請用此 Handle URI 來引用此文件: http://hdl.handle.net/11455/60801
標題: Clinical Implications of High MET Gene Dosage in Non-Small Cell Lung Cancer Patients without Previous Tyrosine Kinase Inhibitor Treatment
作者: Chen, Y.T.
陳盈璁
Chang, J.W.C.
Liu, H.P.
Yu, T.F.
Chiu, Y.T.
Hsieh, J.J.
Chen, Y.R.
Wu, H.D.I.
Huang, S.F.
關鍵字: MET amplification
EGFR
NSCLC
Tyrosine kinase inhibitor
Chemotherapy
Gene dosage
growth-factor receptor
in-situ hybridization
c-met
copy number
juxtamembrane domain
somatic mutations
amplification
gefitinib
adenocarcinoma
carcinomas
期刊/報告no:: Journal of Thoracic Oncology, Volume 6, Issue 12, Page(s) 2027-2035.
摘要: Introduction: Recently, two studies revealed that MET amplification was associated with secondary epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) resistance in non-small cell lung cancer (NSCLC) patients. But it remains uncertain whether MET amplification could be related to primary TKI resistance in NSCLC because of limited data. Materials and Methods: MET gene dosage of the tumor tissues from 208 NSCLC patients was investigated by real time quantitative polymerase chain reaction and compared with molecular and clinical features, including EGFR mutations, KRAS mutations, EGFR gene copy numbers, and patient survivals. Three copies were used as the cutoff. Among them, 25 patients were also evaluable for EGFR TKI responsiveness. Results: The proportion of high MET gene dosage was 10.58% (22/208) with higher incidence in squamous cell carcinoma (11.86%) and smokers (16.18%), although the differences with adenocarcinoma and nonsmokers were nonsignificant. Coexisting EGFR mutations were identified, and the incidence (8.54%) was similar to wild type (12.0%). High MET gene dosage was significantly associated with higher tumor stage (stage I + II versus stage III + IV; p = 0.0254) and prior chemotherapy for stage III + IV adenocarcinoma patients (35.71% versus 7.41%; p = 0.0145) but not correlated with primary TKI resistance. Among the 155 surgically resectable patients (stage I to IIIA), high MET gene dosage was significantly associated with shorter median survival (21.0 months versus 47.1 months; p = 0.042) by univariate analysis. Conclusions: High MET gene dosage was not related to primary TKI resistance and the incidence was increased after chemotherapy, suggesting high MET gene dosage may also be related to chemotherapy resistance.
URI: http://hdl.handle.net/11455/60801
ISSN: 1556-0864
文章連結: http://dx.doi.org/10.1097/JTO.0b013e3182307e92
顯示於類別:基因體暨生物資訊學研究所

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