TUBB3/STMN1基因表达与非小细胞肺癌EGFR通路的相关性

背景与目的已有研究表明分子标志物在指导肺癌个体化治疗中起着重要作用。本研究旨在探讨非小细胞肺癌（non-small cell lung cancer, NSCLC）抗微管类药物靶点TUBB3（tubulin, beta 3 class III)/STMN1（stathmin 1）基因表达水平与EGFR（epidermal growth factor receptor）、KRAS（Kirsten rat sarcoma viral oncogene homolog）、BARF（v-raf murine sarcoma viral oncogene homolog B）、PI3K（phosphatidylinositol-4,5-bisphosphate 3-kinase）基因突变的相关性,为NSCLC预后及药物疗效判断提供参考依据。方法回顾性分析我院经病理确诊的46例NSCLC患者手术切除的肿瘤标本,通过分支DNA-液相芯片法检测TUBB3、STMN1基因mRNA表达水平,通过xTAG液相芯片法检测EGFR、KRAS、BRAF、PI3K基因突变,对检测结果应用SPSS 19.0软件采用Spearman相关进行分析基因表达与基因突变的关系。结果抗微管靶点TUBB3和STMN1存在很强的共表达性,TUBB3基因高表达时,STMN1趋向于高表达（P=0.006）。EGFR E21突变与TUBB3存在负相关关系：EGFR E21无突变时TUBB3趋向于高表达（P=0.004,6）。KRAS E2突变与STMN1存在正相关关系：KRAS E2突变时STMN1趋向于高表达（P=0.038,6）。结论抗微管耐药相关因子TUBB3和STMN1与EGFR通路的关键因子突变相关,提示了EGFR突变和KARS突变是调控TUBB3/STMN1表达的重要因素,为研究化疗药物耐药性提供了重要的参考因素。     

非小细胞肺癌EGFR、KRAS基因突变与RRM1、TUBB3 mRNA表达水平的相关性

目的:探讨非小细胞肺癌（NSCLC）EGFR、KRAS基因突变与核苷酸还原酶亚基M1（RRM1）、Ⅲ型β微管蛋白（TUBB3）mRNA表达水平的相关性及其临床意义。方法:69例NSCLC组织标本来自解放军空军总医院胸外科2010年6月至2014年10月手术中从肿瘤中心切取。使用xTAG-液相芯片法检测EGFR、KRAS基因突变,分支DNA-液相芯片法检测RRM1、TUBB3 mRNA表达水平。结果:在69例NSCLC组织样本中,28例为EGFR基因突变（40.6%,28/69）,13例为KRAS基因突变（18.8%,13/69）,EGFR基因突变与性别（P=0.005）、病理类型（P=0.036）、吸烟史（P=0.029）相关。KRAS基因突变与性别相关（P=0.007）。TUBB3 mRNA的表达水平与病理类型相关（P=0.008）,RRM1 mRNA的表达水平与患者各临床病理特征无关（P＞0.05）。EGFR基因突变与RRM1、TUBB3 mRNA表达水平无关（P＞0.05）,KRAS基因突变与RRM1 mRNA表达水平无关（P＞0.05）,KRAS突变型患者TUBB3 mRNA表达水平比KRAS野生型患者高（P＜0.05）。结论:在NSCLC患者中,EGFR及KRAS基因的突变状态对评估患者使用吉西他滨及抗微管类药物的疗效有重要意义,尤其在KRAS突变型NSCLC患者中,抗微管类化疗药物的疗效可能不佳,这有利于指导化疗药物方案的制定,促进NSCLC的个体化治疗。     

基于GEO数据库的胃癌耐药基因表达谱分析及其对预后的影响

目的通过对相关数据库数据分析,探讨胃癌组织耐药基因表达与患者生存和预后的关系。方法对NCBI中GEO数据库中的数据集数据进行表达量分析、生存分析和相关性分析。结果 (1)研究分析表明,ABCB1、LRP、GCS和GST-π基因在胃癌组织中存在明显的高表达(ABCB1,P<0.0001;LRP,P<0.0001;GCS,P=0.0035;GST-π,P<0.0001)。(2)在胃癌组织中ABCB1与LRP及GCS与GST-π的表达均呈正相关(P<0.0001,γ=0.6666);而ABCB1与GCS的表达呈负相关(P=0.032,γ=-0.02301)。(3)ABCB1与GCS的高表达会导致胃癌患者的总生存率和无复发生存率明显降低。结论通过分析表明,在胃癌中部分相关耐药基因的存在差异表达,这些差异表达的基因之间存在相关性,而且对患者的生存及预后又具有重要影响。     

ERCC1、TYMS、RRM1、TUBB3表达与非小细胞肺癌化疗疗效的相关性和意义

[目的]探讨非小细胞肺癌(NSCLC)术后标本中ERCC1、TYMS、RRM1、TUBB3表达与化疗疗效的相关性.[方法]回顾性分析我院病理确诊的72例NSCLC患者手术切除的肿瘤标本,通过分支DNA-液相芯片法,检测ERCC1、TYMS、RRM1、TUBB3基因mRNA表达水平.[结果]ERCC1、TYMS、RRM1、TUBB3阳性表达率分别为38.9％ (28/72)、62.5％(15/72)、55.6％ (46/72)和47.2％(34/72);4者表达与年龄、性别、吸烟、组织学类型、TNM分期、淋巴结转移均无关(P＞0.05),TYMS、TUBB3在高、中分化组中的阳性表达率显著低于低分化组(P=0.003,P＜0.001).ERCC1、TYMS、RRM1和TUBB3阳性表达的化疗患者1年生存率均显著低于阴性表达者(61.5％vs95.5％,P=0.048;53.5％vs 94.9％,P=0.035;58.6％vs 92.9％,P=0.039;47.8％vs 97.4％,P=0.014).[结论]ERCC1、TYMS、RRM1、TUBB3阴性表达者化疗生存率高.ERCC1、TYMS、RRM1、TUBB3阴性表达可作为NSCLC患者临床化疗受益的指标.     

EGFR和KRAS突变对手术切除NSCLC患者预后预测价值分析

目的:探讨EGFR和KRAS突变在未经系统酪氨酸激酶抑制剂(tyrosine kinases inhibitors,TKIs)治疗的非小细胞肺癌(non-small cell lung cancer,NSCLC)患者中的预后预测价值。方法:收集56例未经过系统TKIs治疗的NSCLC患者手术组织样本,通过液相芯片技术进行EGFR与KRAS突变检测,随访2.9~30.0个月,收集患者的临床资料与死亡资料,分析患者2年生存率。结果:56例NSCL组织中,19例(33.9%)存在EGFR突变,其中9例为E19突变,10例为E21突变;8例(14.3%)存在KRAS突变,其中7例为E2突变,1例为E3突变。单因素分析显示,携带KRAS突变的患者2年生存率低于KRAS无突变患者,P=0.023 2;而EGFR突变的患者2年生存率高于EGFR无突变患者,但差异无统计学意义,P=0.060 5。双基因分析显示,3组NSCLC患者的2年生存率差异有统计学意义,P=0.033 9。组间比较显示,EGFR E19/E21突变组2年生存率优于KRAS E2/E3突变组,校正P=0.031 5,EGFR E19/E21突变组与野生型组、KRAS E2/E3突变组与野生型组的2年生存率均差异无统计学意义,校正P值分别为0.506 0和0.628 6。多因素Cox回归分析显示,KRAS突变与KRAS和EGFR综合突变情况是NSCLC患者2年生存率的独立预测因子。其中,KRAS突变/KRAS无突变,P=0.037;EGFR E19/E21突变组/KRAS E2/E3突变组,P=0.039。结论:KRAS突变与KRAS和EGFR综合突变情况是未经系统TKIs治疗NSCLC患者生存的独立预测因子,对患者预后具有指示意义。     

754例Ⅰ期-Ⅲa期可手术切除非小细胞肺癌患者EGFR和KRAS基因突变状态及其临床意义

背景与目的 表皮生长因子受体(epidermal growth factor receptor,EGFR)和KRAS基因是非小细胞肺癌(non-small cell lung cancer,NSCLC)重要的分子靶点,但目前研究主要集中在晚期NSCLC组织和血浆标本的EGFR检测,早期NSCLC组织样本中EGFR和KRAS突变特征尚不清楚.本研究将探讨Ⅰ期-Ⅲa期NSCLC EGFR和KRAS基因突变与相关临床病理特征的关系.方法 采用突变扩增系统(amplification refractory mutation system,ARMS)PCR方法检测北京协和医院病理科提供的754例Ⅰ期-Ⅲa期NSCLC组织样本的EGFR和KRAS基因突变状况,分析基因突变率及其与临床病理特征的关系.结果 EGFR和KRAS基因热点突变的突变率分别为34.5％和13.1％,其中有3例样本具有EGFR和KRAS基因的双突变.EGFR基因在女性中的突变率高于男性(39.5％vs 29.4％,P=0.076),在腺癌中的突变率(38.7％)高于鳞癌、腺鳞癌、大细胞癌(P＜0.01),但仍明显低于其他研究报道的亚裔晚期腺癌突变率(-50％).KRAS基因突变在男性中的突变率高于女性(16.6％vs 9％,P=0.048),且在腺癌中的突变率也高于其他类型,但差异不显著(P=0.268).与KRAS基因突变阳性组相比,EGFR基因突变阳性组在年龄分布上有年轻化的趋势(P=0.031,5),在性别分布上有显著性差异(P＜0.01).结论 Ⅰ期-Ⅲa期NSCLC EGFR基因突变率较晚期患者低,且EGFR和KRAS基因双突变的发生率为0.9％.     

非小细胞肺癌原发灶和转移灶EGFR和KRAS状态比较的meta分析

背景与目的非小细胞肺癌EGFR和KRAS基因状态对肺癌一线靶向治疗的选择尤为关键,而原发肿瘤和转移瘤之间可能存在不同的EGFR和KRAS基因状态.本研究旨在系统评价比较配对的原发肺癌灶和转移灶EGFR和KRAS基因状态以指导临床实践.方法通过Pubmed数据库检索所有符合检索条件的文献,末次检索日期2010年5月10日,根据纳入和排除标准进一步筛选.采用meta分析方法比对肺癌原发灶和转移灶中EGFR基因突变、扩增、EGFR蛋白表达和KRAS基因突变状态之间的差异.结果 14篇文献纳入meta分析,具有配对的原发灶和转移灶,598例vs 598例.原发灶中EGFR蛋白表达和KRAS基因的突变频率高于转移灶,RR分别为1.13(95%CI:0.98-1.31,P=0.09)和1.39(95%CI: 0.95-2.03,P=0.09).转移灶中EGFR的基因拷贝数高于原发灶,RR=0.74(95%CI:0.53-1.02,P=0.06).EGFR基因在原发灶和转移灶中的突变频率无统计学差异(P=0.31).原发灶和转移灶基因状态不一致率分别为:EGFR突变率为17.09%;EGFR扩增率为27.07%;EGFR蛋白表达率为27.84%;KRAS突变率为25.91%.结论肺癌原发灶和相应转移灶中EGFR基因突变较KRAS基因状态更为稳定,原发灶中KRAS基因突变更能反映肺癌周身癌灶KRAS基因特征,单独对转移灶做KRAS状态分析可能会引入更多抵抗EGFR酪氨酸激酶抑制剂治疗的患者.联合检测原发灶中EGFR和KRAS基因突变可作为肺癌靶向治疗的疗效预测指标.     

表皮生长因子受体和肝细胞生长因子受体在非小细胞肺癌中的表达及其与预后的关系

目的 探讨非小细胞肺癌(NSCLC)组织中表皮生长因子受体(EGFR)和肝细胞生长因子受体(c-Met)基因和蛋白的表达情况,及其与NSCLC临床病理特征和预后的关系.方法 采用免疫组化法检测61例NSCLC组织中EGFR和c-Met蛋白的表达情况,采用实时荧光定量PCR法检测EGFR和c-Met DNA的相对拷贝数.结果 61例NSCLC组织中,EGFR和c-Met蛋白的阳性表达率分别为77.0%和57.4%.EGFR和c-Met蛋白在高、中分化NSCLC组织中的阳性表达率分别为61.5%和38.5%,均明显低于低分化的肿瘤组织(均P＜0.05).EGFR和c-Met DNA在吸烟患者中的相对拷贝数分别为0.22±0.22和0.20±0.21,均明显高于不吸烟患者(均P＜0.05);在腺癌中的相对拷贝数分别为0.24±0.26和0.23±0.25,均明显高于鳞癌患者(均P＜0.05).EGFR蛋白与c-Met蛋白表达、EGFR DNA相对拷贝数与c-Met DNA相对拷贝数、EGFR蛋白表达与EGFR DNA相对拷贝数之间均具有显著的相关性(均P＜0.05),但c-Met蛋白表达与c-Met DNA相对拷贝数之间没有相关性(P=0.259).EGFR DNA低拷贝组和高拷贝组患者的术后中位生存时间分别为48和36个月,差异有统计学意义(P=0.039);c-Met DNA低拷贝组和高拷贝组患者的术后中位生存时间分别为44和31个月,差异亦有统计学意义(P=0.022).结论 EGFR和c-Met的蛋白表达与NSCLC的分化程度有关;EGFR和c-Met DNA的相对拷贝数与NSCLC患者的吸烟史以及病理类型有关,有助于预测NSCLC患者的预后.     

血清miRNA-1296联合表皮生长因子受体检测对非小细胞肺癌患者预后评估价值的分析

目的 研究血清miRNA-1296联合表皮生长因子受体(EGFR)检测对非小细胞肺癌(NSCLC)患者的预后评估价值.方法 选取61例NSCLC患者为NSCLC组,选取同期61例健康体检者为对照组.检测血清miRNA-1296、EGFR水平,分析两者在NSCLC患者中的相关性,观察两者对NSCLC患者预后的评估价值.结果 NSCLC组患者血清miRNA-1296水平明显低于对照组(P﹤0.01),EGFR水平明显高于对照组(P﹤0.01).死亡组NSCLC患者的血清miRNA-1296水平明显低于生存组(P﹤0.01),EGFR水平明显高于生存组(P﹤0.01).受试者工作特征(ROC)曲线分析结果显示,血清miRNA-1296与EGFR联合预测NSCLC预后的曲线下面积(AUC)、灵敏度、特异度均高于二者单独预测结果.NSCLC患者血清miRNA-1296水平与EGFR水平呈负相关(P﹤0.01).随访期间,miRNA-1296高表达组患者累积生存率明显高于低表达组(P﹤0.01),EGFR高表达组累积生存率明显低于低表达组(P﹤0.05).多因素Cox比例风险回归模型分析表明,血清EGFR水平高表达是NSCLC患者预后的独立危险因素(P﹤0.01),血清miRNA-1296水平高表达是NSCLC患者预后的保护因素(P﹤0.01).结论 血清miRNA-1296水平低表达、EGFR水平高表达均与NSCLC的发生和预后有关,二者联合检测能够对患者预后进行更有效的评估,从而对患者进行针对性的治疗,可能是NSCLC患者潜在治疗靶点.     

胃癌中hMSH2表达缺失对EGFR及KRAS基因突变影响的研究

目的:探讨胃癌中hMSH2表达缺失对EGFR和KRAS基因突变的影响.方法:收集大连地区胃癌标本63例,所有患者均未经放疗或化疗.应用免疫组织化学方法检测63例胃癌标本和38例癌旁组织的hM-SH-2、EGFR和KRAS蛋白的表达情况;应用HRM技术检测其中58例胃癌标本的EGFR基因19-21外显子和KRAS基因2外显子的突变情况,筛选出的阳性标本应用DNA测序证实.结果:hMSH2表达缺失率在胃癌组为34.9％,显著低于癌旁组的60.5％(P=0.012);在Ⅲ-Ⅳ期胃癌组为47.4％,显著高于Ⅰ-Ⅱ期胃癌组的16.0％ (P =0.011).58例胃癌标本中,hMSH2表达缺失组的EGFR突变率为10.5％,高于hMSH2表达组的2.6％ (P=0.513);hMSH2表达缺失组的KRAS突变率为15.8％,高于hMSH2表达组的7.7％(P =0.623).EGFR蛋白表达率在胃癌组为47.6％,显著高于癌旁组的26.3％ (P =0.034);在淋巴结转移组为57.4％,显著高于无淋巴结转移组的18.8％ (P =0.007);在Ⅲ-Ⅳ期胃癌组为57.9％,显著高于Ⅰ-Ⅱ期胃癌组的32.0％ (P =0.044).KRAS蛋白表达率在胃癌组为63.5％,显著高于癌旁组的36.8％(P=0.009);在Ⅲ-Ⅳ期胃癌组为73.7％,显著高于Ⅰ-Ⅱ期胃癌组的48.0％(p=0.038).结论:hMSH2表达缺失的胃癌组织可能更易携带EGFR及KRAS基因突变;hMSH2、EGFR和KRAS蛋白表达的增加可能早于胃癌的发生;hMSH2表达缺失、EGFR和KRAS蛋白表达增加在胃癌的进展中发挥作用.     

KRAS mutation is an important predictor of resistance to therapy with epidermal growth factor receptor tyrosine kinase inhibitors in non-small-cell lung cancer.

PURPOSE: EGFR gene mutations and increased EGFR copy number have been associated with favorable response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKI) in patients with non-small-cell lung cancer (NSCLC). In contrast, KRAS mutation has been shown to predict poor response to such therapy. We tested the utility of combinations of these three markers in predicting response and survival in patients with NSCLC treated with EGFR-TKIs. EXPERIMENTAL DESIGN: Patients with advanced NSCLC treated with EGFR-TKI with available archival tissue specimens were included. EGFR and KRAS mutations were analyzed using PCR-based sequencing. EGFR copy number was analyzed using fluorescence in situ hybridization. RESULTS: The study included 73 patients, 59 of whom had all three potential markers successfully analyzed. EGFR mutation was detected in 7 of 71 patients (9.8%), increased EGFR copy number in 32 of 59 (54.2%), and KRAS mutation in 16 of 70 (22.8%). EGFR mutation (P<0.0001) but not increased EGFR copy number (P=0.48) correlated with favorable response. No survival benefit was detected in patients with either of these features. KRAS mutation correlated with progressive disease (P=0.04) and shorter median time to progression (P=0.0025) but not with survival. Patients with both EGFR mutation and increased EGFR copy number had a >99.7% chance of objective response, whereas patients with KRAS mutation with or without increased EGFR copy number had a >96.5% chance of disease progression. CONCLUSION: KRAS mutation should be included as indicator of resistance in the panel of markers used to predict response to EGFR-TKIs in NSCLC.     

肺癌驱动基因与非小细胞肺癌生存关系的相关性研究

目的探讨非小细胞肺癌驱动基因EGFR、KRAS、BRAF、PIK3CA、ALK、MET、HER-2、RET、ROS-1与患者预后相关性,寻找更有效防治分子靶标。方法利用Kaplan-Meier(KM)plotter在线数据库分析EGFR、KRAS、BRAF、PIK3CA、ALK、MET、HER-2、RET、ROS-1表达与非小细胞肺癌患者总生存期(overall survival OS),性别与吸烟状态等参数的相关性,并得出相应的危险比(Hazard ratio,HR)、95%置信区间(CI)和P值。结果研究结果显示:高表达EGFR、BRAF、MET、RET、ROS-1的患者有较好的OS。进一步引入吸烟状态和性别参数显示,BRAF、MET,PIK3CA、HER-2、ALK的表达与患者的吸烟状态存在相关性(P<0.05)。BRAF、MET、EGFR、ALK表达与OS的相关性存在性别差异(P<0.05)。结论各驱动基因在患者预后评判中既是独立因素,又相互作用,吸烟状态与性别也是决定患者预后的关键因素,提示临床治疗时要对患者进行综合的评判,要进行多基因的共同分析、多靶点的联合治疗才能使病人获得更大的收益。     

Mutations in the epidermal growth factor receptor and in KRAS are predictive and prognostic indicators in patients with non-small-cell lung cancer treated with chemotherapy alone and in combination with erlotinib.

PURPOSE: Epidermal growth factor receptor (EGFR) mutations have been associated with tumor response to treatment with single-agent EGFR inhibitors in patients with relapsed non-small-cell lung cancer (NSCLC). The implications of EGFR mutations in patients treated with EGFR inhibitors plus first-line chemotherapy are unknown. KRAS is frequently activated in NSCLC. The relationship of KRAS mutations to outcome after EGFR inhibitor treatment has not been described. PATIENTS AND METHODS: Previously untreated patients with advanced NSCLC in the phase III TRIBUTE study who were randomly assigned to carboplatin and paclitaxel with erlotinib or placebo were assessed for survival, response, and time to progression (TTP). EGFR exons 18 through 21 and KRAS exon 2 were sequenced in tumors from 274 patients. Outcomes were correlated with EGFR and KRAS mutations in retrospective subset analyses. RESULTS: EGFR mutations were detected in 13% of tumors and were associated with longer survival, irrespective of treatment (P < .001). Among erlotinib-treated patients, EGFR mutations were associated with improved response rate (P < .05) and there was a trend toward an erlotinib benefit on TTP (P = .092), but not improved survival (P = .96). KRAS mutations (21% of tumors) were associated with significantly decreased TTP and survival in erlotinib plus chemotherapy-treated patients. CONCLUSION: EGFR mutations may be a positive prognostic factor for survival in advanced NSCLC patients treated with chemotherapy with or without erlotinib, and may predict greater likelihood of response. Patients with KRAS-mutant NSCLC showed poorer clinical outcomes when treated with erlotinib and chemotherapy. Further studies are needed to confirm the findings of this retrospective subset analysis.     

PD-1/PD-L1 expression in non-small-cell lung cancer and its correlation with EGFR/KRAS mutations

This study was aimed to detect the correlation among EGFR/KRAS status and PD-1/PD-L1 expression in non-small-cell lung cancer (NSCLC) patients. PD-1 and PD-L1 expressions were detected by immunohistochemistry in 100 surgically resected lung adenocarcinoma tissues and were statistically correlated with clinicopathological characteristics including EGFR and KRAS statuses. Besides, the overall survival (OS) times were analyzed. There was a statistical significances between PD-1 expression in tumor and KRAS status (P = 0.043), with a higher mutation rate in with lower PD-1 expression patients. There was a statistical significance between PD-L1 expression in tumor and EGFR status (P = 0.012), with a higher mutation rate in patients with lower PD-L1 expression. The OS of patients with EGFR mutation was significantly longer than those without EGFR mutation. The OS of patients with lower PD-L1 in tumor was significantly longer than those with higher PD-L1 expression. We found negative associations between PD-L1 expression in tumor and mutated EGFR status, as well as between PD-1 expression in tumor and mutated KRAS status.     

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。      

Expression of TS,RRM1, ERCC1, TUBB3 and STMN1 Genes in Tissues of Non-small Cell Lung Cancer and its Significance in Guiding Postoperative Adjuvant Chemotherapy

Background: To explore the expression of TS, RRM, ERCC1, TUBB3 and STMN1 genes in the tissues ofpatients with non-small cell lung cancer (NSCLC) and its significance in guiding the postoperative adjuvantchemotherapy. Materials and Methods: Real time polymerase chain reaction (PCR) was applied to detect theexpression of TS, RRM, ERCC1, TUBB3 and STMN1 genes in the tissues of NSCLC patients so as to analyze therelationship between the expression of each gene and the clinical characteristics and to guide the postoperativeindividualized chemotherapy according to the detection results of NSCLC patients. Results: Expression of TSgene was evidently higher in patients with adenocarcinoma than those with non-adenocarcinoma (P=0.013) andso was the expression of ERCC1 (P=0.003). The expression of TUBB3 gene was obviously higher in NSCLCpatients in phases Ⅰ/Ⅱ and Ⅳ than those in phase Ⅲ (P1=0.021; P2=0.004), and it was also markedly higher inpatients without lymph node metastasis than those with (P=0.008). The expression of STMN1 gene was apparentlyhigher in patients in phase Ⅰ/Ⅱ than those in phase Ⅳ (P=0.002). There was no significant difference betweenthe rest gene expression and the clinical characteristics of NSCLC patients (P>0.05). Additionally, the diseasefreesurvival (DFS) was significantly longer in patients receiving gene detections than those without (P=0.021).Conclusions: The selection of chemotherapeutic protocols based singly on patients’ clinical characteristics hascertain blindness. However, the detection of tumor-susceptible genes can guide the postoperative adjuvantchemotherapy and prolong the DFS of NSCLC patients.