| 103 | 5 | 103 |
| 下载次数 | 被引频次 | 阅读次数 |
目的:探讨AP(培美曲塞+顺铂)和TP(多西紫杉醇+顺铂)方案对EGFR-TKIs耐药的晚期非小细胞肺癌(NSCLC)患者的疗效。方法:回顾性分析2009年2月至2010年3月广州医科大学附属第一医院收治的232例EGFR-TKIs耐药的晚期NSCLC患者的临床资料,根据化疗方案不同分为AP组(培美曲塞+顺铂)和TP组(多西紫杉醇+顺铂),每组各116例。根据RECIST标准评价近期疗效(RR、DCR)、总生存期(OS),无进展生存期(PFS)。结果:TP组和AP组有效率、自靶向药物进展后总生存期分别为34.5%和24.1%、12.4个月和12.0个月,两组比较,差异无统计学意义(P>0.05)。TP组和AP组PFS分别为8.0个月和6.2个月,两组比较,差异有统计学差异(P<0.01)。AP组中不吸烟与吸烟患者的总生存期、PFS分别为12.0和9.0个月、6.5和5.6个月,两者比较,差异有统计学意义(P<0.01)。两组吸烟与不吸烟患者疾病控制率比较,差异无统计学意义(P>0.05)。TP组中不吸烟与吸烟患者的总生存期分别为14和8.8个月,两者比较,差异无统计学意义(P=0.725);TP组中不吸烟与吸烟患者的PFS分别为8.0和6.0个月,两者比较,差异有统计学意义(P<0.01)。结论:AP和TP方案对EGFR-TKI靶向治疗耐药进展的晚期NSCLC患者疗效相似;吸烟者疗效较不吸烟者差。
Abstract：Objective: To investigate the effect of AP( pemetrexed + cisplatin) protocol versus TP( docetaxel + cisplatin) protocol in advanced non-small-cell lung cancer( NSCLC) patients with EGFR-TKI resistance. Methods: The clinical data of 232 advanced NSCLC patients with EGFR-TKI resistance hospitalized in First Affiliated Hospital of Guangzhou Medical University between February 2009 and March 2010 were retrospectively analyzed. Based on different protocols of chemotherapy,all patients were divided into two groups( n = 116 each) : the AP( premetrex + cisplatin) group and TP( docetaxel + cisplatin) group. The short-term efficacy [response rate( RR) and disease control rate( DCR) ],overall survival( OS),progression free survival( PFS) were evaluated by Response Evaluation Criteria in Solid Tumors( RECIST) criteria. Results: The RR and OS after the targeted drug developed in TP group and AP group were 34. 5% vs. 24. 1% and 12. 4 months vs. 12. 0 months,respectively. And there were no statistically significant differences between the two groups( P> 0. 05). The PFS in TP group and AP group was 8. 0 months vs. 6. 2 months,with statistically significant difference( P < 0. 01). The OS and PFS in non-smokers and smokers of the AP group were 12. 0 months vs. 9.0 months and 6. 5 months vs. 5. 6 months,respectively,with statistically significant differences between the two groups( P < 0. 01). No statistically significant difference was found in DCR between smokers and non-smokers of the two groups( P > 0. 05). The OS in non-smokers and smokers of the TP group was 14 months vs. 8. 8 months,respectively,with statistically significant difference( P = 0. 725); while the PFS in non-smokers and smokers of the TP group was 8. 0 months vs. 6. 0 months,respectively,with statistically significant difference( P < 0. 01).Conclusion: The effect of AP protocol and TP protocol in advanced NSCLC patients was similar in the development of EGFR-TKI resistance in targeted therapy. And the efficacy in smokers was worse than non-smokers.
[1]Lee YJ,Choi HJ,Kim SK,et al.Frequent central nervous system failure after clinical benefit with epidermal growth factor receptor tyrosine kinase inhibitors in Korean patients with non-small-cell lung cancer[J].Cancer,2010,116(5):1336-1343.
[2]Jackman D,Pao W,Riely GJ,et al.Clinical definition of acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small-cell lung cancer[J].J Clin Oncol,2010,28(2):357-360.
[3]Lynch TJ,Bell DW,Sordella R,et al.Activating mutations in the epidermal growth factor receptor under lying responsiveness of non-small-cell lung cancer to gefitinib[J].N Engl J Med,2004,350(21):2129-2139.
[4]Mok TS,Wu YL,Thongprasert S,et al.Gefitinibor carboplatin-paclitaxel in pulmonary adenocarcinoma[J].N Engl J Med,2009,361(10):947-957.
[5]Han JY,Park K,Kim SW,et al.First-SIGNAL:firstlinesingle-agent iressa versus gemcitabine and cisplatin trial in never-smokerswith adenocarcinoma of the lung[J].J Clin Oncol,2012,30(10):1122-1128.
[6]Maemondo M,Inoue A,Kobayashi K,et al.Gefitinibor chemotherapy for non-small-cell lung cancer with mutated EGFR[J].N Engl J Med,2010,362(25):2380-2388.
[7]Mitsudomi T,Morita S,Yatabe Y,et al.Gefitinibversus cisplatin plus docetaxel in patients with non-small-cell lung cancerharbouring mutations of the epidermal growth factor receptor(WJTOG3405):an open label,randomised phase3 trial[J].Lancet Oncol,2010,11(2):121-128.
[8]Zhou C,Wu YL,Chen G,et al.Erlotinib versus chemotherapy as first-line treatment for patients with advanced EGFR mutation-positivenon-small-cell lung cancer(OPTIMAL,CTONG-0802):a multicentre,openlabel,randomised,phase 3 study[J].Lancet Oncol,2011,12(8):735-742.
[9]Clarke SJ,Abratt R,Goedhals L,et al.Phase II trial ofpemetrexeddisodium(ALIMTA,LY23 1 514)in chemotherapynaive patients with advanced nonsmallcelllung cancer[J].Ann Oncol,2002,13(5):737-741.
[10]Scagliotti GV,Parikh P,von Pawel J,et al.Phase III study comparing cisplatinplusgemcitabine with cisplatin plus pemetrexed in chemotherapy-naive patients withadvanced-stage non-small-cell lung cancer[J].J Clin Oncol,2008,26(21):3543-3545.
[11]Gomez HL,Santillana SL,Vallejos CS,et al.A phase II trial of pemetrexedinadvanced breast cancer:clinical response and association with molecular targetexpression[J].Clin Cancer Res,2006,12(3ptl):832-838.
[12]Gridelli C,Brodowicz T,Langer CJ.Pemetrexed therapy in elderly patients with good performance status:analysis of two phase III trials of patients with nonsquamous nonsmall-cell lung cancer[J].Clin Lung Cancer,2012,13(5):340-346.
[13]Manson GV,Ma PC.Response to Pemetrexed Chemotherapy in Lung adenocarcinoma-Bronchioloalveolar Carcinoma.Insensitive to Erlotinib[J].Clinical Lung Cancer,2010,11(1):57-60.
[14]Oxnard GR,Arcila ME,Sima CS,et al.Acquired resistance to EGFR tyrosine kinase inhibitors in EGFRmutant lung cancer:distinct natural history of patients with tumors harboring the T790M mutation[J].Clin Cancer Res,2011,17(6):1616-1622.
[15]Kobayashi S,Boggon TJ,Dayaram T,et al.EGFR mutation and resistance of non-small-cell lung cancer to gefitinib[J].N Engl J Med,2005,352(8):786-792.
[16]Pao W,Miller VA,Politi KA,et al.Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain[J].PLo S Med,2005,2(3):73.
[17]Engelman JA,Zejnullahu K,Mitsudomi T,et al.MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling[J].Science,2007,316(5827):1039-1043.
[18]Cappuzzo F,Janne PA,Skokan M,et al.MET increased gene copy number and primary resistance to gefitinib therapy in non-small-cell lung cancer patients[J].Ann Oncol,2009,20(2)298-304.
[19]Morgillo F,Kim WY,Kim ES,et al.Implication of the insulin-like growth factor-IR pathway in the resistance of non-small cell lung cancer cells to treatment with gefitinib[J].Clin Cancer Res,2007,13(9):2795-2803.
[20]何卫国,马军,张梅春,等.P53表达预测非小细胞肺癌化疗的耐药性及养肺解毒方的干预治疗[J].中华生物医学工程杂志,2010,16(3):210-213.
[21]Hainaut P,Pfeifer GP.Patterns of p53 G->T transversions in lung cancers reflect the primary mutagenic signature of DNA-damage by tobacco smoke[J].Carcinogenesis,2001,22(3):367-374.
[22]Subramanian J,Govindan R.Molecular profile of lung cancer in never smokers[J].EJC Suppl,2013,11(2):248-253.
基本信息:
中图分类号:R734.2
引用信息:
[1]张洁霞,蔡迪,李时悦,等.AP与TP方案在EGFR-TKI耐药的非小细胞肺癌患者中的疗效比较[J].广州医科大学学报,2015,43(01):4-8.
2015-02-15
2015-02-15