Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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Sub-category:, @; y. |! J8 O% z
Molecular Targets 9 W6 s3 d) e0 P0 v# F7 K0 U
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Category:
" U0 u7 {1 [% i- L* TTumor Biology 3 F2 l6 K' i! F" D( j m
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Meeting:
% _" H4 [ q' r" R1 H& L" g( ^2011 ASCO Annual Meeting
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8 [& ^+ z4 z. O" E OSession Type and Session Title:8 n3 h7 R1 O2 i7 y% i) {
Poster Discussion Session, Tumor Biology / ~* a% w) ?# a1 Q$ b0 L0 f3 h r# q
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3 `( O+ I' o" N0 E) U) CAbstract No:
$ S, y! L1 @) h3 ?# W3 z# x. I; \10517 " G! j# ]; Y( r3 ` s
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& W% B K9 u' |1 a; \# r) M: gCitation:
6 @. e( t# H% F" W6 t! ^) K Y rJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):
6 Y/ d* h$ f& k; h& tJ. Yang, X. Zhang, J. Su, H. Chen, H. Tian, Y. Huang, C. Xu, Y. L. Wu; Guangdong Lung Cancer Institute, Guangdong General Hospital & Guangdong Academy of Medical Sciences, Guangzhou, China; Guangdong Lung Cancer Institute, Medical Research Center of Guangdong General Hospital, Guangzhou, China; Guangdong Lung Cancer Institute, Guangzhou, China; Guangdong Lung Cancer Institute, Guangdong General Hospital & Guangdong Academy of Medical Sciences, Guangzhou, China
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Abstracts that were granted an exception in accordance with ASCO's Conflict of Interest Policy are designated with a caret symbol (^) here and in the printed Proceedings.
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% H0 F' k( Y$ C( l! e" PAbstract Disclosures& U/ L! G1 \. X4 o, ~' @
f o. D: M% ]7 u" A$ wAbstract:5 s# a; X7 ?' t+ t
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2 X5 u7 N4 R" VBackground: The fusion of the anaplastic lymphoma kinase (ALK) with the echinoderm microtubule-associated protein-like 4 (EML4) and epidermal growth factor receptor (EGFR) mutations are considered mutually exclusive. Advanced non-small cell lung cancer (NSCLC) patients with EML4-ALK did not benefit from EGFR tyrosine kinase inhibitors (TKIs). Methods: Multiplex reverse transcriptase-polymerase chain reaction (RT-PCR) followed by sequencing was performed for EML4-ALK fusion status detection. EGFR and KRAS mutations were determined by direct DNA sequencing. Positive results of EML4-ALK fusion were also confirmed by RACE-coupled PCR sequencing. Results: From April 2010 to January 2011, 412 patients (398 with NSCLC; 14 with SCLC) were tested for mutation status of EGFR, KRAS and EML4-ALK respectively. Frequency of EML4-ALK fusion was 10.6% (42/398) in NSCLC patients. No patients with SCLC were found to have positive EML4-ALK fusion. Frequency of concomitant EGFR and EML4-ALK gene mutations was 1.0% (4/398) in NSCLC patients, and their variants of EML4-ALK gene mutations were Variant 1 (3 patients) and Variant 6 (1 patient); being never smokers, all of them were diagnosed with advanced (3 with stage †W and 1 with stage IIIB) adenocarcinoma harbouring wild type KRAS. Two female stage †W patients with double gene mutations (1 with L858R and Variant 1; 1 with exon19 deletion and Variant 6) received first-line gefitinib which is one kind of EGFR TKIs and achieved partial response. Conclusions: Though being rare events, NSCLC patients harbouring concomitant EGFR mutation and EML4-ALK gene fusion are sensitive to first-line EGFR TKIs. Whether they could also benefit from ALK inhibition after failure to EGFR TKIs warranted further investigation.$ b- H* T+ x& _; H" u- E# d) f
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二十三个月跋涉：在生命的悬崖边，为
二十三个月。
放在漫长的人生里，不过是弹指一挥间。但对我而言，这几百个日夜，却是
三代药泰瑞沙五年骨转，请教后续方案
17年右锁骨异常，穿刺确诊肺CA，基因检测19突变，无其他转移。服用易瑞沙，至2019肺部
都说免疫不入脑，入了就不得了
免疫治疗以后的疗效反应，当病灶增大时，不一定是进展，还有一种可能，叫做CR，这个现
四期伴骨转移，没有靶向药，希望多交
父亲于9月份查出肺部问题，一直非常焦虑、迷茫，对这个病的害怕、对治疗方案的不
MET变异肺癌患者必备宝典：20余位专
间质上皮细胞转化因子（MET）基因的异常，是非小细胞肺癌（NSCLC）发展、转移和耐药的
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显身卡
