Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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# i. E f8 X; j5 E3 h k( Q k" zMolecular Targets # ], {* h f+ a1 ?) j
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Category:4 J% S) Q/ o: t8 E* M0 Z: ?& e4 `
Tumor Biology
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( B' v1 B0 N( Y5 PMeeting:
0 x3 N; u7 e( D. a( E2011 ASCO Annual Meeting , W5 c4 v5 T3 l2 e* a- n
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7 i* |- T, X6 C5 }# _1 uSession Type and Session Title:
8 o/ U' s. G2 P4 J1 R$ ~- sPoster Discussion Session, Tumor Biology * U/ H$ D0 O2 z7 T# w
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Abstract No:4 i. r+ W9 _9 S, j' r2 {6 K
10517
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J Clin Oncol 29: 2011 (suppl; abstr 10517) * T+ g1 }! l( p/ c1 V
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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 6 a- ]5 G4 U# ?3 o \6 [
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. t2 w3 V7 w9 S- n& UAbstracts 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., x" J( D" \+ S# w b: Z
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Abstract Disclosures% r5 o1 l) E& r0 O8 h
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Abstract:
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- R2 _4 F8 j/ I+ K9 I, mBackground: 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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