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The Co-Expression of Programmed Death-Ligand 1 (PD-L1) in Untreated EGFR-Mutated Metastatic Lung Adenocarcinoma

Authors :
Shu-Min Lin
Li-Chung Chiu
Ping-Chih Hsu
Yu-Lun Lo
Scott Chih-Hsi Kuo
Cheng-Ta Yang
Allen Chung-Cheng Huang
Chih-Wei Wang
Source :
Biomedicines, Volume 8, Issue 2, Biomedicines, Vol 8, Iss 2, p 36 (2020)
Publication Year :
2020
Publisher :
Multidisciplinary Digital Publishing Institute, 2020.

Abstract

Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) is the standard first-line therapy for metastatic lung adenocarcinoma harboring sensitive EGFR mutations. Tumor surface programmed death-ligand 1 (PD-L1) is expressed in some metastatic EGFR-mutated lung adenocarcinoma, but its impact on the efficacy of EGFR-TKIs is unclear. We retrospectively investigated 117 untreated metastatic lung EGFR mutated adenocarcinoma patients with a PD-L1 immunohistochemistry test. The PD-L1 expression level was classified by tumor proportion scores (TPS). Forty-five patients had negative expression (TPS &lt<br />1%), 45 had a weak expression (TPS 1&ndash<br />49%), and 27 had a strong expression (&ge<br />50%). All patients recruited in this study received EGFR-TKIs as a first-line therapy. No significant differences were observed for objective response rates (68.9% versus 62.2% versus 73.1%, p = 0.807) and median time to treatment failure (TTF) (12.17 versus 13.17 versus 11.0 months, p = 0.443) of first-line EGFR-TKIS among the three groups of patients (negative versus weak versus strong). The median overall survival was 21.27 versus 20.63 versus 19.43 months among the three groups of patients (p = 0.77). Our results demonstrated that PD-L1 did not affect the efficacy of first-line EGFR-TKIs in metastatic EGFR mutated lung adenocarcinoma. Thus, EGFR-TKIs are suggested as the preferred clinical therapy for these patients, despite their PD-L1 levels.

Details

Language :
English
ISSN :
22279059
Database :
OpenAIRE
Journal :
Biomedicines
Accession number :
edsair.doi.dedup.....26d65fdc37ed903be3ca303bcee732cb
Full Text :
https://doi.org/10.3390/biomedicines8020036