系。方法 :应用PCR -SSCP方法 ,检测 2 8例手术标本、2 1例支气管镜活检及 2 7例恶性胸水NSCLC患者中P16基因的表达。结果 :2 8例Ⅰ期手术标本中 8例P16基因发生改变 (2 8 6 % ) ,其中 5例纯合性缺失 ,3例点突变 ;2 1例支气管镜活检中 ,8例P16基因发生改变 (38 1% ) ,其中 3例纯合性缺失 ,5例点突变 ;2 7例恶性胸水标本中 ,17例P16基因发生改变 (6 3 0 % ) ,其中 16例纯合性缺失 ,1例点突变。恶性胸水患者的P16基因改变率与Ⅰ期手术标本、支气管镜活检相比较 ,有显著性差异 (分别为P <0 0 1、P<0 0 0 5 )。在 76例NSCLC中 ,Ⅰ期患者的P16基因改变率为 30 0 % (9/ 30 ) ,Ⅱ期患者为 5 0 % (2 / 4 ) ,Ⅲ期患者为 5 1 6 % (16 /31) ,Ⅳ期患者为 5 4 5 % (6 / 11)。Ⅰ期患者的P16基因改变率与Ⅱ、Ⅲ、Ⅳ期患者相比较 ,均有显著性差异 (P <0 0 5 )。腺癌患者的P16基因改变率为 4 5 0 % (18/ 4 0 ) ,鳞癌患者为 4 2 3% (11/ 2 6 ) ,而腺鳞癌混合型为 4 0 0 % (4/ 10 ) ,经统计学分析 ,三者无显著性差异。而鳞癌患者的P16基因突变率为 2 3 1% (6 / 2 6 ) ,腺癌患者为 7 5 % (3/ 4 0 ) ,二者有显著性差异 (P <0 0
Objective: To investigate the relationship between the expression of P16 gene in tissue samples of different types and stages of non-small cell lung cancer (NSCLC). Methods: PCR-SP method was used to detect the expression of P16 gene in 28 cases of surgical specimens, 21 bronchoscopic biopsies and 27 cases of malignant pleural effusion NSCLC. Results: There were 8 cases of P16 gene mutation (286%) in 28 cases of stage Ⅰ surgical specimens, of which 5 cases were homozygous deletion and 3 cases were point mutation. Among 21 cases of bronchoscopic biopsy, 8 cases of P16 gene changed (38 1%), of which 3 cases were homozygous deletion and 5 cases were point mutation. Among 27 samples of malignant pleural effusion, 17 cases changed P16 gene (63.0%), of which 16 cases were homozygous deletion and 1 case Point mutation. The rate of P16 gene mutation in patients with malignant pleural effusion was significantly different from that of stage Ⅰ surgical specimens and bronchoscopic biopsy (P <0.01, P <0.05). Among 76 NSCLC patients, the rate of P16 gene mutation was 30 0% (9/30) in stage Ⅰ, 50% (2/4) in stage Ⅱ and 51.6% (16/31) in stage Ⅲ, , And 54.5% (6/11) patients in stage Ⅳ. The rate of P16 gene mutation in stage Ⅰ patients was significantly different from that in stage Ⅱ, Ⅲ and Ⅳ (P <0.05). The rate of P16 gene mutation in adenocarcinoma was 45.0% (18/40), that in squamous cell carcinoma was 42.3% (11/26), and that in adenosquamous carcinoma was 400% (4/10) ), The statistical analysis, the three no significant difference. The mutation rate of P16 gene in squamous cell carcinoma was 231% (6/26) and that in adenocarcinoma was 75% (3/40), both of which were significantly different (P <0 0