Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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Sub-category:
2 L. D' d; Z& w+ C D5 EMolecular Targets
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Tumor Biology $ j7 Z- X+ l! U! u" t8 p0 S. V* A
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+ y. K; L5 T8 J0 ^% gMeeting:
% J; W& O$ t0 p8 ]$ `6 k* S! _2011 ASCO Annual Meeting
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0 u" U3 J6 p1 d! n& HSession Type and Session Title:
: s4 E+ a1 e, r7 lPoster Discussion Session, Tumor Biology
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10517 $ j5 v8 @4 m \. @) S) R
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Citation:9 I8 Z5 X/ c9 e( ~3 a
J Clin Oncol 29: 2011 (suppl; abstr 10517) 1 R! x. d) t/ f: B1 N: l
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Author(s):
/ _8 r @0 h u" R: {" d- {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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0 O- E# ]6 F8 P% R OAbstracts 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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4 f9 r( c8 i6 w" i, N7 e' f! UAbstract Disclosures) O% \& Z0 B6 `( q8 ~% i
. Q1 O' E6 g. W* j" QAbstract:- M0 T. ], W' D6 V/ [
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, U0 E% V' a" \* a! b$ g3 eBackground: 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.$ w4 a4 R" }- z- X
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