Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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& B5 Y# a9 Q% x7 h8 l9 p7 BSub-category:
) c0 _3 z& m9 {& W; VMolecular Targets
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! j7 G' s1 U( ?Tumor Biology % W5 S w6 c. @
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Meeting:9 t3 ~6 \9 k4 ~) A) I/ l/ y
2011 ASCO Annual Meeting
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Session Type and Session Title:
7 b2 l* \7 `' Z: u8 r- hPoster Discussion Session, Tumor Biology ; r5 c+ P( l8 q" K
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Abstract No:; z5 ` j( G5 l0 q0 o. ], h6 W
10517
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Citation:
- n5 _- {8 V0 Q$ g' PJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):, L- E; N4 @6 ^9 h
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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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.* E3 `% w/ t: z9 M) w' V5 F
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Abstract Disclosures
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! f5 I4 S" |% IAbstract:1 I# n6 D" i, h3 P$ Z$ l a8 f
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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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