国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2012年
19期
1511-1513
,共3页
C-MET%酪氨酸激酶抑制剂%非小细胞肺癌%表皮生长因子受体%耐药,肝细胞生长因子
C-MET%酪氨痠激酶抑製劑%非小細胞肺癌%錶皮生長因子受體%耐藥,肝細胞生長因子
C-MET%락안산격매억제제%비소세포폐암%표피생장인자수체%내약,간세포생장인자
C-MET%Tyrosine Kinase Inhibitors%Non-small cell lung cancer%Epidermal growth factor receptor%Resistance%Hepatocyte growth factor
以表皮生长因子受体(EGFR)为靶点的酪氨酸酶抑制剂(TKI)是近年来非小细胞肺癌(NSCLC)治疗的重大突破.但是随着临床的广泛应用,耐药成为新的难点.新近研究已发现对EGFRTKI的耐药产生主要涉及原癌基因C-MET的扩增突变.C-MET是原癌基因,是蛋白产物肝细胞生长因子/离散离子(HGF/SF)的受体,具有酪氨酸酶活性,C-MET基因扩增激活ErbB3-PI3K信号途径导致NSCLC对EGFR-TKI产生耐药,大量研究证实NSCLC患者对EGFR-TKI耐药约20％归因于C-MET基因扩增.
以錶皮生長因子受體(EGFR)為靶點的酪氨痠酶抑製劑(TKI)是近年來非小細胞肺癌(NSCLC)治療的重大突破.但是隨著臨床的廣汎應用,耐藥成為新的難點.新近研究已髮現對EGFRTKI的耐藥產生主要涉及原癌基因C-MET的擴增突變.C-MET是原癌基因,是蛋白產物肝細胞生長因子/離散離子(HGF/SF)的受體,具有酪氨痠酶活性,C-MET基因擴增激活ErbB3-PI3K信號途徑導緻NSCLC對EGFR-TKI產生耐藥,大量研究證實NSCLC患者對EGFR-TKI耐藥約20％歸因于C-MET基因擴增.
이표피생장인자수체(EGFR)위파점적락안산매억제제(TKI)시근년래비소세포폐암(NSCLC)치료적중대돌파.단시수착림상적엄범응용,내약성위신적난점.신근연구이발현대EGFRTKI적내약산생주요섭급원암기인C-MET적확증돌변.C-MET시원암기인,시단백산물간세포생장인자/리산리자(HGF/SF)적수체,구유락안산매활성,C-MET기인확증격활ErbB3-PI3K신호도경도치NSCLC대EGFR-TKI산생내약,대량연구증실NSCLC환자대EGFR-TKI내약약20％귀인우C-MET기인확증.
In recent years epidermal growth factor receptor (EGFR) inhibitor is atreatment a major treatment of non-small cell lung cancer (NSCLC).But with the widespread clinical application of resistance as a new difficulty.Now researchers have discovered the main resistance mechanisms is C-MET oncogene amplification.C-MET is a proto oncogene,a protein product of hepatocyte growth factor/scatter factor (HGF/SF) receptor with tyrosine activity.The amplification of C-MET can activated Erb3-PI3K signaling pathway which result in NSCLC resistant to the EGFR-TKI.The patients who resist to EGFR-TKI for about 20％ were due to the amplification of C MET gene.
