Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page . k9 k0 S. B3 W$ Y
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0 _. c2 N- u, n; D8 t* SMolecular Targets
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2 L, ?& x* X. M y$ t+ {6 YTumor Biology
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2011 ASCO Annual Meeting 4 [. U& n0 U/ d: q" V5 U
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Session Type and Session Title:8 M3 }. f5 m6 a3 }' C* C7 \- o* v, f( Q
Poster Discussion Session, Tumor Biology . a3 z. T; L! k( f1 T" H6 J
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Abstract No:. s6 j. v. R- P
10517
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J Clin Oncol 29: 2011 (suppl; abstr 10517) , F! E) x! H& j. s. E; s
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$ f8 H" g; J+ c+ z) gJ. 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.9 }2 P% O I5 q c3 R& k
2 S$ C8 C/ R* _" s# z6 o4 o5 q* I( PAbstract Disclosures; J' Y9 @, `3 N) b8 X! Z
4 M+ l5 z7 I# o) f9 @: uAbstract:3 g' y0 c- X! E) X' J7 t k
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0 U6 G! ?/ b/ E2 w2 bBackground: 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.' D1 l+ Q3 F0 P' \9 u% h
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