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

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    Fulltext not available
    Authors
    Ye, L.
    Leslie, C.
    Jacques, Angela
    Mesbah Ardakani, N.
    Amanuel, B.
    Millward, M.
    Date
    2018
    Type
    Journal Article
    
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    Citation
    Ye, L. and Leslie, C. and Jacques, A. and Mesbah Ardakani, N. and Amanuel, B. and Millward, M. 2018. Programmed death ligand-1 expression in non-small cell lung cancer in a Western Australian population and correlation with clinicopathologic features. Modern Pathology.
    Source Title
    Modern Pathology
    DOI
    10.1038/s41379-018-0173-9
    ISSN
    0893-3952
    School
    School of Physiotherapy and Exercise Science
    URI
    http://hdl.handle.net/20.500.11937/71839
    Collection
    • Curtin Research Publications
    Abstract

    © 2018, United States & Canadian Academy of Pathology. 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.

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