Targeted therapies forpatients withadvanced NSCLC harboring wild-type EGFR：what’s new andwhat’s enough

Historically, non?small cell lung cancer (NSCLC) is divided into squamous and nonsquamous subtypes based on histo?logic features. With a growing number of oncogenic drivers being identiifed in squamous...     

肺癌患者外周血中EGFR-mRNA、LUNX-mRNA的表达及意义

目的建立以EGFR-mRNA、LUNX-mRNA为靶基因,逆转录聚合酶链反应(RT-PCR)检测肺癌患者肿瘤组织和外周血微转移的方法,探寻靶基因作为肺癌微转移检测分子标志物的可行性。方法应用RT-PCR技术检测40例非小细胞肺癌组织和15例肺良性病变组织中EGFR-mRNA、LUNX-mRNA的表达;检测40例肺癌患者外周血中靶基因的表达,并以15例良性肺疾病患者和10名健康人外周血作为对照。结果40例肺癌患者病理组织中EGFR-mRNA、LUNX-mRNA的表达率为77.5%(31/40)、100%(40/40),外周血中EGFR-mRNA、LUNX-mRNA表达阳性率为55.0%(22/40)、57.5%(23/40);对照组中,15例肺良性病变患者病理组织中EGFR-mRNA表达率为13.3%(2/15),无LUNX-mRNA表达,15例肺良性病变患者和10名健康人的外周血中无EGFR-mRNA、LUNX-mRNA表达。结论EGFR-mRNA、LUNX-mRNA是检测肺癌组织及肺癌外周血微转移的良好的分子标志物,两者表达与肺癌TNM分期和癌细胞分化程度关系密切。     

表皮生长因子受体与肺癌化疗的临床研究

目的：利用ARMS法分析与检测IB-IIIA非小细胞肺癌患者表皮生长因子受体（EGFR）基因总体突变率,探讨其对肺癌化疗的影响。方法：选取本院2013年8月-2014年8月在同一医疗组IA-IIIA期进行根治术后肺癌患者80例为研究资料,对IB-IIIA期48例全部根治术后肺癌患者进行标准含铂两药的化疗并作病情观察分析,对不同性别、病理类型及吸烟史患者EGFR突变率、术后化疗EGFR基因突变阳性与阴性的无病生存期（DFS）、WHO标准下药物毒副作用差异进行比较。结果：80例肺癌研究患者中检测EGFR基因突变31例,突变率38.75%。37例鳞癌患者, EGFR基因突变2例,突变率5.41%;43例腺癌患者,EGFR基因突变29例,突变率67.44%,突变率的病理类型比较差异有统计学意义（P<0.05）。IB-IIIA期患者共48例,术后做标准含铂两药化疗,20例EGFR基因突变阳性组与28例基因突变阴性组胃肠道副作用反应比较差异无统计学意义（P>0.05）,两组DFS比较差异有统计学意义（P<0.05）。吸烟肺癌患者38例,不吸烟患者42例,前者EGFR基因突变20例,突变率52.6%,后者EFGR基因突变11例,突变率26.2%,突变率比较差异有统计学意义（P<0.05）。结论：非小细胞肺癌患者的EGFR基因突变和患者病理的种类密切相关,通过对突变率的比较得知,腺癌突变率高于鳞癌,患者的EGFR突变状态可以使酪氨酸激酶抑制剂十分有益于预测肺癌化疗治疗。     

吉非替尼在晚期肺腺癌中的临床疗效观察

目的观察吉非替尼治疗晚期肺腺癌的近期疗效及毒副反应。方法选取经放、化疗治疗无效或不能耐受的晚期肺腺癌患者27例。口服吉非替尼(250 mg/次/d),服用至病情进展或出现不可耐受的毒副反应。结果 27例患者CR2例,PR14例,SD10例,PD1例。客观缓解率59.26%,疾病控制率96.40%。PFS 14.17个月。中位生存期20.23个月。EGFR基因突变阳性者生存时间长于基因未突变患者(P<0.05),女性生存时间长于男性(P<0.05)。结论对晚期肺腺癌患者进行EG-FR基因检测,选择优势人群使用吉非替尼疗效肯定,安全易耐受,无明显毒副反应。     

Comprehensive Study on Associations Between Nine SNPs and Glioma Risk

Aim: Glioma cancer is the most common type of adult brain tumor. Recent genome-wide association studies(GWAS) have identified various new susceptibility regions and here we conducted an extensive analysis ofassociations between 12 single nucleotide polymorphisms (SNPs) and glioma risk. Methods: A total of 197glioma cases and 197 health controls were selected, and 9 SNPs in 8 genes were analyzed using the SequenomMassARRAY platform and Sequenom Assay Design 3.1 software. Results: We found the MAF among selectedcontrols were consistent with the MAF from the NCBI SNP database. Among 9 SNPs in 8 genes, we identifiedfour significant SNP genotypes associated with the risk of glioma, C/C genotype at rs730437 and T/T genotypeat rs1468727 in ERGF were protective against glioma, whereas the T/T genotype at rs1799782 in XRCC1 andC/C genotype at rs861539 in XRCC3 conferred elevated risk. Conclusion: Our comprehensive analysis of nineSNPs in eight genes suggests that the rs730437 and rs1468727 in ERGF, rs1799782 in XRCC1 gene, and rs861539in XRCC3 gene are associated with glioma risk. These findings indicate that genetic variants of various genesplay a complex role in the development of glioma.