Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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8 g9 I* V' x" z9 V/ rMolecular Targets ! j. t+ H) L4 N- U; H
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7 [ @: e1 A2 p/ m$ HCategory:$ N3 a) a9 B! Z# q' F( x
Tumor Biology
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Meeting:
, T3 {& I; }7 e, b2011 ASCO Annual Meeting - \+ N# U" P) q8 Q, R/ L
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, A2 J# _: u, ~. h0 O6 dSession Type and Session Title:' `" L, t. }, q# {- T' L, n: v
Poster Discussion Session, Tumor Biology 7 f1 W& D$ K7 L6 Z" t
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Abstract No:" }9 _( Z& _) A" F0 I4 Q3 L$ i4 v
10517
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) t, I* W' X1 L. a; Z$ }; f/ zJ Clin Oncol 29: 2011 (suppl; abstr 10517) / L% I4 G3 b; q! w
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J. 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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. R" s& X+ R: FAbstracts 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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7 e( \% S7 [3 U) |! h6 zAbstract Disclosures- i( L9 v7 y' a) e( n# ]4 |
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Abstract:% v$ F, c$ M2 I0 q: C# q
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% [; B* w- ^7 V# H: gBackground: 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.
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