Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page @/ f1 G4 v5 A! J. A, u j
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% I8 c# m% F& v2 }! P" R* d; h0 ~Molecular Targets ! H* M- K2 Y0 a7 u: o1 _! S
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Category:8 j* o7 Y3 S; P. K6 t/ M
Tumor Biology + O, { z3 ~ [! p$ P* P u
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Meeting:
5 }" j k d4 D) u g2 M- F' G2011 ASCO Annual Meeting
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Session Type and Session Title:% a9 \0 T' A( O3 }6 u
Poster Discussion Session, Tumor Biology
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: u2 {4 v2 c2 t8 N4 YAbstract No:" ]8 u) @% H+ w; T7 w/ ~
10517
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- V* F1 F" M5 T, S( k0 sJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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' `; \- a! m. b5 F. d% U3 k: mAuthor(s):
( O0 ~+ o' V1 g) M. kJ. 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 + f* L; b3 U, R
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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.1 {* B/ @' L9 z4 f( Q0 ?
( d3 m! S1 x3 Q0 e5 e/ AAbstract Disclosures E$ N" N: `$ F
7 U! z0 }6 F2 gAbstract:
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Background: 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.' g% a+ k2 ?# K6 Z$ j# _; E% u
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KRASQ61H突变，1A2期，后续治疗选择
我母亲59岁。22年左右CT发现肺部多发结节，右肺下叶磨玻璃结节较大。24.10.22肺炎出院
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