Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page : i2 {2 J' n9 k$ U0 ~" B1 ]3 K
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Sub-category:
* v$ O r8 o4 ?3 _ Q/ f5 ?7 KMolecular Targets
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Category:
4 c1 g1 V* L$ L* a8 _$ hTumor Biology
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Meeting:
( Y! i) o# U, T0 ^* Q) A2011 ASCO Annual Meeting % Q5 q% E5 ^' q- O+ W& b4 g8 L
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Session Type and Session Title:
/ N( ~) h; Z/ Q# w# o" h0 X, I" G1 [Poster Discussion Session, Tumor Biology & s- d2 c0 H- j4 B( T& H
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Abstract No:4 W8 L: @3 U/ F$ Y8 W
10517
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J Clin Oncol 29: 2011 (suppl; abstr 10517)
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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 5 R& ]+ G, G& b2 n% b1 b9 l1 g9 Q7 E
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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.; t2 Y' o4 z. ]3 e
; E4 }* R6 z' BAbstract Disclosures
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Abstract:8 Z$ x, w+ B f8 k
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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.$ ^% t% v1 w+ G: u- o
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