Deng Qiuhua, Qiu Yuan, Jia Junmei, Tang Hailing, Liu Liping, Huang Liyan, He Dongyun, Dong Xiaomeng, Yang Haihong
The Center for Translational Medicine, National Clinical Research Center of Respiratory Disease, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou 510120, China.
Department of Thoracic Oncology, State Key Laboratory of Respiratory Diseases, National Clinical Research Center of Respiratory Disease, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou 510120, China.
Transl Lung Cancer Res. 2019 Dec;8(6):838-846. doi: 10.21037/tlcr.2019.10.19.
Genetic alteration profile of epidermal growth factor receptor () mutant resected non-small cell lung cancer (NSCLC) and its relationship with clinical outcomes remains to be illustrated and genetic biomarkers that can predict recurrence need to be figured out.
Clinicopathological and follow-up information were collected for 99 -mutant resected NSCLC. Tumor sections were collected for genetic alteration detection. Targeted next-generation sequencing (NGS) was performed to detect somatic mutations within each sample using a 285-gene panel on the Ion Torrent platform.
Concurrent driver gene mutations were detected in 86 participants. Adjuvant therapy was a positive factor in disease-free survival (DFS) period, and patients receiving tyrosine kinase inhibitors (TKIs) gained the longest DFS. A total of 34 concurrent mutant driver genes were found. The median number of mutated driver genes for each sample was 2 (range, 0-12). and were the most frequent concurrent mutant driver genes with rates of 53.54% and 25.25% respectively. The number of concurrent mutant genes did not have a significant effect on recurrence. Multivariable analysis found that mutations of (P=0.021), (P=0.002), (P<0.001), (P=0.015), (P=0.042), (P=0.006), and wildtype (P=0.032), (P=0.012), (P=0.035) were independent risk factors for the recurrence of resected mutant NSCLC.
and was the most common concurrent mutant driver gene. Mutations of , and wildtype were independent risk factors for the recurrence of resected mutant NSCLC.
表皮生长因子受体（）突变的可切除非小细胞肺癌（NSCLC）的基因改变图谱及其与临床结局的关系仍有待阐明，且需要找出能够预测复发的基因生物标志物。
收集99例经手术切除的 - 突变NSCLC患者的临床病理和随访信息。采集肿瘤切片用于基因改变检测。使用Ion Torrent平台上的285基因panel进行靶向二代测序（NGS），以检测每个样本中的体细胞突变。
86名参与者检测到同时存在的驱动基因突变。辅助治疗是无病生存期（DFS）的一个积极因素，接受酪氨酸激酶抑制剂（TKIs）治疗的患者DFS最长。共发现34个同时突变的驱动基因。每个样本中突变驱动基因的中位数为2（范围0 - 12）。 和 是最常见的同时突变驱动基因，发生率分别为53.54%和25.25%。同时突变基因的数量对复发没有显著影响。多变量分析发现， （P = 0.021）、 （P = 0.002）、 （P < 0.001）、 （P = 0.015）、 （P = 0.042）、 （P = 0.006）以及野生型 （P = 0.032）、 （P = 0.012）、 （P = 0.035）是经手术切除的 突变NSCLC复发的独立危险因素。
和 是最常见的同时突变驱动基因。 、 以及野生型 的突变是经手术切除的 突变NSCLC复发的独立危险因素。
