Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
2 P5 z$ L4 @8 q* Z- {8 m& R% @& w; Y/ |9 V% z4 c
: W8 w6 s2 `: k r7 bSub-category:
; J8 b' a7 z( u( Z) sMolecular Targets
8 i! y/ u' Y8 {5 r0 Z8 P/ ]1 ]; H' C, Z4 ~
3 h- n" r2 P) t+ E0 e
Category:
& ?1 }( Q% j, l7 k, Y3 gTumor Biology . r9 M8 H5 h% ?& [
/ |; v: H; p$ X+ G" P% J1 I1 ~) k9 A6 M6 o& q
Meeting:! O# L! B) u* X: E: W/ o, R+ m. G, v! ?
2011 ASCO Annual Meeting , s$ m) F1 h5 ~9 e6 q
: I% J& l; |# H
2 A8 Q, ]/ R1 D4 T9 kSession Type and Session Title:
, S3 P7 V6 l, \6 APoster Discussion Session, Tumor Biology
) k5 Y2 H: U7 A3 l: c- O; O" e$ y& q
) b3 O. w" W# W, U% `
- n7 \- K& ~7 e1 d- y! g: lAbstract No:1 w* W. x1 R, \, I; w9 |" Z/ I
10517 , b$ y, ]2 _4 N6 y
6 c; D; o2 `0 m9 P
( W9 r- g. v+ S: Q# x; I
Citation:7 |& x; b2 \. K! D
J Clin Oncol 29: 2011 (suppl; abstr 10517)
* |! z$ F' s6 s. B8 O& y; m" ^( I# _& D2 \" L% H0 P' \2 ~
' T3 y6 [4 P- [- nAuthor(s):
$ ?* \3 e$ W0 bJ. 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 $ z" f+ F6 ? [" T
) R1 s$ y9 \; O/ _5 h
: a* B$ @' {7 b7 a
8 S) {# Q, @* ~0 D# Y
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.
0 `; _- z4 z7 J! R; J$ M
% ]2 R- C0 z# E7 @% E4 ?Abstract Disclosures
' Z: Z9 k, g9 Z; c- U. I
0 F9 w5 y; V: e' q7 P* eAbstract:
# Y2 J \# Z7 P# Y( b' s) A8 T- }* H& H- W6 O7 E W+ F
7 D. `$ ]: j/ ^% ^3 x& lBackground: 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.
1 t' N4 U x1 u! L0 c7 G0 w# N9 ~% {. j1 p
! S) ~1 E: _0 R/ x$ o |
当靶向治疗遇到胸水：肺癌患者必须了
作者：雨过天晴“复查发现胸水是靶向药物耐药了吗？”“胸水增多是不是疾病进展了？”
肿瘤患者放化疗后如何补充营养，专家
整理者：pear审核人：王闫飞教授放化疗在对抗肿瘤的过程中起着至关重要的作用，但同时
获批了！耐药后有这一突变的肺癌患者
作者：seacat
6月30日，中国国家药品监督管理局（NMPA）批准，赛沃替尼联合奥希替尼用
一线三代29个月，四次培美加卡铂出现
患者信息：女，57岁。确诊时肺内广泛转移+脑部多发转移+肝部转移+骨转移。组织检测600
母亲晚期肺癌跨越11年了！我们的5点
讲述者：小白兔整理者：pear
2014年母亲确诊晚期肺腺癌，一路摸索抗癌前行，幸得病友
6 R T6 [% Y* |4 W q1 R" T
显身卡
