Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page ' `9 t# A- Z0 y; H* n% B7 i$ i$ `* r
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Sub-category:
. h) w I$ m, b; HMolecular Targets
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Tumor Biology
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Meeting:
1 V$ I' V; V! o. k' m! o2011 ASCO Annual Meeting . h; s; c- O5 S, m* Z" F
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Session Type and Session Title:
9 _. @7 h Z# G" U5 P" T1 iPoster Discussion Session, Tumor Biology
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4 w; j. Y9 v6 G) ^3 o2 ?' {Abstract No:
4 m) t1 @& ~4 r a, A+ {10517
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Citation:1 O: C/ [* t. G2 Y7 I) l( O
J Clin Oncol 29: 2011 (suppl; abstr 10517) ) I1 P4 N; w7 S$ I; i9 @/ l
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Author(s):4 k M D; I2 C. N3 V) H' y
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 * f8 _0 a/ w& j- R, b
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; o% f! _) k1 R. oAbstracts 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.! p- A# a2 b2 r6 O6 |
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Abstract Disclosures3 r5 w" q6 b! F5 i
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Abstract:5 ]2 ~+ G3 V% d; S8 Q1 M' H. Q
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! o; _2 R0 v3 V, R$ ]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.# e' P0 T3 C9 _# U
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