【佳学基因检测】非小细胞肺癌患者的异常启动子甲基化谱及其与生存的关联

基因检测要多少钱—答案

在高峰论坛中dota2吧雷电竞 基因检测位点的全面性与正确性了解《Clin Cancer Res》在. 2006 Dec 15;12(24):7329-38.发表了一篇题目为《非小细胞肺癌患者的异常启动子甲基化谱及其与生存的关联》dota2吧雷电竞 dota2吧雷电竞 治疗基因检测临床研究文章。该研究由Jian Gu , David Berman, Charles Lu, Ignacio I Wistuba, Jack A Roth, Marsha Frazier, Margaret R Spitz, Xifeng Wu等完成。促进了dota2吧雷电竞 的正确治疗与个性化用药的发展，进一步强调了基因信息检测与分析的重要性。

肿瘤转移恶化的基因根源临床研究内容关键词：

非小细胞肺癌,NSCLC,甲基化,肺腺癌,肺磷癌,老年患者,年轻患者

肿瘤靶向治疗基因检测临床应用结果

肿瘤甲基化基因检测目的：肿瘤致病基因及甲基化基因检测的研究的目的是探讨肿瘤抑制基因高甲基化对非小细胞肺癌 (NSCLC) 患者的预后价值。实验设计：呼吸科基因检测技术开发验证小组使用定量甲基化特异性 PCR检测了 155 例非小细胞肺癌 (NSCLC) 患者肿瘤中 9 个基因的甲基化状态。肿瘤基因解码团队分析了基因甲基化状态与患者总体存活率之间的关联。肿瘤基因序列变化及甲基化影响的研究结果：甲基化指数（定义为甲基化基因数与测试基因数之比）在腺癌中显着高于（0.38 +/- 0.20）鳞状细胞癌 (0.30 +/- 0.22; P = 0.027)，老年患者的肿瘤 (0.37 +/- 0.20) 比年轻患者 (0.30 +/- 0.22; P = 0.040)高，重度吸烟者的肿瘤 (0.39 +/- 0.21) 比轻度吸烟者 (0.29 +/- 0.20; P = 0.042)的甲基化比例高。在 Cox 比例风险模型中，p16 甲基化与显着较差的生存率相关[风险比，1.95； 95% 置信区间 (95% CI), 1.21-3.39]。 Kaplan-Meier 生存曲线显示，p16 高甲基化患者的生存期（中位数 = 21.7 个月）明显短于 p16 高甲基化患者（中位数 = 62.5 个月；P = 0.0001，对数秩检验）。 CDH1 或 TIMP3 基因的高甲基化与显着更好的生存相关，风险比分别为 0.51（95% CI，0.29-0.90）和 0.59（95% CI，0.36-0.97）。这三个基因的联合分析显示，随着不利事件数量的增加，生存率下降的显着趋势（P = 0.0007）。结论：多个基因的高甲基化对NSCLC患者的生存率表现出显着的差异影响。需要评估每个甲基化基因对生存的影响，以提供贼佳的预后价值。

肿瘤发生与反复转移国际数据库描述：

Purpose: The aim of this study was to investigate the prognostic value of hypermethylation of tumor suppressor genes in patients with non-small cell lung cancer (NSCLC).Experimental design: We examined the methylation status of nine genes in 155 tumors from patients with NSCLC using quantitative methylation-specific PCR. We analyzed the associations between gene methylation status and overall patient survival.Results: The methylation index, defined as the ratio between the number of methylated genes and the number of genes tested, was significantly higher in adenocarcinomas (0.38 +/- 0.20) than in squamous cell carcinomas (0.30 +/- 0.22; P = 0.027), in tumors from older patients (0.37 +/- 0.20) than younger patients (0.30 +/- 0.22; P = 0.040), and in tumors from heavier smokers (0.39 +/- 0.21) than lighter smokers (0.29 +/- 0.20; P = 0.042). In the Cox proportional hazards model, p16 methylation was associated with significantly poorer survival [hazard ratio, 1.95; 95% confidence interval (95% CI), 1.21-3.39]. Kaplan-Meier survival curves showed that patients with hypermethylated p16 had significantly shorter survival (median = 21.7 months) than patients without p16 hypermethylation (median = 62.5 months; P = 0.0001, log-rank test). Hypermethylation of CDH1 or TIMP3 gene was associated with significantly better survival with hazard ratios of 0.51 (95% CI, 0.29-0.90) and 0.59 (95% CI, 0.36-0.97), respectively. Joint analysis of these three genes showed a significant trend for poorer survival as the number of unfavorable events increased (P = 0.0007).Conclusion: Hypermethylation of multiple genes exhibited significant differential effect on NSCLC patient survival. Assessment of the effect of each methylated gene on survival is needed to provide optimal prognostic value.