Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page # ]) V, `* L; m/ N B. H, h
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Sub-category: s5 H# r g8 E
Molecular Targets
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Category:
: O4 n* K# ?# F; `7 w/ e; ^; Z. pTumor Biology / M1 Q) ^6 ~* W( m: B/ [' H, C( S
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2011 ASCO Annual Meeting ! ~! N: }6 M1 e2 Y% ^
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Poster Discussion Session, Tumor Biology ; V% X& N. {8 m+ d$ v$ v5 d
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Abstract No:) o9 [4 q; F6 ]/ c
10517
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7 A$ E3 k# G% ~" u5 Q9 Q. RCitation:
; k, u$ k: g) j. KJ Clin Oncol 29: 2011 (suppl; abstr 10517) - K- O0 T v" P {3 v/ d' E* \
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( M6 R& S! U9 J) V- HJ. 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 : h5 R# v2 ?2 q8 {+ P6 i
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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.8 c* B; m! B1 g; z/ X, {6 v
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Abstract: e5 F0 `0 d. u5 s4 |% l
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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.
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