Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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& P0 }7 F4 z6 U( n3 M4 TMolecular Targets
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Category:
- I* Q% T8 X( Z3 D5 n* H) s) JTumor Biology $ C& a2 c- n0 x( y' {
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Meeting:
$ [' M2 p) v% H2011 ASCO Annual Meeting
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Session Type and Session Title:
- d5 L) m9 l# C8 g/ f, q- FPoster Discussion Session, Tumor Biology
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6 A) c" g5 O2 T" PAbstract No:
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7 l* \- ~* q* E; C8 ^Citation:
* i0 d- G& e! o. g! j3 M+ _J Clin Oncol 29: 2011 (suppl; abstr 10517) ' q9 m$ N, ~* q* a3 f7 P( v) r
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x0 f7 V/ T# |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 H# W0 [ ^+ S$ a; e% D* o7 C
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0 U5 r; n/ G0 i' T9 W; |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.3 V8 V+ i$ [ [4 t7 z
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Abstract Disclosures
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& L a* S4 v8 Y+ T1 Y5 xAbstract:6 t1 b T' A {4 D4 l5 T$ h: \1 ?
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k2 ]6 V" k! o4 m; J) VBackground: 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. w0 M0 e3 B& P
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