Objective To explore the pathogenesis and prognostic biomarkers of non-small cell lung cancer（NSCLC） in female patients by bioinformatic analysis and functional prediction of potential NSCLC-associated genes. Methods Gene expression profile data for female patients with NSCLC were downloaded from the Gene Expression Omnibus（GEO） database, and differentially expressed genes（DEGs） were identified using limma package. Gene Ontology（GO）, Kyoto Encyclopedia of Genes and Genomes（KEGG） and protein-protein interaction（PPI） analyses were performed for DEGs. The igraph package was used to screen the key DEGs from PPI. The expression pattern of key DEGs were confirmed in Oncomine database and NSCLC cell lines. The Log-rank test was used to assess the association between key DEGs and overall survival. Results A total of 500 DEGs were identified, and GO analysis showed that these genes were mainly involved in cell proliferation, cell migration, and extracellular structure organization（P＜0.05）. The KEGG analysis indicated that these genes were primarily related to ECM-receptor interactions, protein digestion and absorption, and leukocyte transendothelial migration signalling. Three key DEGs [interleukin-6（IL-6）, epidermal growth factor（EGF）, matrix metalloprotein-9（MMP-9）] were screened from the PPI network. The expression of IL-6 was downregulated in NSCLC tissues and cell lines, while EGF and MMP-9 expressions were upregulated. The log-rank test found that IL-6 and EGF were associated with overall survival of female patients with NSCLC. Conclusions In female patients, IL-6（χ~2 =6.90, P=0.009） and EGF（χ~2 =7.73, P=0.005） may be key genes for pathogenesis and prognosis of NSCLC, and represent novel therapeutic targets.

目的 探索采用Runthrough导丝辅助下,结合X线透视技术完成无碘对比剂房间隔穿刺的方法.方法 2021 年 2 月至 10 月在皖南医学院第一附属医院接受导管射频消融治疗的阵发性房颤患者60 例,随机分为常规房间隔穿刺组 30 例和Runthrough导丝辅助房间隔穿刺组 30 例.比较两组患者在房间隔穿刺过程中的总操作时间、透视时间、X线放射剂量,评估安全性.结果 两组患者房间隔穿刺过程中的总操作时间[(1.98±0.29)min比(2.11±0.14)min]、透视时间[(1.83±0.30)min比(1.98±0.14)min]、X线放射剂量[(27.77±3.08)μGy·m2 比(29.13±1.54)μGy·m2]差异均有统计学意义(均P＜0.05).所有患者均无心包填塞、主动脉穿孔等并发症发生.结论 X线透视下Runthrough导丝辅助的房间隔穿刺技术安全、经济、易行、可重复性强,可作为碘对比剂过敏患者房间隔穿刺的一种新方法.

目的 长链非编码RNA是肿瘤细胞影响周围环境的重要方式之一,其机制仍然是目前研究的热点.文中旨在探讨肺腺癌细胞是否通过长链非编码RNA00467诱导巨噬细胞极化,进而促进肺腺癌细胞的增殖.方法 100 ng/mL佛波酯(PMA)处理人THP-1细胞48 h,RT-PCR检测细胞CD68的表达水平.巨噬细胞分别与A549细胞和16HBE细胞共培养,A549细胞与巨噬细胞共培养为实验组,16HBE细胞与巨噬细胞共培养为对照组,共培养实验验证肺腺癌细胞对巨噬细胞极化的影响.RT-PCR实验检测巨噬细胞极化后linc00467表达水平变化.通过慢病毒shRNA敲低A549细胞中linc00467水平并进行巨噬细胞共培养实验,观察巨噬细胞极化情况.随后通过慢病毒shRNA敲低巨噬细胞linc00467水平并分别与A549细胞共培养,MTT实验检测敲低巨噬细胞linc00467水平后对A549细胞增殖能力的影响.结果 实验组CD68mRNA水平(1.95±0.49)较对照组(0.41±0.15)明显增加(P<0.01).肺腺癌细胞组中巨噬细胞IL-12的表达水平(8.27±1.06)较对照组(16.28±2.11)下降(P<0.01);IL-10的表达水平(12.86±2.17)较对照组(7.91±1.85)上升(P<0.01).与对照组(0.42±0.19)相比,A549细胞与巨噬细胞共培养组中巨噬细胞linc00467的表达水平(1.87±0.41)增加(P<0.01).与对照组相比,转染shRNA-linc00467的巨噬细胞组,A549细胞增殖能力显著降低(P<0.01).结论 肺腺癌细胞的linc00467会被巨噬细胞摄取,诱导巨噬细胞极化,进而促进肺腺癌细胞的增殖能力,这为肺腺癌的治疗提供了新的可能的靶点.

Objective: To explore the pathogenesis and prognostic biomarkers of non-small-cell lung cancer (NSCLC) in female patients via a bioinformatic analysis and functional prediction of potential NSCLC-associated genes in females. Methods: Data for female patients with NSCLC were downloaded from the Gene Expression Omnibus (GEO) database, and differentially expressed genes (DEGs) were identified using GEO2R. The DAVID online database was used to perform Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) analyses, and STRING online software was used to perform protein-protein interaction (PPI) analyses. Next, the plug-in (M-CODE) was used to screen the key DEGs; the Oncomine database was analysed for IL6, EGF and MMP9 expression in NSCLC tissues and normal lung tissues and the Kaplan-Meier plotter was used to perform prognostic analyses of key DEGs. Finally, RT-PCR was used to verify the expression of key DEG in NSCLC cells. Results: A total of 500 DEGs were screened, and the functional and pathway enrichment analysis showed that these genes were mainly involved in cell proliferation, cell migration, and vasculature development regulation. The KEGG analysis showed that the pathways were primarily related to ECM-receptor interactions, protein digestion and absorption, and leukocyte transendothelial migration signalling. Three key DEGs were obtained by the PPI network analysis: IL6, EGF and MMP9. The expression of IL6 was low in NSCLC tissues, while that of EGF and MMP9 was high. IL6 and EGF may be biomarkers for predicting the prognosis of female patients with NSCLC. Compared with human bronchial epithelial cell line (16HBE), EGF and MMP-9 were high expressed in NSCLC cells. Conclusion: In female patients, IL6, EGF and MMP9 may be research targets for characterizing the pathogenesis of NSCLC, and IL6 and EGF may be biomarkers for predicting the prognosis of this cancer.

Background Janus-activated kinase-1 ( JAK1 ) plays a crucial role in many aspects of cell proliferation, differentiation, apoptosis and immune regulation. However, correlations of JAK1 with prognosis and immune infiltration in NSCLC have not been documented. Methods We analyzed the relationship between JAK1 expression and NSCLC prognosis and immune infiltration using multiple public databases. Results JAK1 expression was significantly decreased in NSCLC compared with that in paired normal tissues. JAK1 overexpression indicated a favourable prognosis in NSCLC. In subgroup analysis, high JAK1 expression was associated with a preferable prognosis in lung adenocarcinoma (OS: HR, 0.74, 95% CI from 0.58 to 0.95, log-rank P = 0.017), not squamous cell carcinoma. In addition, data from Kaplan–Meier plotter revealed that JAK1 overexpression was associated with a preferable prognosis in male and stage N2 patients and patients without distant metastasis. Notably, increased levels of JAK1 expression were associated with an undesirable prognosis in patients with stage 1 (OS: HR, 1.46, 95% CI from 1.06 to 2.00, P = 0.02) and without lymph node metastasis (PFS: HR, 2.18, 95% CI from 1.06 to 4.46, P = 0.029), which suggests that early-stage NSCLC patients with JAK1 overexpression may have a bleak prognosis. Moreover, multiple immune infiltration cells, including NK cells, CD8 + T and CD4 + T cells, B cells, macrophages, neutrophils, and dendritic cells (DCs), in NSCLC were positively correlated with JAK1 expression. Furthermore, diverse immune markers are associated with JAK1 expression. Conclusions JAK1 overexpression exhibited superior prognosis and immune infiltration in NSCLC.

目的 探讨基于ESA(engage—投入、study—学习、activate—活用)的翻转课堂教学模式在呼吸内科实践教学中的应用效果.方法 选取在皖南医学院弋矶山医院呼吸内科实习的临床医学专业实习医生80名,随机分为试验组和对照组,每组40名.在授课内容相同的情况下,试验组实习医生采用基于ESA的翻转课堂教学模式,对照组采用传统教学模式,待实习结束后,比较两组学生的教育处调查评分和出科考核成绩,同时采用问卷调查方式对基于ESA的翻转课堂教学模式的内容进行评价.结果 出科时,基于ESA的翻转课堂教学组学生的教育处调查评分和考核成绩均高于对照组(P<0.05),且试验组医学生对基于ESA的翻转课堂教学模式的评价认可度均超过90％.结论 基于ESA的翻转课堂教学模式应用在呼吸内科实践教学中,不但可以提高临床实习医生的教学满意度和出科考核成绩,而且实习医生对新的教学模式认可度较好.

目的:探索基于小规模限制性在线课程(SPOC)的翻转课堂教学模式在呼吸内科实践教学中的运用.方法:选取在弋矶山医院呼吸内科实习的临床医学专业学生80名,随机分为基于SPOC的翻转课堂教学组和传统教学组,每组40名.在授课内容相同的情况下,比较两组教学效果和学生测验成绩的差异.结果:基于SPOC的翻转课堂教学组的学生对教学满意度高于传统教学组,学生理论知识和临床病例分析测验成绩也有提升,差异具有统计学意义(P<0.05).结论:在呼吸内科临床实践教学中,应用基于SPOC的翻转课堂教学模式可提高学生的学习兴趣和学习成绩,取得较好的教学效果.

Background: Lung adenocarcinoma (LAD) is the most prevalent type of lung cancer. The abnormal expression of UDP-N-acetylglucosamine pyrophosphorylase 1 (UAP1) has been reported to be involved in many biological processes of cancer cells, but the expression of UAP1 in LAD is unclear. Methods: Bioinformatics was used to analyse the LAD gene expression data and related clinical data in the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. DAVID6.8 was used to perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genome (KEGG) signal pathway enrichment analyses of UAP1 expression-related genes. The STRING database was used to analyse protein-protein interaction (PPI) networks. RNA isolation and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assay were used to detect the expression of UAP1 in tissues and blood samples. Results: We found that UAP1 was upregulated in LAD tissues and correlated with poor clinical outcome. GO analysis showed that these genes were enriched in biological processes and functions including intracellular transport, cellular protein catabolic process, and mitochondria (P<0.05). The KEGG pathway analysis showed that these genes were mainly involved in the signalling pathways of amino sugar and nucleotide sugar metabolism, the aminoacyl-tRNA biosynthesis signalling pathway, and protein export (P<0.05). The PPI analysis showed that EPRS, COPB1, CCT3, ALDH18A1 and ARF1 genes had marked or potential interaction with UAP1 (P<0.01). In addition, UAP1 expression was upregulated in LAD tissues compared to normal tissues. High levels of UAP1 expression were associated with larger tumour sizes and later TNM stages. RT-qPCR detection in serum further showed that UAP1 expression was upregulated in the plasma of LAD patients compared to that of healthy volunteers. High expression of UAP1 in serum suggests a poor prognosis for LAD patients. Conclusion: UAP1 could be a novel diagnostic biomarker and a promising therapeutic target for LAD.

目的:探讨敲降长链非编码RNA00467(long intergenic non-coding RNA00467,linc00467)对肺腺癌(lung adenocarcinoma,LAD)患者预后的影响及其机制.方法:收集LAD患者和健康志愿者血清样本,采用定量逆转录PCR(qRT-PCR)方法检测LAD患者和健康志愿者血清中linc00467的表达水平.绘制ROC曲线检测linc00467在LAD中的诊断效能.通过Kaplan-Meier生存曲线和对数秩检验分析患者总生存期(overall survival,OS).使用细胞增殖测定法和裸鼠皮下瘤实验来证实敲降linc00467表达在体外和体内对肿瘤发生的影响.结果:与健康志愿者相比,LAD患者血清中的linc00467表达上调,并且linc00467在肿瘤直径大于3 cm的LAD患者、有淋巴结转移和晚期LAD患者血清中的表达水平明显上调(P=0.038、P=0.018和P=0.019).血清中高表达的linc00467提示LAD患者预后较差,多因素分析表明linc00467的表达可以作为LAD总生存期的独立预后因素.功能实验表明,敲降linc00467表达可以在体外和体内抑制LAD细胞增殖.结论:研究表明linc00467参与了LAD的发生发展,并且linc00467可能是一种新型的诊断和预后生物标志物,也是LAD的潜在治疗靶标.

Abstract Geranylgeranyl diphosphate synthase (GGPPS) is an enzyme that catalyzes the synthesis of geranylgeranyl pyrophosphate (GGPP). GGPPS is implicated in many disorders, but its role in idiopathic pulmonary fibrosis (IPF) remains unclear. This study aimed to investigate the role of GGPPS in IPF. We established bleomycin-induced lung injury in a lung-specific GGPPS-deficient mouse (GGPPS−/−) and detected GGPPS expression in lung tissues by Western blot and immunohistochemistry analysis. We found that GGPPS expression increased during lung injury and fibrosis in mice induced by bleomycin, and GGPPS deficiency augmented lung fibrosis. GGPPS deficiency activated lung fibroblast by facilitating transforming growth factor β1 while antagonizing bone morphogenetic protein 4 signaling. Notably, the supplementation of exogenous GGPP mitigated lung fibrosis in GGPPS−/− mice induced by bleomycin. In conclusion, our findings suggest that GGPPS provides protection against pulmonary fibrosis and that the restoration of protein geranylgeranylation may benefit statin-induced lung injury.

Long non-coding RNAs (lncRNAs) have been identified to serve an important role in the occurrence, development and metastasis of tumours. However, the role of linc00467 in lung adenocarcinoma (LAD) is unclear. In the present study, it was demonstrated that linc00467 expression was upregulated in human lung tumour tissues compared with normal tissues. In addition, high levels of linc00467 expression were associated with larger tumour sizes and later TNM stages. Functional experiments suggested that linc00467 promoted LAD cell proliferation, migration and invasion, and inhibited apoptosis in vitro. Knockdown of linc00467 altered the expression of downstream genes, including HtrA serine peptidase 3 (HTRA3), and RNA immunoprecipitation and chromatin immunoprecipitation assays indicated that linc00467 recruited EZH2 to the HTRA3 promoter to inhibit its expression. Taken together, the results of the present study indicated that linc00467 served an oncogenic role in LAD tumourigenesis, suggesting that it may be used as a novel diagnostic biomarker and therapeutic target for LAD.

Introduction: Most non-small-cell lung cancer (NSCLC) patients who exhibit good clinical responses to EGFR-tyrosine kinase inhibitors (EGFR-TKIs) will inevitably develop disease progression. Herein, through next-generation sequencing (NGS), we aimed to investigate three new disease-progression modes of NSCLC patients after EGFR-TKI treatment. Materials and Methods: Patients with sensitive EGFR-mutations who acquired resistance to EGFR-TKIs and whose tissues were subjected to post-progression NGS were enrolled. The clinical characteristics, progression-free survival (PFS), genomic alterations and expression of EGFR-mutations among the three disease-progression modes were retrospectively analyzed. Results and Conclusion: The sites of disease progression were as follows: primary foci in 19.5% (8/41) (Mode 1), metastatic foci in 31.7% (13/41) (Mode 2), and both primary and metastatic foci in 48.8% (20/41) (Mode 3). The median PFS in Mode 1 was 6 months (95% CI 1-8), which was significantly shorter than the 11 months (95% CI 8-14) in Mode 2 and the 10 months (95% CI 3-16) in Mode 3 (p = 0.0084). The expression of Del19 was significantly different among the three modes (p = 0.02). The numbers and species of mutant genes in Mode 3 were obviously greater than those in Modes 1 and 2, and no gene amplifications were observed in Mode 2. Mutations in the TP53 gene were the most frequent genetic alteration found in our study, and these accounted for 48.8% (20/41) of all alterations. TP53 mutations in Mode 1 were mainly in exons 6 and 8, while in Mode 2 and Mode 3, all mutations were located from exon 4 to exon 8. A significant benefit in PFS was observed in the metastatic foci progression mode and in the dual primary and metastatic foci progression mode rather than in the primary foci progression mode, which had significant value in the design of therapeutic strategies.

目的:探讨循环肿瘤DNA(circulating tumor DNA,ctDNA)鉴定的EGFR基因20位外显子T790M突变状态与晚期肺腺癌(lung adenocarcinoma,LUAD)患者一线使用EGFR-TKI获得性耐药和预后的相关性.方法:回顾性分析2012年1月至2016年1月南京总医院一线使用EGFR-TKI获得性耐药的晚期LUAD患者93例,按照QIAamp循环核酸试剂盒说明提取外周血ctDNA,采用二代测序(nextgeneration sequencing,NGS)的方法对ctDNA中T790M突变进行鉴定,分析其与临床特征和预后的相关性.结果:在93例一线使用EGFR-TKI获得性耐药的晚期LUAD患者,T790M阳性突变率为52.7％(49/93),T790M突变与晚期LUAD患者的年龄、临床分期、组织学亚型、ECOG评分、初始EGFR突变类型、EGFR-TKI种类差异均无统计学意义(P＞0.05);但与性别、吸烟史、EGFR-TKI耐药后进展类型、EGFR-TKI耐药后血CEA水平、EGFR-TKI耐药后治疗方案比较差异有统计学意义(P＜0.05),EGFR-TKI耐药后血CEA预测T790M阳性的cut-off值为90.1 μg/L,其中敏感度44.9％、特异度90.9％,曲线下面积0.639(95％CI 0.526～0.752);T790M阳性突变患者的中位无进展生存期(progression-free survival,PFS)和总生存期(overall survival,OS)分别为12.4,29.5个月,均较T790M突变阴性的6.2,18.1个月显著延长(P＜0.001);Cox单因素和多因素回归分析均提示T790M突变阳性是PFS(RR=0.302,95％CI 0.162～0.560;P＜0.001)和OS (RR=0.422,95％CI 0.250～0.715;P=0.001)的独立影响因素.结论:T790M突变与晚期LUAD患者的性别、吸烟史、EGFR-TKI耐药后进展类型、EGFR-TKI耐药后血CEA水平、EGFR-TKI耐药后治疗方案有关,同时是PFS和OS的独立影响因素.

目的 探讨肝激酶(LK)B1基因表达水平与非小细胞肺癌(NSCLC)患者的临床病理特征及与预后的相关性.方法 应用实时荧光定量-聚合酶链式反应(RT-PCR)和Western印迹法检测LKB1基因mRNA和蛋白表达,并结合23例NSCLC临床资料进行分析.结果 LKB1基因在癌组织和癌旁正常组织均有表达,癌组织表达明显低于癌旁正常组织(P<0.05).LKB1基因在鳞癌和腺癌表达无统计学差异(P>0.05).LKB1表达水平与分化程度相关(P<0.05),与患者年龄、临床分期、肿瘤大小不相关(P>0.05).LKB1基因mRNA低表达组中位无进展生存期(PFS)〔8.20(95％CI:6.29～10.11)个月〕显著低于高表达组〔16.57(95％CI:11.20～21.94)个月〕(P<0.05).LKB1基因蛋白低表达组PFS〔9.07(95％CI:5.80～12.34)个月〕显著低于高表达组〔15.36(95％CI:12.52～18.20)个月〕(P<0.05).结论 LKB1基因表达水平与NSCLC组织分化程度相关,且LKB1低表达可能提示预后不良.

目的:探讨外周血中血小板/淋巴细胞比值(PLR)在肺腺癌诊断中的价值.方法:收集80例肺腺癌患者和100例健康对照者外周血中PLR、中性粒细胞/淋巴细胞比值(NLR)、淋巴细胞/单核细胞比值(LMR)及血清癌胚抗原(CEA),观察外周血PLR与肺腺癌临床病理特征的相关性,运用受试者工作特征(ROC)曲线评价PLR在肺腺癌患者中的诊断效能.结果:与健康体检者相比较,肺腺癌患者PLR值升高,而NLR、LMR在肺腺癌患者和健康对照组间差异无统计学意义.肺腺癌患者PLR表达水平与患者吸烟及TNM分期具有相关性(P=0.025和P=0.039),ROC曲线结果显示,采用PLR诊断肺腺癌的曲线下面积(AUC)为0.752,灵敏度为0.600,特异度为0.830,节点值为134.840,95％CI:0.677～0.825;采用CEA诊断肺腺癌的AUC为0.753,灵敏度为0.563,特异度为0.880,节点值为4.375,95％CI:0.679～0.827;PLR和CEA联合检测诊断肺腺癌的AUC为0.861,灵敏度为0.750,特异度为0.850,95％CI:0.803～0.919;结论:PLR表达水平具有初步诊断肺腺癌的价值,且诊断能力不亚于CEA,两者联合检测可以提高诊断的准确性,同时PLR表达水平与肺腺癌患者的吸烟状态及TNM分期具有相关性.

Objective: To observe the effects of simvastatin on transforming growth factor-β1 (TGF-β1) expression in the lung tissue of asthmatic mice with airway remodeling. Methods: A total of 60 SPF grade female BALB/C mice were randomized into groups of asthma, simvastatin administration, and control (n = 20 for each group). Pathological changes of the lung tissues and airways were observed and compared among groups of mice. Image analysis software was used to measure the internal wall area (WAi), smooth muscle area (WAm) and the perimeter of basement membrane (Pbm) in bronchial lung tissues, and real time PCR and Western blot were used to determine the expression levels of TGF-β1mRNA and protein in the lung tissues. Results: Pathological change was the severest in mice in asthma group. Although mice in the simvastatin administration group had severer pathological change than the controls, yet the change was minor compared to mice in the asthma group. Mice in the asthma group had thicker bronchial wall and smooth muscle layer as well as higher TGF-β1mRNA expression and protein level in the lung tissues than those in control group. The difference was statistically significant. Conclusion: Simvastatin may inhibit airway remodeling through reducing TGF-β1 expression in the lung tissues.

目的 探讨新辅助化疗联合肺癌根治术在肺癌治疗中的应用效果.方法 选取我院收治的肺癌患者82例作为研究对象.将入选的患者随机分为对照组与研究组,每组各41例.对照组患者直接采用肺癌根治术治疗,研究组患者采用新辅助化疗联合肺癌根治术治疗.结果 研究组及对照组患者缓解率分别为80.49%、31.71%,两组比较,差异具有统计学意义(P<0.05).研究组患者术后并发症发生率低于对照组,差异具有统计学意义(P<0.05).结论 新辅助化疗联合肺癌根治术可有效减少并发症,疗效安全可靠,在肺癌的治疗中具有重要的临床意义.

目的:分析重组人血管内皮抑制素联合顺铂化疗方案治疗老年晚期非小细胞肺癌的效果.方法:将2016年2月-2016年12月80例老年晚期非小细胞肺癌患者作为研究对象并根据随机数字表分组,分别40例.化疗组采取吉西他滨联合顺铂化疗方案治疗,联合组在化疗组基础上给予重组人血管内皮抑制素.比较两组晚期非小细胞肺癌治疗总有效率;中位生存期、无进展生存期;干预前后患者生存质量.结果:联合组晚期非小细胞肺癌治疗总有效率高于化疗组,P＜ 0.05;联合组中位生存期、无进展生存期长于化疗组,P＜ 0.05;干预前两组生存质量相近,P＞ 0.05;干预后联合组生存质量优于化疗组,P＜0.05.结论:重组人血管内皮抑制素联合顺铂化疗方案治疗老年晚期非小细胞肺癌效果肯定,可有效延长中位生存期、无进展生存期,改善患者生存质量,值得推广.

Objective To investigate the clinical value of ultrasound -guided and CT -guided percutaneously transthoracic lung biopsy for peripheral lung cancer. Methods The clinical characteristics and data of 331 patients with suspected peripheral lung cancer who received ultrasound-guided or CT-guided percutaneously transthoracic lung biopsy were retrospectively analyzed. These patients were divided into ultrasound-guided group(42 cases) and CT-guided group(289 cases). The accuracy of diagnosis and the incidences of complications were comparatively analyzed. Results The accuracy of diagnosis was 85.71% for ultrasound-guided group,and 94.12% for CT-guided group, there was no significance difference between two groups(χ2=4.005,P=0.056). The incidences of pneumothorax and hemopytsis were 7.14% and 9.52% in ultrasound-guided group, respectively. The incidences of pneumothorax and hemopytsis were 4.84%and 3.81%in CT-guided group, respectively, there was no significance difference between two groups(χ2=2.698,P=0.156). Conclusion Both ultrasound-guided and CT-guided percutaneously transthoracic lung biopsies are minimally invasive,safe and accurate diagnostic procedure for peripheral lung cancer.

目的:观察埃克替尼—线治疗晚期非小细胞肺癌表皮生长因子受体(EGFR)敏感性突变患者的疗效及毒副反应.方法:22例接受盐酸埃克替尼治疗的EGFR敏感性突变的NSCLC患者,口服埃克替尼125 mg,3次/d,持续至疾病进展或不良反应无法耐受,评价近期疗效及毒副反应.结果:22例患者中19外显子缺失突变9例,21外显子L858R点突变13例,客观缓解率59.1％,疾病控制率72.7％,中位无进展生存期7.77个月;主要不良反应为皮疹和腹泻,多为Ⅰ～Ⅱ级.结论:盐酸埃克替尼—线治疗EGFR敏感性突变的NSCLC患者疗效较好,不良反应轻.