Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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Sub-category:
9 Y+ l' B# c7 t% lMolecular Targets 7 z' r9 |# M: H" r6 D. u
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Category:7 F5 ?. U: {0 R, x
Tumor Biology
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! o' z3 D B g5 h6 {; s, n4 vMeeting:
/ J0 D4 t* }9 D2011 ASCO Annual Meeting ( u) F# C5 `3 @% s8 l4 |( w
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8 p" B/ r- v4 W1 N% u) w+ TSession Type and Session Title:4 g& H5 u9 j! D, A( f1 x3 R* N
Poster Discussion Session, Tumor Biology
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Abstract No:1 T w2 D5 Z2 i5 h$ n; g
10517
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7 g7 H" h& c3 k5 S0 ~- [- g: nCitation:! L9 `9 a& K& c; M
J Clin Oncol 29: 2011 (suppl; abstr 10517) ! R7 n, W+ ?% H
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Author(s):; w1 `6 Z/ q9 [3 _+ M a
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 6 k' z' t( K L+ a5 r
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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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) t8 W) S" i- H3 X5 x' xAbstract Disclosures
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8 e0 E( w7 O: q/ j: |# gAbstract:$ [, B$ T5 s* ?: U; q5 d
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8 g. b# {' N1 @6 z9 g0 uBackground: 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.7 O0 E3 \, G. C8 b
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