<i><scp>CD</scp>274</i> (<i><scp>PDL</scp>1</i>) and <i><scp>JAK</scp>2</i> genomic amplifications in pulmonary squamous‐cell and adenocarcinoma patients

<jats:sec><jats:title>Aims</jats:title><jats:p><jats:italic><jats:styled-content style="fixed-case">CD</jats:styled-content>274</jats:italic> (<jats:italic><jats:styled-content style="fixed-case">PDL</jats:styled-content>1</jats:italic>) and <jats:italic><jats:styled-content style="fixed-case">JAK</jats:styled-content>2</jats:italic> (9p24.1) gene amplifications have been recently described in pulmonary carcinomas in association with programmed death‐ligand 1 (<jats:styled-content style="fixed-case">PD</jats:styled-content>‐L1) expression. Furthermore, <jats:styled-content style="fixed-case">PTEN</jats:styled-content> loss has been explored preclinically in relation to <jats:styled-content style="fixed-case">PD</jats:styled-content>‐L1 expression. Our aim was to determine whether these genomic alterations affect <jats:styled-content style="fixed-case">PD</jats:styled-content>‐L1 expression levels in non‐small‐cell lung cancer.</jats:p></jats:sec><jats:sec><jats:title>Methods and results</jats:title><jats:p><jats:styled-content style="fixed-case">PD</jats:styled-content>‐L1 and <jats:styled-content style="fixed-case">PTEN</jats:styled-content> expression determined by immunohistochemistry (<jats:styled-content style="fixed-case">IHC</jats:styled-content>), and <jats:italic><jats:styled-content style="fixed-case">CD</jats:styled-content>274</jats:italic>,<jats:italic> <jats:styled-content style="fixed-case">JAK</jats:styled-content>2</jats:italic> and <jats:italic><jats:styled-content style="fixed-case">PTEN</jats:styled-content></jats:italic> copy number alterations (<jats:styled-content style="fixed-case">CNA</jats:styled-content>s) determined by fluorescence <jats:italic>in‐situ</jats:italic> hybridisation, were studied in 171 pulmonary carcinoma specimens. <jats:styled-content style="fixed-case">PD</jats:styled-content>‐L1 expression was positive in 40 cases (23.3%), and <jats:italic><jats:styled-content style="fixed-case">CD</jats:styled-content>274</jats:italic> amplification was present in 14 tumours (8.8%). Concordance between both events was found in 12 of 14 amplified cases (<jats:italic>P</jats:italic> = 0.0001). We found nine <jats:italic><jats:styled-content style="fixed-case">JAK</jats:styled-content>2</jats:italic>‐amplified cases (5.7%), seven with <jats:styled-content style="fixed-case">PD</jats:styled-content>‐L1 expression (<jats:italic>P</jats:italic> = 0.0006). Moreover, six of the seven cases had <jats:italic><jats:styled-content style="fixed-case">JAK</jats:styled-content>2</jats:italic> and <jats:italic><jats:styled-content style="fixed-case">CD</jats:styled-content>274</jats:italic> coamplification (9p24.1 genomic amplification). Remarkably, the average <jats:styled-content style="fixed-case">PD</jats:styled-content>‐L1 <jats:styled-content style="fixed-case">IHC</jats:styled-content> score was higher in these amplified cases (230 versus 80; <jats:italic>P</jats:italic> = 0.001). Non‐statistical associations were observed between <jats:styled-content style="fixed-case">PD</jats:styled-content>‐L1 expression and <jats:styled-content style="fixed-case">PTEN</jats:styled-content> loss and <jats:italic><jats:styled-content style="fixed-case">PTEN</jats:styled-content></jats:italic> deletions.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>We describe a subset of patients (8.2%) who had 9p24.1 amplifications resulting in high expression of <jats:styled-content style="fixed-case">PD</jats:styled-content>‐L1. Our results provide evidence for genomic up‐regulation of <jats:styled-content style="fixed-case">PD</jats:styled-content>‐L1 expression in non‐small‐cell lung cancer.</jats:p></jats:sec>