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1.
表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI)因其高效低毒等特点,广泛运用于非小细胞肺癌的治疗,临床发现部分患者在治疗初期就对EGFR-TKI不敏感,即发生EGFR-TKI原发性耐药。本文对EGFR-TKI原发性耐药机制进行综述,以期更有效地指导非小细胞肺癌个体化治疗。  相似文献   

2.
《中国现代医生》2020,58(32):187-192
分子靶向治疗是在驱动基因指导下的治疗,开启了非小细胞肺癌“个体化”与“精准”治疗时代。非小细胞肺癌驱动基因包括表皮生长因子受体(EGFR)、间变淋巴瘤激酶(ALK)和原癌基因-1(Ros-1)等。EGFR 突变是非小细胞肺癌最常见的靶点,表皮生长因子受体-酪氨酸激酶抑制剂(EGFR-TKI)是治疗EGFR 突变晚期非小细胞肺癌的最有效药物,已广泛用于临床治疗,但后期耐药问题不可避免。近年来,为优化TKI 治疗,EGFR-TKI 联合治疗应运而生,不断探索有效的EGFR-TKI 联合治疗的方案。如EGFR-TKI 联合抗血管生成药物、化疗和免疫治疗等。本文就一线EGFR-TKI 药物及EGFR-TKI 联合治疗在一线探索的有关临床研究进展进行综述。  相似文献   

3.
EGFR-TKI治疗非小细胞肺癌耐药机制的研究进展   总被引:1,自引:0,他引:1       下载免费PDF全文
近年来,随着医学分子生物学的发展,分子靶向治疗作为恶性肿瘤治疗的新手段,正日益受着临床工作者们的重视.其中表皮生长因子受体酪氨酸激酶抑制剂(epidermal growth factor receptor tyrosine kinases inhibitor,EGFR-TKI)在非小细胞肺癌中的作用也逐渐受到肯定.然而在临床中,有些患者对EGFR-TKI的治疗并不敏感或对该类药物产生耐药,故对EGFR-TKI耐药机制的探索成为国内外研究的热点.本文现就EGFR-TKI耐药机制的研究进展进行综述.  相似文献   

4.
张璇  孙建立 《医学综述》2012,(8):1222-1224
肺癌是最常见的恶性肿瘤之一,随着分子研究的不断发展,以表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI)为靶点的肿瘤治疗——分子靶向治疗,成为了治疗非小细胞肺癌的新领域。虽然临床上一些对EGFR-TKI药物敏感的人群在控制病灶、改善症状方面都取得了很好的疗效,但多数患者在服药6~12个月后就会出现疾病进展,即产生获得性耐药。目前,多数患者在应用靶向药物治疗的同时也在服用中医药。靶向药物结合中医药已成为大多数晚期肺癌患者最佳的治疗模式。  相似文献   

5.
肺癌是最常见的恶性肿瘤之一,随着分子研究的不断发展,以表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI)为靶点的肿瘤治疗--分子靶向治疗,成为了治疗非小细胞肺癌的新领域.虽然临床上一些对EGFR-TKI药物敏感的人群在控制病灶、改善症状方面都取得了很好的疗效,但多数患者在服药6 ~12个月后就会出现疾病进展,即产生获得性耐药.目前,多数患者在应用靶向药物治疗的同时也在服用中医药.靶向药物结合中医药已成为大多数晚期肺癌患者最佳的治疗模式.  相似文献   

6.
随着对肿瘤发病机制及其生物学行为的深入研究,分子靶向治疗成为目前治疗非小细胞肺癌(non-small celllung cancer,NSCLC)最具前景的研究领域。其中表皮生长因子受体酪氨酸激酶抑制剂(epidermal growth factor receptor tyrosinekinase inhibitor,EGFR-TKI)可延长患者无进展生存期并明显提高患者生活质量,然而耐药已成为影响该类药物临床应用的最大障碍。因此对EGFR-TKI耐药机制的研究已成为关注的热点。现已发现其耐药可能与受体突变、细胞内信号转导相关蛋白、EGFR以外的TK受体介导的通路活化等有关。文中就NSCLC对EGFR-TKI耐药机制的最新研究进展进行综述。  相似文献   

7.
《海南医学院学报》2017,(8):1109-1112
目的:研究免疫治疗联合表皮生长因子受体-酪氨酸激酶抑制剂(EGFR-TKIs)药物治疗对EGFR突变晚期非小细胞肺癌(NSCLC)患者肿瘤恶性程度的影响。方法:选择在西安市第一医院和陕西省肿瘤医院接受治疗的EGFR突变的晚期NSCLC患者作为研究对象,随机分为DC-CIK组和对照组,前者接受免疫治疗联合EGFR-TKI药物治疗,后者接受EGFR-TKI药物治疗。治疗前后分别测定血清中癌细胞活力相关标志物的含量、外周血单个核细胞中抗肿瘤免疫应答标志分子的表达量,治疗后测定肺癌病灶中增殖相关基因的表达量。结果:治疗后2、4周时,两组血清中CEA、Cyfra21-1、SCCA的含量均显著低于治疗前且DC-CIK组血清中CEA、Cyfra21-1、SCCA的含量均显著低于对照组,DCCIK组外周血单个核细胞中CD3、CD4、CD8的荧光强度显著高于治疗前,对照组外周血单个核细胞中CD3、CD4、CD8的荧光强度与治疗前比较无显著性差异;DC-CIK组肺癌病灶中TCF3、MEF2D、cFLIP(L)的表达量显著低于对照组,FRMD8、PDCD5、caspase-3、caspase-8的表达量显著高于对照组。结论:免疫治疗联合EGFR-TKI药物治疗EGFR突变晚期非小细胞肺癌能够增强抗肿瘤免疫应答、促进癌细胞凋亡。  相似文献   

8.
目的探讨非小细胞肺癌患者血清癌胚抗原(carcinoembryonic antigen,CEA)水平与EGFR-TKI治疗疗效及预后之间的关系。方法收集88例(腺癌69例,非腺癌19例)经吉非替尼或厄罗替尼治疗、疗效可评价的晚期非小细胞肺癌患者,有完整的血清CEA检测结果,分析CEA水平与EGFR-TKI药物治疗反应及预后之间的关系。结果血清CEA<5 ng/ml者的有效率(CR+PR)为18.2%(6/33),稳定率(SD)为18.2%(6/33),进展率为63.6%(21/33);CEA≥5 ng/ml者的有效率为30.9%(17/55),稳定率为43.6%(24/55),进展率为25.5%(14/55)。2组EGFR-TKI治疗的疗效差异有统计学意义(P=0.003)。血清CEA水平高的患者,服用TKI药物后疗效更好,而较低CEA值的患者效果较差。生存分析结果表明,血清CEA≥5 ng/ml组患者经EGFR-TKI治疗后有更长的无疾病进展时间及生存优势,差异有统计学意义(P=0.020,P=0.019)。结论血清CEA水平可作为预测晚期非小细胞肺癌患者服用EGFR-TKI药物疗效及预后指标。  相似文献   

9.
目的探讨表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI)联合化疗治疗EGFR-TKI获得性耐药晚期非小细胞肺癌(NSCLC)的临床疗效。方法 EGFR突变阳性且经EGFR-TKI治疗后缓慢进展的患者43例,根据治疗方案分为C组(培美曲塞联合顺铂或卡铂化疗,化疗6周期仍未进展者,改培美曲塞单药维持化疗)和EC组(EGFR-TKI联合化疗组,化疗方案同C组),对两组患者的疗效进行评价。结果 EC组患者的有效率和疾病控制率均高于C组(P<0.05),但无进展生存时间差异无统计学意义(P>0.05)。两组毒副反应均较轻,两组比较差异无统计学意义(P>0.05),没有治疗相关性死亡。结论对于晚期NSCLC患者,在EGFR-TKI获得性耐药后继续使用EGFR-TKI并联合化疗可以获益。  相似文献   

10.
近年来,表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI)成为治疗晚期非小细胞肺癌(NSCLC)的新趋势,但仍存在毒副作用以及耐药性,而中医学特有的辨证论治以及减毒增效的特点则可以缓解相应不良反应,将二者结合可取得更好的疗效。本文对第一代EGFR-TKI、中医药联合靶向治疗晚期NSCLC的研究进展进行综述,参考文献37篇。  相似文献   

11.
1文献来源 Oxnard GR, Arcila Acquired resistance to ME, Sima CS, EGFR tyrosine inhibitors in EGFR-mutant lung cancer: et al. kinase Distinct natural history of patients with tumors harboring T790M mutation [J]. Clin Cancer Res, 2011 the ,17(6):1616—1622. 2证据水平  相似文献   

12.
13.
程颖  郭珑华 《循证医学》2013,13(1):30-33
1文献来源 Su KY, Chen HY, Li KC, et al. Pretreatmentepidermal mutation growth predicts factor receptor (EGFR) T790M shorter EGFR tyrosine kinase inhibitor response duration in patients with non-small cell lung cancer[J]. J Clin Oncol, 2012, 30(4): 433 -440.  相似文献   

14.
王洁  黄玲 《循证医学》2011,11(1):25-27
1文献来源 Makoto M, Akira I, Kunihiko K, et al. Gefitinib or chemotherapy for non-small cell lung cancerwith mutated EGFR [J]. N Engl J Med, 2010, 362(25) : 2380-2388.  相似文献   

15.
16.
Objective Diabetic nephropathy (DN) is the major cause of end-stage renal disease worldwide and its prevalence continues to increase.Currently,therapies for DN provide only partial renoprotection; hence new targets for therapeutic intervention need to be identified.In this review,we summarized the new target,sphingosine kinase-1/sphingosine 1-phosphate (SphK1/S1P) pathway,explored its potential therapeutic role in the prevention and treatment of DN.Data sources Most relevant articles were mainly identified by searching PubMed in English.Study selection Mainly original articles and critical review articles by major pioneer investigators in this field were selected to be reviewed.Results SphK1/S1P pathway can be activated by hyperglycemia,advanced glycation end products,and many proinflammatory cytokines,which leads to fibronectin,transforming growth factor-31 up-regulation and AP-1 activation.And then it could promote glomerular mesangial cells proliferation and extracellular matrix accumulation,mediating the initiation and progression of diabetic renal fibrosis.Conclusions SphK1/S1P pathway is closely correlated with the pathogenesis of DN.The results suggest that SphK1/ S1P pathway as a new target for clinically improving DN in future is of great prospect.  相似文献   

17.
Background Considering the existence of a large number of liver cell degeneration and necrosis in fibrotic liver, liver function was damaged severely and could not effectively regenerate after partial hepatectomy (PHx). The aim of this study was to investigate whether decorin (DCN) could promote the liver regeneration after PHx in fibrotic mice. Methods Forty mice (5-week-old, Balb/c) were injected with CCI4 intraperitoneally and liver fibrosis model was established after 5 weeks. The survival mice were randomly divided into two groups: control group and DCN group. Then, we performed 70% PHx on all these mice and injected DCN or phosphate-buffered saline plus normal saline (NS) to each group, respectively, after surgery. Liver body weight ratio (LBR), quantitative real-time polymerase chain reaction, and immunohistochemistry were used to analyze liver regeneration and fibrosis degree in both groups, and to find out whether exogenous protein DCN could promote the regeneration of fibrosis liver after PHx. Results Expressions of a-smooth muscle actin (SMA) mRNA and LBR had significant increases in the DCN group at postoperative Day 3 (POD 3, P〈0.05). The protein expressions of CD31, a-SMA, and tumor necrosis factor (TNF)-a were higher in the DCN group than those in the control group by immunohistochemistry at POD 3 (P〈0.05). Conclusion Exogenous protein DCN could promote liver regeneration after PHx in fibrotic mice. Chin Med J 2014;127 (14): 2679-2685  相似文献   

18.
黄诚  徐崇锐 《循证医学》2011,11(1):31-33
1文献来源 Mok TS, Wu YL, Thongprasert S, et at.Gefitinib or Carboplatin-Paclitaxel in pulmonaryadenocarcinoma [J]. N Engl J Med, 2009,361(10):947-957.  相似文献   

19.
1文献来源 Tetsuya M, Satoshi M, Yasushi Y, et al. Gefitinib versus Cisplatin plus Docetaxel in patients with non-small-cell lung cancer harbouring mutations of theepidermal growth factor receptor (WJTOG3405) : Anopen label, randomised phase 3 trial [J]. LancetOncol,2010, 11(2) : 121-125.  相似文献   

20.
Background Studies have shown that the drug resistance of gastric cancer cells can be modulated by abnormal expression of microRNAs (miRNAs).We investigated the role of miR-503 in the development of cisplatin resistance in human gastric cancer cell lines.Methods MiR-503 expression was measured by quantitative real-time PCR.MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and clonogenic assays were used to examine changes in cell viability and the drug resistance phenotype of cancer cells associated with upregulation or downregulation of the miRNA.A dual-luciferase activity assay was used to verify target genes of miR-503.Immunohistochemistry,Western blotting analysis,and a flow cytometric apoptosis assay were used to elucidate the mechanism by which miR-503 modulates drug resistance in cancer cells.Results MiR-503 was significantly downregulated in gastric cancer tissues and several gastric cancer cell lines.Additionally,downregulation of miR-503 in the cisplatin (DDP)-resistant gastric cancer cell line SGC7901/DDP was concurrent with the upregulation of insulin-like growth factor-1 receptor (IGF1R) and B-cell lymphoma 2 (BCL2) expression compared with the parental SGC7901 cell line.An in vitro drug sensitivity assay showed that overexpression of miR-503 sensitized SGC7901/DDP cells to cisplatin.The luciferase activity of reporters driven by IGF1R and BCL2 3'-untranslated regions in SGC7901/DDP cells suggested that IGF1R and BCL2 were both direct target genes of miR-503.Enforced miR-503 expression in SGC7901/DDP cells reduced expression of the target proteins,inhibited proliferation,and sensitized the cells to DDP-induced apoptosis.Conclusion Our findings suggest that hsa-miR-503 modulates cisplatin resistance of human gastric cancer cells at least in part by targeting IGF1R and BCL2.  相似文献   

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