Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page * q) Z R! N8 H& q3 p
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Sub-category:
& y5 s: R; q2 u- ^Molecular Targets ' ^% X$ y! f& }( W1 g/ i8 A8 B1 z8 l s
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Tumor Biology 7 n+ E6 Q& S: {: T% C% A. c( [
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2011 ASCO Annual Meeting ; I7 U% {% q/ e+ g @
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Poster Discussion Session, Tumor Biology 2 D; P, m4 K6 c j7 R
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Citation:
4 e: c% K" W( x0 V& G9 }J Clin Oncol 29: 2011 (suppl; abstr 10517) / Q( p# j8 L# n( h- P3 _8 L
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+ F6 g+ A% p" T* g0 h' jJ. 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 ( W" ?. j' W; D- s* y% V2 I' ?
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8 z9 z1 M! a, Z3 T% D/ PAbstract Disclosures
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6 V' a' }' [8 E+ {4 WAbstract:
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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.% v% A5 M$ Y1 Z
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