Overexpression of YAP1 in EGFR mutant lung adenocarcinoma prior to tyrosine kinase inhibitor therapy is associated with poor survival
- Abstract
- EGFR tyrosine kinase inhibitor (EGFR TKI) is approved as first-line treatment for advanced-stage EGFR mutant lung adenocarcinoma (LADC). Yes-associated protein 1 (YAP1), a main effector of the Hippo pathway, is associated with adverse prognosis and disruption of EGFR TKI modulation of non-small cell lung cancer. In this study, we demonstrated a prognostic role of YAP1 in EGFR mutant LADC and efficacy of EGFR TKI therapy. A total of 63 patients, including 41 with paired lung cancer specimens before and after EGFR TKI therapy and 22 with non-paired lung cancer specimens prior to EGFR TKI, were enrolled for examination. Expression of YAP1 protein was evaluated using immunohistochemistry. Fifteen paired cases (36.6%) with high nuclear YAP1 expression were detected in the pre-EGFR TKI LADC group and 21 paired cases (52.5%) after treatment with EGFR TKI. Nuclear YAP1 expression was significantly upregulated after EGFR TKI therapy (P = .002). Fifteen paired cases with high nuclear YAP1 expression before EGFR TKI LADCs showed poorer overall survival (OS) (P = .023) and progression-free survival (PFS) (P = .041). Among the 63 patients under study, those with high nuclear YAP1 expression before EGFR TKI showed shorter OS (P = .038) and PFS (P < .001). High nuclear YAP1 expression in cases with acquired EGFR exon 20 T790 M mutant LADCs showed poorer OS (P < .001). We demonstrated that YAP1 burden before clinical application of EGFR TKI plays a crucial role in prognosis of EGFR mutant LADC treated using EGFR TKI.
- All Author(s)
- S. A. Hong
; S. H. Jang
; M. H. Oh
; S. J. Kim
; J. H. Kang
; S. H. Hong
- Issued Date
- 2018
- Type
- Article
- Keyword
- EGFR tyrosine kinase inhibitor; Lung adenocarcinoma; Prognosis; YAP1
- Publisher
- European Society of Pathology
- ISSN
- 0344-0338
; 1618-0631
- Citation Title
- Pathology, research and practice
- Citation Volume
- 214
- Citation Number
- 3
- Citation Start Page
- 335
- Citation End Page
- 342
- Language(ISO)
- eng
- DOI
- 10.1016/j.prp.2018.01.010
- URI
- http://schca-ir.schmc.ac.kr/handle/2022.oak/2597
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