Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 1 h2 s7 @2 L( i& ]+ I" o6 g
% B" k! q) \, r
" P: _0 F: w/ f$ i, v# w: {) V, V, kSub-category:% j, l6 D, f6 ~, Z+ R
Molecular Targets % j6 V* z9 u- r; Y6 x! I
$ r8 ?" v0 U0 r3 c* |! M9 r, z: [+ C
Category:4 V7 D6 O1 ?8 x: o) d
Tumor Biology " M& g% p& I( N8 l
0 g+ u- e3 |; a' d2 r9 M& Y" A7 h% N) p9 |' n+ J* W0 N
Meeting:
: |* o% U+ |5 _. w2011 ASCO Annual Meeting & Y' Z& Q# C$ \, @
, ]+ _6 g+ E1 r9 W& K/ A3 ^; m5 g/ _& \( J
Session Type and Session Title:
' y/ K+ o; |4 }2 `Poster Discussion Session, Tumor Biology
. A6 i# d/ R3 I+ c0 V
0 S3 T( B, d! {4 G: H
) z; P( E( X2 g) R4 q0 ]7 pAbstract No:, n) H* u) Y) N. k4 G/ x; w3 e0 F
10517
" \+ H! C1 Y/ |
7 O% B0 T/ E8 N* ^$ ?; J' F; Z- t9 Z# Q
Citation:+ v& t" o" N$ Y' ^9 q
J Clin Oncol 29: 2011 (suppl; abstr 10517)
# p) [) ?7 ?- E+ ~ u
6 r7 R3 L4 Z9 f
* e( q8 m9 A& m& ZAuthor(s):2 [# @: `) P/ n$ n4 j- r+ X' h
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 9 o5 {, \- P& r! v- [4 c8 ^
2 h$ ~: X6 Q, k6 t- _0 h) _
2 U) ~7 e" h+ H6 L# ^& ~
' |- n/ m! k) |( ~ |6 ^6 f3 q1 SAbstracts 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.7 s# \- `0 w0 _
7 X$ z6 \ i- ^. x1 G
Abstract Disclosures
/ m) _) z3 a4 R/ p- ^/ s- [6 Q9 L# x( s: K. ]: }
Abstract:
1 Y* W! o& \5 J' j( Y# \* ^
4 ]7 p5 K- c9 Z7 U+ `0 ?" Z+ I
* H/ W, a6 i* k* E- ?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.; D- ]9 b: d7 m" j8 Y1 x
/ l, i7 u Z0 C p) g; P: P; [+ W9 r
|
求助 K药和替雷利珠如何选择
父亲9月刚查出非小细胞低分化癌伴随左肾上腺和第10胸椎转移PDL1高表达(TPS=90%) SMARC
妈妈晚期确诊治疗18个月后的疑惑和不
我的妈妈于2023年12月份确诊肺癌，术中发现胸膜转移，术后基因检测后有EGFR 21
生病1年后复查脑MR情况
自生病1年以来，主冶医生也没有开过脑部MR的检查，既然主冶没开就自已做了一个。通过d
肺鳞癌晚期各病灶大幅缩小，骨转不断
62岁的父亲几个月前查出肺鳞癌晚期全身多处转移，目前K药单免中，主病灶和转移灶都在
肺癌靶向治疗耐药的“解药”来了！缓
作者：seacat
SYS6010是石药集团旗下新诺威巨石生物研发的靶向EGFR的ADC。4月底举行的
: z6 @% h) a$ |/ W! Z
显身卡
