Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 4 i/ X- \3 d' z0 W: p' j: f
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Sub-category:# ~2 R6 h% h, T4 ]! X5 U
Molecular Targets . h0 M9 g# l7 m% Q
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Category:
1 X3 U$ B* r2 ZTumor Biology ; D' V- Z8 p1 g* j$ \3 c8 O5 k
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3 n0 {; E5 W7 S/ sMeeting:
# Y5 b$ j; M, n7 ]2011 ASCO Annual Meeting , Q) [' k2 L+ v7 H5 M! i, O
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Session Type and Session Title:' V: B2 N- a% A {! H
Poster Discussion Session, Tumor Biology ; v& y: O, P, Y1 _9 Q. a) L
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% q5 V5 b4 H1 l+ s: ]: S" m- @Abstract No:
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J Clin Oncol 29: 2011 (suppl; abstr 10517)
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, b* U2 @# |' y: @/ Z5 FAuthor(s):
J. @* K, H" k/ c7 ^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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# o* E$ e9 c* b* S+ L( Z1 A. W+ d' ^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.' K- ?6 O- V$ {2 P
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Abstract Disclosures9 b0 V$ k+ a2 f' r& O* h* F+ {* d
$ g5 d1 ~) C, [3 m1 M/ m; OAbstract:6 a: ~- ^' A! G0 X
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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.
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