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Letter
Response to: ‘Patterns of PD-L1 expression and CD8 T cell infiltration in gastric adenocarcinomas and associated immune stroma’
  1. Sascha Rahn1,
  2. Sandra Krüger2,
  3. Christoph Röcken2,
  4. Ole Helm1,
  5. Susanne Sebens1
  1. 1 Institute for Experimental Cancer Research, Christian-Albrechts-University Kiel (CAU) and University Medical Center Schleswig-Holstein (UK-SH), Kiel, Schleswig-Holstein, Germany
  2. 2 Department of Pathology, Christian-Albrechts-University Kiel (CAU) and University Medical Center Schleswig-Holstein (UK-SH), Kiel, Schleswig-Holstein, Germany
  1. Correspondence to Professor Susanne Sebens, Institute for Experimental Cancer Research, Christian-Albrechts-University Kiel (CAU) and University Medical Center Schleswig-Holstein (UK-SH), Kiel, 24105 SH, Germany; susanne.sebens{at}email.uni-kiel.de

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We read with interest the manuscript by Thompson et al recently published in Gut 1 highlighting the expression of programmed death ligand 1 (PD-L1) within the stromal compartment of gastric adenocarcinomas (GC). This study showed that PD-L1 is rather expressed by stromal than neoplastic cells and primarily at the tumour margin of PD-L1positive GC. Moreover, they identified a high proportion of CD8+ T cells within these areas that, in contrast to previous studies, correlated with worse progression-free survival and overall survival.1 We fully agree with their findings because of very similar results obtained regarding PD-L1 expression in a well-characterised cohort of pancreatic ductal adenocarcinomas (PDAC).2 Immunohistochemical PD-L1 staining revealed marked PD-L1 expression in 17 of 59 cases (30.4%) (figure 1A). Furthermore, pan-cytokeratin/PD-L1 costainings validated that in 76.5% of the PD-L1positive subgroup PD-L1 is predominantly or exclusively expressed …

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Footnotes

  • Contributors SR, SK and OH performed the experiments. SR and CR evaluated immunohistochemical stainings. SR, OH and SS analysed the data. SR and SS wrote the manuscript. All authors have read and corrected the manuscript.

  • Funding This work was supported by the Stiftung für Krebsentstehung & Immunologie.

  • Competing interests None declared.

  • Ethics approval Ethics Committee of the University Hospital Schleswig-Holstein (reference number: D430/09).

  • Provenance and peer review Not commissioned; externally peer reviewed.