Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page , Q& n& u& u$ W6 L% }+ |
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Sub-category:
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Category:
7 m Q7 g. i4 i a# o. g. }: WTumor Biology
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7 R5 k) }/ z$ I: a5 x% Q1 D/ ^Meeting:
! J# X' H; ]$ g4 K+ ~, e, g% d2011 ASCO Annual Meeting - t6 w1 E+ k; `. C* r( h( X* N
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Session Type and Session Title:
& L" ?) a+ `; m2 N6 w- g D$ ~ QPoster Discussion Session, Tumor Biology 2 U) k" B1 k+ z9 @+ a+ l
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) w# M: q& F, ]/ b, cCitation:
9 m6 ~% {% D" B9 M# xJ Clin Oncol 29: 2011 (suppl; abstr 10517) 5 a2 l, V) J G# L
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Author(s):
) W. U" l% [. ~# \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.
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! a5 ^& I. s8 ?9 W7 `, V' }( JAbstract Disclosures
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! ?( Y. J! e+ S3 OAbstract:7 L& X, s$ R- A! ^- ~$ y) R1 x x% K
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. m! G& V0 o bBackground: 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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