Programmed death ligand-1 expression in non-small cell lung cancer in a Western Australian population and correlation with clinicopathologic features

Document Type

Journal Article

Publication Title

Modern Pathology

ISSN

1530-0285

Volume

32

Issue

4

First Page

524

Last Page

531

PubMed ID

30401947

Publisher

Springer Nature Publishing AG

School

School of Medical and Health Sciences

RAS ID

31190

Comments

Ye, L., Leslie, C., Jacques, A., Ardakani, N. M., Amanuel, B., & Millward, M. (2019). Programmed death ligand-1 expression in non-small cell lung cancer in a Western Australian population and correlation with clinicopathologic features. Modern Pathology, 32(4), 524–531. Available here

Abstract

Immune checkpoint inhibition is an important therapeutic option in patients with non-small cell lung cancer. Programmed cell death ligand-1 (PD-L1) expression may serve as a predictive marker for anti-PD-1/PD-L1 therapies. The relationship between non-small cell lung cancer PD-L1 expression and clinicopathological characteristics remains unclear and there is no population level Australian data. We report the results of PD-L1 testing in patients with non-small cell lung cancer diagnosed at major Western Australian public hospitals served by a single state Pathology provider. We analyzed PD-L1 expression by immunohistochemistry in 241 non-small cell lung cancer specimens using the 22C3 clone on a Dako autostainer platform. Tumor cell PD-L1 expression was scored as Tumor Proportion Score and categorized using pre-specified subsets of  1%, 1-49% and  ≥  50% for correlation with clinicopathologic features. PD-L1 Tumor Proportion Score was  1% in 65 (27%) cases, 1-49% in 100 (41%) cases and  ≥  50% in 76 (32%) cases. PD-L1-positive rate was 92% in squamous cell carcinomas and 67% in adenocarcinomas. PD-L1 Tumor Proportion Score was higher in squamous cell carcinomas (p  =  0.004) and lower in adenocarcinomas (p  =  0.003). Of the 196 non-squamous carcinomas, 35% had rat sarcoma viral oncogene homolog (RAS) mutations, 13% had epidermal growth factor receptor (EGFR) mutations, 2% had anaplastic lymphoma kinase (ALK) translocations and 2% had ROS1 translocations. Tumor Proportion Score  ≥  50% was seen in 34% (23/68), 28% (7/25) and 25% (1/4) of RAS, EGFR mutant, and ALK translocated carcinomas, respectively. There was no significant correlation between PD-L1 expression and molecular or genetic abnormalities, or other parameters including age, gender, stage, and smoking status. In our patient cohort, PD-L1 Tumor Proportion Score was significantly higher in squamous cell carcinomas and lower in adenocarcinomas. The overall prevalence of Tumor Proportion Score  ≥  50% is consistent with that reported in clinical trials.

DOI

10.1038/s41379-018-0173-9

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