Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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3 v" @; B* t9 `: B' i5 _Molecular Targets 5 ~7 F9 w/ v% R+ @% o8 M
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Category:
( e) `7 I" v9 k* @3 P. qTumor Biology & y) s5 R% K; q1 ~+ B& } u u
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0 G/ {$ H" N" B; _4 D9 C2 ^ FMeeting:( }4 p! b4 |5 y% b( N9 ]4 f
2011 ASCO Annual Meeting
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Poster Discussion Session, Tumor Biology
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! i- R% G% A) P+ o4 YAbstract No:
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2 f0 r& \$ P3 v! c+ BJ Clin Oncol 29: 2011 (suppl; abstr 10517) 7 K. L) c& R$ Z9 m0 D I4 q# _
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Author(s):) H) k! P* a$ }# s
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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8 Q% ~/ E; o8 e9 g. T8 ^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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' d1 _/ b7 I \$ d/ |5 UAbstract Disclosures
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) D" E2 `1 F9 d8 D* h% F( n& a! JAbstract:6 D0 j2 K; |/ Y$ O2 ^
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4 h9 r1 K$ l$ ABackground: 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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