Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page * u1 I& m0 _; V4 y6 f# O
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Sub-category:: V0 E: S& |% b9 X8 L, X% u( o
Molecular Targets ) Z8 V# I4 \2 g4 m+ \0 K* i
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Tumor Biology ! `8 C' p2 F! h) w; @! d+ X
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2011 ASCO Annual Meeting N( _9 e( X# q" I' v
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Session Type and Session Title:
: W" l' q. r O" P6 GPoster Discussion Session, Tumor Biology ! g6 O# m; G# O* ?& B% a8 c
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Abstract No:$ c3 {8 v& q% J8 v7 c* i
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1 i0 C2 r* Z5 S# bJ Clin Oncol 29: 2011 (suppl; abstr 10517) : d* ~5 K) N( U' y3 P$ t5 _
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Author(s):% D$ P2 A# d# k7 i; H; b& \5 K8 p
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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( v1 u* K: q6 ^: {. gAbstracts 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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Abstract Disclosures
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Abstract:6 W/ @* H5 v2 c) L/ G6 X
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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.3 j& p% V2 q u# ^- b
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张红梅教授10个肺癌案例精彩答疑丨医
整理者：雨过天晴审核人：鹰版为帮助肺癌患者解决诊疗过程中的难题与困惑，与癌共舞论
依沃西用药后，该怎么办？
依沃西用药后，该怎么办？
我爸爸于2024年7月确诊肺鳞癌，整个治疗过程如附件里表格
化疗+免疫“黄金时机”被发现，晚期
作者：雨过天晴以免疫检查点抑制剂为代表的免疫治疗在非小细胞肺癌（NSCLC）治疗中具
求助：肺腺癌3年，脑转脑膜转骨转，E
肺腺癌3年，脑转脑膜转、骨转，E19+797S突变，免疫阴性，阿美29个月，期间放疗2次，后
求助，请大家帮忙出出主意，奥西+280
病人是我妈妈，43年8月的，81周岁。
19年10月28日确诊，肺腺癌晚期，右上肺肺癌并双
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显身卡
