晚期非小细胞肺癌中淋巴结转移与EGFR突变的相关性及对患者预后的影响

目的 探索晚期非小细胞肺癌中淋巴结转移与表皮生长因子受体(EGFR)突变状态的相关性及对患者总生存的预测价值.方法 回顾性分析1358例晚期非小细胞肺癌患者的临床病理资料和随访资料,Kaplan-Meier法进行疾病总生存率(OS)分析,并采用Log-rank检验进行比较.结果 吸烟与不吸烟患者、EGFR突变型与EGFR野生型患者、M1a与M1b患者的N分期间,差异均有统计学意义(P﹤0.05);淋巴结转移阴性或仅有肺门淋巴结转移患者(N0~1)多为不吸烟、EGFR突变型及M1a患者.Kaplan-Meier生存分析结果 显示,N0~1组患者总生存时间明显长于N2~3组患者(P﹤0.001).按EGFR因素分层分析显示,N0~1/EGFR突变组患者的预后最好,N2~3/EGFR野生组患者的预后最差,而N0~1/EGFR野生组与N2~3/EGFR突变组患者的生存时间比较,差异无统计学意义(P=0.642);按M分期分层分析显示,N0~1/M1a组患者的预后最好,N2~3/M1b组患者的预后最差,而N0~1/M1b组与N2~3/M1a组患者的生存时间比较,差异无统计学意义(P=0.450).结论 非小细胞肺癌中淋巴结分期与EGFR突变状态有关,N0~1期患者预后明显优于N2~3期患者,同时EGFR状态及M分期可进一步影响不同淋巴结分期患者的预后.     

靶向高通量测序在非小细胞肺癌中的临床应用

  目的  对8种与非小细胞肺癌（non-small cell lung cancer,NSCLC）个性化治疗高度相关的驱动基因进行检测,分析基因变异与临床病理特征的关系。  方法  收集天津医科大学肿瘤医院2016年6月至2017年8月212例NSCLC患者样本,对EGFR、KRAS、BRAF、ALK、MET、ERBB2、ROS1、RET 8种基因进行高通量测序。  结果  8种基因中EGFR基因变异率高达52.8%,其次为KRAS（8.5%）、ALK（8.0%）、ERBB2（6.1%）、MET（3.8%）、BRAF（1.4%）、RET（0.9%）、ROS1（0.9%）,75%样本检出至少1个驱动基因变异,驱动基因变异间呈现强烈互斥。最常见的EGFR突变为19外显子缺失和L858R突变,EGFR T790M突变与前面两个突变位点伴随出现。19外显子缺失患者携带非EGFR T790M突变比例低于L858R突变患者携带非EGFR T790M突变比例（P=0.04）。15.2%EGFR突变伴EGFR扩增,携带EGFR扩增且EGFR突变率 > 40%患者比例高于无EGFR扩增且EGFR突变率 > 40%患者（P < 0.01）。女性、不吸烟、腺癌患者易发生EGFR特别是EGFR敏感突变（P < 0.01）。肺腺癌（P=0.013）、临床分期晚（P=0.048）、淋巴结转移（P=0.027）患者携带EGFR扩增比例高。男性（P=0.009）、左侧肺癌（P=0.048）,吸烟患者（P=0.037）KRAS突变发生率较高。携带非KRAS突变、ALK融合的患者更年轻（P=0.005,P=0.031）,而携带KRAS突变患者年龄较高（P=0.055）。  结论  高通量测序可同时高效检测NSCLC患者中8种与靶向治疗相关驱动基因的变异谱,为临床医生的个体化诊疗提供参考,以多基因为基础的高通量测序为NSCLC诊疗提供更多的可能性。      

湖南地区肺腺癌EGFR基因突变及突变位点的临床病理特点

目的:研究湖南地区肺腺癌EGFR基因突变及突变位点的临床病理特点。方法:收集中南大学湘雅医院胸外科肺腺癌患者组织标本134例,采用扩增阻滞突变系统(ARMS)检测EGFR外显子18、19、20、21号突变状态。结果:134例肺腺癌患者中EGFR突变68例,突变率50.7%。其中男、女突变率分别为40.7%、58.7%（P=0.039）,吸烟、不吸烟患者突变率分别为30.6%、62.4%（P=0.000）。外显子18、19、20、21号突变分别为2例（2.9%）、32例（47.1%）、3例（4.4%）、31例（45.6%）。19、21号外显子突变在肺癌TNM分期中I-II期与III-IV期比较有差异,21号外显子突变在I-II期多见,P=0.048。结论:湖南地区肺腺癌中女性、不吸烟患者EGFR突变率高,EGFR突变以19、21号外显子为主,19与21号外显子突变相比较,21号外显子突变在肺癌TNM分期中I-II期多见。     

绵阳北川羌族肺腺癌患者EGFR基因突变特点的研究

目的：研究绵阳北川羌族肺腺癌患者EGFR突变的特点。方法：采用ARMS法对120例羌族肺腺癌组织进行EGFR突变检测,并分析EGFR突变与临床特征的关系。结果：120例肺腺癌患者中,57例携带EGFR突变,突变率47.5%,以L858R突变和19号外显子缺失为主,分别占52.6%（30例）和42.1%（24例）。在120例患者中,男、女突变率分别为60.7% 、35.9%,差异有统计学意义（P =0. 016）,而吸烟、不吸烟患者突变率分别为31.0%、56.4%,差异亦有统计学意义 (P =0. 012）。以患者年龄、肿瘤大小、淋巴结有无转移、肿瘤分化程度、分期对患者分组后分析发现,EGFR突变率的差异均无统计学意义（P﹥0. 05）。结论：绵阳羌族肺腺癌的EGFR突变率较高,以L858R突变和19号外显子缺失为主,EGFR突变率与性别、吸烟状况有关,而与患者年龄、肿瘤大小、淋巴结有无转移、肿瘤分化程度、分期均无明显相关性。     

不同病理分期肺腺癌EGFR、ALK基因状态与EGFR-TKI靶向治疗的关系

目的：探讨不同病理分期肺腺癌表皮生长因子受体（EGFR）、间变性淋巴瘤激酶（ALK）基因状态与EGFR-TKI靶向治疗的关系。方法选取接受EGFR-TKI靶向治疗的肺腺癌患者87例,检测患者EGFR、ALK基因状态,分析其与临床特征及疗效的关系。结果 EGFR突变患者与非EGFR突变患者年龄、性别及TNM分期比较,差异无统计学意义（P﹥0.05）;EGFR突变患者吸烟比例低于非EGFR突变患者（26.32%vs 48.98%）,差异有统计学意义（P﹤0.05）;ALK阳性与ALK阴性患者的性别、吸烟比例及TNM分期比较,差异均无统计学意义（P﹥0.05）;ALK阳性患者平均年龄低于ALK阴性患者,差异有统计学意义（P﹤0.05）;EGFR突变患者EGFR-TKI治疗的总缓解率优于ALK阳性和WT/WT患者,差异均有统计学意义（P﹤0.05）;ALK阳性患者和WT/WT患者治疗疗效比较,差异无统计学意义（P﹥0.05）。结论肺腺癌患者应首先进行EGFR检测,如有条件可同时检测EGFR突变和ALK重排;EGFR突变患者应首选EGFR-TKI靶向治疗。     

肺腺癌EGFR突变及与TTF-1、CK7、NapsinA蛋白表达的关系

摘 要：［目的］ 探讨新分类肺腺癌中EGFR突变情况与TTF-1、CK7、NapsinA表达的关系及临床意义。［方法］ 收集南京市胸科医院2013~2015年外科手术切除标本307例,根据2011年IASLC/ATS/ERS肺腺癌国际多学科新分类进行病理分型,用ARMS法检测EGFR基因,用免疫组化法检测TTF-1、CK7、NapsinA蛋白的表达。［结果］ EGFR在肺腺癌中突变率为51.1%(157/307),19外显子缺失突变(del)和21外显子（L858R）突变率分别为43.9%和51.0%,乳头和实体型腺癌突变率分别为65.4%和 29%。EGFR突变与性别、吸烟及肺腺癌病理分型均有相关性（P<0.001）,与TTF-1、CK7蛋白表达有相关性（均P<0.05）,与NapsinA无相关性（P=0.108）。［结论］ EGFR基因突变多见于女性非吸烟患者,较少见于实体为主型肺腺癌,突变以21（L858R）和19外显子缺失突变为主,TTF-1蛋白表达及肺腺癌病理分型对EGFR突变有着较好的提示作用。     

GPER1在EGFR突变的肺腺癌中的表达

  目的  探讨肺腺癌中表皮生长因子受体（epidermal growth factor receptor,EGFR）与G蛋白偶联雌激素受体1（G-protein cou? pled estrogen receptor 1,GPER1）/GPR30之间的关系。  方法  采用免疫组织化学方法检测83例术后肺腺癌组织样本中GPER1的表达,同时收集患者的临床病理资料,采用二代基因测序方法检测相应组织中EGFR基因突变状态,并分析GPER1与EGFR之间的相关性,Western blot检测EGFR野生型肺腺癌细胞A549,EGFR突变型肺腺癌细胞PC-9以及使用吉非替尼处理的PC-9细胞的GPER1表达水平。  结果  GPER1的阳性表达与患者性别、年龄、肿瘤大小、吸烟、分化程度无显著性差异（均P > 0.05）;EGFR突变与肿瘤TNM分期无显著性差异（P=0.542）;GPER1阳性表达与EGFR突变呈正相关（P=0.003）;GPER1在Ⅲ、Ⅳ期肺腺癌中较Ⅰ、Ⅱ期高表达（P=0.008）;在PC-9细胞中使用吉非替尼抑制EGFR活性引起GPER1表达下调。  结论  GPER1在EGFR基因突变型的肺腺癌中的表达高于EGFR野生型肺腺癌,GPER1的表达可能受EGFR活性调控。      

18F-FDG PET-CT显像在预测不可切除肺腺癌EGFR突变的价值

目的 探讨氟脱氧葡萄糖F18正电子发射计算机断层显像（18F-FDG PET-CT）在不可切除肺腺癌表皮生长因子受体（EGFR）突变中的预测价值。方法 收集2012年4月至2016年5月151例ⅢB期或Ⅳ期的肺腺癌患者的临床资料,所有患者治疗前均行18F-FDG PET-CT检查及EGFR突变检测。采用受试者工作特征（ROC）曲线计算最大标准摄取值（SUVmax）的截断值,Logistics回归分析影响EGFR突变的预测因素。结果 ROC曲线分析显示,SUVmax预测EGFR突变的截断值为10.28。151例不可切除肺腺癌患者中,68例（45.0％）为EGFR突变型。单因素分析结果显示,性别、吸烟、癌胚抗原、SUVmax与EGFR突变有关（P＜0.05）,而CT征象包括空洞、空气支气管征、密度、分叶、胸膜凹陷与EGFR突变无关（P＞0.05）。Logistic多因素分析显示,吸烟和SUVmax是预测EGFR突变的独立因素（P＜0.05）。结论 SUVmax是18F-FDG PET-CT预测不可切除肺腺癌EGFR突变的独立因素,在预测EGFR突变中具有一定的参考价值。     

晚期肺腺癌EGFR基因突变状态检测及分析

目的分析晚期肺腺癌表皮生长因子受体（epidermal growth factor receptor,EGFR）基因突变率及其与临床特征的相关性。方法收集2010-09-07-2011-07-21首都医科大学附属北京胸科医院收治的晚期初治肺腺癌患者102例,有可供检测的肿瘤组织标本。利用扩增受阻突变系统（amplification refractory mutation system,ARMS）进行EGFR基因突变检测,统计分析EGFR基因突变状态和临床特征的相关性。结果 102例晚期肺腺癌组织中,共检测到EGFR基因突变55例（53.9%）,其中18外显子突变1例（1.0%）,19外显子突变25例（24.5%）,20外显子突变2例（2.0%）,21外显子突变26例（25.5%）,同时存在19和20外显子突变1例（1.0%）。Ⅳ期患者EGFR基因突变率为57.6%（53/92）,高于ⅢB期患者20.0%（1/10）,差异有统计学意义,P=0.041;女性患者EGFR基因突变率56.9%（33/58）高于男性患者的50.0%（22/44）,不吸烟患者EGFR基因突变率58.1%（36/62）高于吸烟患者的36.0%（9/25）,〈65岁患者EGFR基因突变率56.8%（42/74）高于≥65岁患者的46.4%（13/28）,但差异均无统计学意义,P〉0.05。不同取材部位及取材方法之间EGFR基因突变率差异无统计学意义,P〉0.05。结论晚期肺腺癌EGFR基因突变率以Ⅳ期、女性和不吸烟患者较高,但性别及吸烟状态之间的差异无统计学意义。不同的肿瘤活检部位及活检方法之间EGFR基因突变率并无差异。     

非小细胞肺癌驱动基因检测及其与临床病理特征的相关性

目的:探讨非小细胞肺癌(NSCLC)驱动基因的变化情况及其与临床病理特征的相关性。方法:回顾性分析我院2016年01月至2020年07月NSCLC患者607例临床及病理学特征资料,采用扩增阻滞突变系统(ARMS)荧光PCR法检测EGFR突变,RT-PCR法检测ALK、ROS1基因融合,荧光原位杂交法（FISH）检测MET基因扩增。结果:607例NSCLC组织中325例(53.5%,325/607)检测到基因改变,分别为EGFR突变（45.5%,276/607）、ALK融合（5.1%,31/607）、ROS1融合（1.3%,8/607）和MET扩增（2.8%,17/607）,EGFR双位点突变15例（2.5%,15/607）,双驱动基因改变7例（1.2%,7/607）,其中EGFR突变与ALK融合阳性共存3例,EGFR突变与ROS1融合阳性共存2例,EGFR突变与MET扩增阳性共存2例。EGFR在女性、非吸烟、腺癌患者中突变率更高（P＜0.05）,EGFR突变更容易发生在以贴壁为主型、腺泡为主型、乳头为主型、微乳头为主型腺癌中（P＜0.05）;ALK融合多见于女性、年轻、非吸烟、实性为主型的腺癌患者（P＜0.05）;MET基因扩增在老年男性患者中发生率更高（P＜0.05）。结论:在NSCLC中EGFR突变率较高,驱动基因联合突变不容忽视,基因分型对临床治疗具有重要指导意义。     

Molecular markers and changes of computed tomography appearance in lung adenocarcinoma with ground-glass opacity

BACKGROUND: High-resolution computed tomography (HRCT) of lung adenocarcinoma at early stage shows pure ground-glass opacity (GGO) and most cases of pure GGO remain stable during follow-up. There is no consensus on the strategy for follow-up. Identification of the molecular mechanisms that are associated with the natural history of lung adenocarcinoma should provide useful information. METHODS: Twenty-three lung adenocarcinomas that were followed-up for more than 6 months pre-operatively by HRCT were included in this study. Patterns of radiological changes during the follow-up period were classified into three groups; type 1, pure GGO without consolidation; type 2, appearance or increase in consolidation within pure GGO; type 3, consolidation without pure GGO. Mutational analysis of the epidermal growth factor receptor (EGFR) and K-ras genes and immunohistochemical staining of p53 protein were performed. RESULTS: EGFR mutations were found in 17 cases (74%), and there was no K-ras mutation. Positive staining of p53 was found in 8 cases (35%). As for radiological findings during the follow-up period, the frequencies of EGFR mutations and positive p53 staining were 67 and 0% in type 1 (n = 9), 89 and 44% in type 2 (n = 9) and 60 and 80% in type 3 (n = 5). CONCLUSIONS: EGFR mutations were frequently found in lung adenocarcinoma with GGO on HRCT in this study. Inactivation of p53 may be associated with the appearance of central consolidation within pure GGO on HRCT which reflects invasive features and may be useful as a molecular marker during the follow-up of pure GGO.     

A correlation between EGFR gene mutation status and bronchioloalveolar carcinoma features in Japanese patients with adenocarcinoma

BACKGROUND: The presence of epidermal growth factor receptor (EGFR) mutations in gefitinib-naive lung cancer patients has been reported to be higher in females, in non-smokers, in Japanese, and in adenocarcinoma patients, especially in bronchioloalveolar carcinoma (BAC). To further investigate the prevalence of EGFR mutations in relation to pathological factors, we evaluated EGFR mutations in series of Japanese adenocarcinoma patients who had never been treated with gefitinib. METHODS: In the previous studies, we examined mutation status in the tyrosine kinase domain of EGFR, exon18 through exon21, in 112 primary lung adenocarcinoma samples. Using these data, adenocarcinomas were histologically classified according to the presence or absence of bronchioloalveolar components. RESULTS: Among 112 patients, 48 had adenocarcinoma with BAC components. Those with adenocarcinomas with BAC components had higher frequency of EGFR mutation (28/48, 58%) than those with non-BAC adenocarcinoma (24/64, 37%, P = 0.036). Male patients had the same trend; 12/23 (52%) male patients with adenocarcinoma with BAC components and 10/47 (21%) of those with non-BAC adenocarcinoma had EGFR mutation (P = 0.0135) but there was no correlation between the EGFR mutation status and with/without BAC components in 42 female patients (P = 0.30). Among 11 male non-smokers, patients with adenocarcinoma with BAC components had a tendency to have EGFR mutation more frequently than those with non-BAC adenocarcinoma (P = 0.061). In clear contrast, the frequency of EGFR mutation did not differ significantly between male smoker patients with adenocarcinoma with BAC components and those with non-BAC. Among patients with adenocarcinoma with BAC components, those with adenocarcinoma with EGFR gene mutation had a significantly better 5 year survival than those with adenocarcinoma with wild-type (85.7 versus 46.0%, P = 0.0017). CONCLUSIONS: Adenocarcinomas with BAC components in male non-smokers seem to predict the presence of EGFR mutation. Half of female adenocarcinoma patients with EGFR mutation exhibit adenocarcinomas with non-BAC suggesting a different behavior from those in males. The prognosis of patients with adenocarcinoma with BAC components with EGFR gene mutation is predicted to be better than that of patients with adenocarcinoma with BAC components with wild-type EGFR gene.     

Different epidermal growth factor receptor gene mutations in a patient with 2 synchronous lung cancers

Recently, the frequency of lung adenocarcinoma has been increasing among nonsmokers, though the etiology remains unclear. Mutations of the epidermal growth factor receptor (EGFR) gene are frequently detected in the lung adenocarcinomas seen in nonsmokers. Thus, EGFR mutations can be implicated in carcinogenesis of lung adenocarcinoma. Herein, we report a case of 2 synchronous lung adenocarcinomas composed of 2 distinct pathological subtypes with different EGFR mutations: homozygous deletion in exon 19 in the papillary subtype of adenocarcinoma and a point mutation of L858R in exon 21 in the tubular adenocarcinoma. These findings suggest that specific mutations can occur randomly in the EGFR hot spot, and that these EGFR mutations can contribute to the distinct carcinogenic process of each adenocarcinoma.     

非小细胞肺癌上皮-间质转化与EGFR突变以及临床病理特征之间的关系

目的探讨非小细胞肺癌(NSCLC)上皮-间质转化(EMT)与表皮生长因子受体(EGFR)突变和临床病理特征之间的关系。方法采用免疫组化法检测NSCLC患者癌组织中E-钙黏素和波蛋白的表达情况。采用卡方检验和Logistic回归分析,探讨临床病理特征和EGFR基因型NSCLC中EMT的影响。结果62例NSCLC标本中,上皮表型35.48%(22/62)。EGFR突变NSCLC中,上皮表型显著高于野生型(77.78%vs18.18%;P<0.0001);女性显著高于男性(54.55%vs25%;P=0.02);腺癌高于其他病理类型(39.47%vs29.17%;P=0.4087);不吸烟者稍高于吸烟者(42.42%vs27.59%;P=0.2231);年龄<60岁和年龄≥60岁组差异无统计学意义(43.33%vs28.12%;P=0.211),早期肺癌与晚期肺癌组差异无统计学意义(38.24%vs32.12%;P=0.6178)。结论EGFR突变型、女性、非吸烟者、腺癌倾向于上皮表型,与EGFR酪氨酸激酶抑制剂疗效分布人群的临床特征相一致。     

血清CEA与癌组织标本中TTF-1检测对肺腺癌EGFR突变的预测价值

目的:血清癌胚抗原(CEA)与癌组织标本中甲状腺转录因子-1(TTF-1)检测对肺腺癌表皮生长因子受体(EGFR)突变的预测价值。方法:选取2018年6月至2019年5月本院胸心外科住院部收治的92例经常规病理检查证实肺腺癌患者作为研究对象,根据突变特异性扩增系统(ARMS)聚合酶链反应(RT-PCR)方法检测EGFR突变结果分为EGFR突变组(n=55)和EGFR野生组(n=37),观察两组患者CEA、TTF-1表达情况,不同浓度CEA及与TTF-1联合对EGFR突变的预测价值。结果:EGFR突变组患者血清CEA水平、阳性率均明显高于EGFR野生组(P<0.05);EGFR突变组患者TTF-1阳性率为89.09%,高于EGFR野生组的13.51%(P<0.05);肺腺癌患者血清CEA水平≥5μg/L、≥20μg/L、≥50μg/L EGFR突变率高于<5μg/L患者(P<0.05),五组间EGFR突变率比较差异有统计学意义(P<0.05);血清CEA≥5μg/L对EGFR突变的敏感度、特异性较高;CEA≥5μg/L+TTF-1预测肺腺癌EGFR突变的敏感度、特异性、阳性预测值、阴性预测值、准确度最高。结论:肺腺癌EGFR突变患者血清CEA水平升高,TTF-1阳性率高,当CEA≥5μg/L且TTF-1阳性表达时对肺腺癌EGFR突变的预测率高。     

Radiotherapy in lung adenocarcinoma with brain metastases: effects of activating epidermal growth factor receptor mutations on clinical response.

PURPOSE: Whole-brain radiation therapy (WBRT) has been applied to inoperable brain metastases in lung adenocarcinoma. Recently, an in vitro study showed reduced clonogenic survival of mutant epidermal growth factor receptor (EGFR) lung cancer cell lines in response to ionizing radiation compared with that of the wild type. To elucidate the role of EGFR mutations in radiation treatment, we evaluated the clinical response to WBRT and survival of lung adenocarcinoma patients with brain metastases. EXPERIMENTAL DESIGN: This was a retrospective analysis of 63 patients with brain metastases from lung adenocarcinoma who were treated with WBRT. Demographic data, EGFR mutation status, response to WBRT, and survival data were collected. Clinical response was assessed 1 month after the start of WBRT. Univariate and logistic regression models were used to test potential predictive factors associated with clinical response. Log-rank test and Cox regression were analyzed to identify factors that affected survival. RESULTS: Clinical response to WBRT was observed in 29 patients (46%), with 34 nonresponder patients (54%). Patients with EGFR mutations had higher response rates to WBRT compared with those with the wild-type (54% versus 24%; P = 0.045). Both the administration of EGFR tyrosine kinase inhibitor (P = 0.034) and EGFR mutation (P = 0.029) were independently associated with response to WBRT. In Cox regression analysis, WBRT responder (P = 0.010) and absence of extracranial metastases (P = 0.002) were associated with better survival. CONCLUSIONS: Both the EGFR mutations and the administration of EGFR TKI during WBRT were independent predictors of response to WBRT in brain metastases of lung adenocarcinoma.     

Bronchial and peripheral murine lung carcinomas induced by T790M-L858R mutant EGFR respond to HKI-272 and rapamycin combination therapy

The EGFR T790M mutation has been identified in tumors from lung cancer patients that eventually develop resistance to erlotinib. In this study, we generated a mouse model with doxycycline-inducible expression of a mutant EGFR containing both L858R, an erlotinib-sensitizing mutation, and the T790M resistance mutation (EGFR TL). Expression of EGFR TL led to development of peripheral adenocarcinomas with bronchioloalveolar features in alveoli as well as papillary adenocarcinomas in bronchioles. Treatment with an irreversible EGFR tyrosine kinase inhibitor (TKI), HKI-272, shrunk only peripheral tumors but not bronchial tumors. However, the combination of HKI-272 and rapamycin resulted in significant regression of both types of lung tumors. This combination therapy may potentially benefit lung cancer patients with the EGFR T790M mutation.     

EGFR不同突变亚型与肺腺癌脑转移预后的相关性分析

目的 探讨肺腺癌脑转移患者EGFR不同突变亚型与预后的相关性。方法 回顾分析2010—2015年本院收治的经EGFR基因突变检测的肺腺癌脑转移患者256例临床资料,筛选脑转移的预后影响因素。Kaplan-Meier法计算生存率Logrank法检验和单因素预后分析,Cox模型多因素预后分析。结果 全组患者中位生存期为10.13个月。单因素分析显示性别、EGFR突变状态、19外显子缺失突变、脑转移时KPS评分、靶向治疗与预后有关(P=0.006、0.001、0.010、0.000、0.003),多因素分析显示脑转移时KPS评分、19外显子缺失突变为脑转移患者预后影响因素(P=0.000、0.045)。将全组病例纳入RPA预后分级指数,检验显示差异有统计学意义(P=0.000)。结论 19外显子缺失突变是肺腺癌脑转移患者的预后影响因素,可以考虑将其纳入肺腺癌脑转移瘤预后评分系统。EGFR-TKI使EGFR基因突变肺腺癌脑转移患者生存获益,尤其是19外显子缺失突变患者。