Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page ! u3 A6 H+ M- N3 J8 g4 S
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Sub-category:
2 H- O2 k7 [3 G, u& \, w" I1 z! KMolecular Targets 4 g2 H m' i1 {+ o
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Category:$ U3 ^% F r/ k& `$ m# r8 ^- P
Tumor Biology
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2011 ASCO Annual Meeting . h$ x7 ~1 `* q& m! o6 W* K
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Session Type and Session Title:
- v, h, y% r2 L- |! }: OPoster Discussion Session, Tumor Biology
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Abstract No:$ e1 v6 H9 w( A5 g9 A+ M, A$ L
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J Clin Oncol 29: 2011 (suppl; abstr 10517)
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9 b$ u- n5 X. _& W% @# z* QJ. 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.
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Q: P# C2 y& ^+ dAbstract Disclosures' Z& g3 T& w5 n
( L6 i- Z1 N4 d8 ?) W- D9 J: l8 xAbstract:5 x) y% Z2 f# O3 ^1 P2 i; t
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6 P x, j! d% \2 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.* w& a: y+ o) h0 y
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