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- Title
CD274 ( PDL1) and JAK2 genomic amplifications in pulmonary squamous-cell and adenocarcinoma patients.
- Authors
Clavé, Sergi; Rodríguez-Rivera, María; Espinet, Blanca; Salido, Marta; Pijuan, Lara; Gimeno, Javier; Lorenzo, Marta; Casadevall, David; Taus, Álvaro; Menéndez, Silvia; Albanell, Joan; Arriola, Edurne; Hernández-Llodrà, Silvia
- Abstract
Aims CD274 ( PDL1) and JAK2 (9p24.1) gene amplifications have been recently described in pulmonary carcinomas in association with programmed death-ligand 1 ( PD-L1) expression. Furthermore, PTEN loss has been explored preclinically in relation to PD-L1 expression. Our aim was to determine whether these genomic alterations affect PD-L1 expression levels in non-small-cell lung cancer. Methods and results PD-L1 and PTEN expression determined by immunohistochemistry ( IHC), and CD274, JAK2 and PTEN copy number alterations ( CNAs) determined by fluorescence in-situ hybridisation, were studied in 171 pulmonary carcinoma specimens. PD-L1 expression was positive in 40 cases (23.3%), and CD274 amplification was present in 14 tumours (8.8%). Concordance between both events was found in 12 of 14 amplified cases ( P = 0.0001). We found nine JAK2-amplified cases (5.7%), seven with PD-L1 expression ( P = 0.0006). Moreover, six of the seven cases had JAK2 and CD274 coamplification (9p24.1 genomic amplification). Remarkably, the average PD-L1 IHC score was higher in these amplified cases (230 versus 80; P = 0.001). Non-statistical associations were observed between PD-L1 expression and PTEN loss and PTEN deletions. Conclusions We describe a subset of patients (8.2%) who had 9p24.1 amplifications resulting in high expression of PD-L1. Our results provide evidence for genomic up-regulation of PD-L1 expression in non-small-cell lung cancer.
- Subjects
ADENOCARCINOMA; SQUAMOUS cell carcinoma; NON-small-cell lung carcinoma; IMMUNOHISTOCHEMISTRY; IMMUNOTHERAPY; PATIENTS
- Publication
Histopathology, 2018, Vol 72, Issue 1, p259
- ISSN
0309-0167
- Publication type
Article
- DOI
10.1111/his.13339