Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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Molecular Targets # J! ]3 \) g; S& q8 g# r& @
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Category:
8 Y6 v0 w' y+ j, C; x3 K" b. [* jTumor Biology
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1 k4 T& Y8 m' R! m0 [" _: HMeeting:6 w) l* }; Q" x* Y2 J
2011 ASCO Annual Meeting ! ?8 B! M8 F1 v) A: k/ n
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1 |0 M! w8 R6 ?7 ?' Q5 g1 {Session Type and Session Title:
+ S8 M1 F- F8 X2 B2 v, rPoster Discussion Session, Tumor Biology + b% s7 ~& n$ E" a8 E2 @! Y3 h
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Abstract No:+ c( [4 ~: K, F, W
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J Clin Oncol 29: 2011 (suppl; abstr 10517) $ r& D1 M, U# j G; q# Z) a/ E/ N
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Author(s):4 U) g( |. g( R) B* q. V; b
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 1 T0 n% l ^; K- N
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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.4 P: G: s" D6 d7 h
+ G3 u% ~! _5 Z8 z6 H, D6 kAbstract Disclosures
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- S6 e- U4 b+ aAbstract:) L1 Z1 o- I( d
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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.9 c. [9 Q) H- X
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