还没做过化疗，EGFR是野生型的病友一定要去做ALK的检测

健康活着 · 发表于 2012-9-18 18:53:34

jzjqian 发表于 2012-7-25 15:45
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, {& {/ A# U5 s7 d4 f7 w& f. w请教，像我这样的，手术22个月了，还能去原手术医院拿到病理作EGFR检查么？

可以，但要有针对性，

落花无意 · 发表于 2012-9-22 15:56:39

请问，肺鳞癌，只做过一次化疗，骨髓抑制严重，后吃特罗凯4个月基本无效，可以参加实验组吗？

godblessmymum · 发表于 2012-9-24 20:13:39

不可以了,要没做过任何治疗的,包括化疗和靶向药

老马 · 发表于 2012-10-14 22:18:42

Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page

Sub-category:
Molecular Targets

Category:
Tumor Biology

Meeting:
2011 ASCO Annual Meeting

Session Type and Session Title:
Poster Discussion Session, Tumor Biology

Abstract No:
10517

Citation:
J Clin Oncol 29: 2011 (suppl; abstr 10517)

Author(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

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.

Abstract Disclosures

Abstract:

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.