Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page , w7 v) \/ y8 Q" ~! ~9 ?
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Sub-category:
~' {% c6 I7 j% e2 o6 AMolecular Targets ' g" P: H+ H: L h9 S$ P, _' `6 g
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% A1 G; ^8 V; m# ]# jTumor Biology
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Meeting:
' ]1 Z( Z; h1 @/ u+ I0 M2011 ASCO Annual Meeting
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Session Type and Session Title:. D! j/ m9 H* {( A# L: U
Poster Discussion Session, Tumor Biology
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) b% \3 h9 M. ?9 M7 Y, {3 N9 Y2 TAbstract No:+ \+ W: Q6 Y; B6 B, ^, ?" R
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J Clin Oncol 29: 2011 (suppl; abstr 10517)
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6 |2 w& W5 G1 v' h3 M3 hAuthor(s):
2 w/ m3 r$ P( M7 ^' e/ I. L0 f& IJ. 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 t8 E7 b2 \. o! ~3 z
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% b0 \/ e' i: J9 EAbstracts 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.+ z$ c8 h1 L" u. I* y# n1 Y5 V
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Abstract Disclosures" k* d" O& e; o/ i1 x
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Abstract:
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1 a* ]/ o% I" x- oBackground: 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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