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Conflicts of interest: R.G. has served as a consultant for Bristol‐Myers Squibb, Roche Pharma, Merck Sharp & Dohme, Novartis, GlaxoSmithKline, Amgen, Almirall Hermal, LEO and Pfizer; has received honoraria for lectures from Bristol‐Myers Squibb, Roche Pharma, Merck Sharp & Dohme, Novartis, GlaxoSmithKline, Amgen, Merck Serono, Almirall Hermal, Galderma and Boehringer Ingelheim; has received travel support from Bristol‐Myers Squibb and Roche Pharma; and has received research grants from Pfizer and Johnson & Johnson. I.S. has received payments for serving on scientific advisory boards for Roche and Bristol‐Myers Squibb; and grant support from Roche, Pfizer and Novartis. K.S. has received grant support from Pfizer.

Dear Editor, the incidence of cutaneous squamous cell carcinoma (cSCC) is rising,1 and as there is a lack of effective therapies for inoperable cSCC, new therapeutic options are needed. Immuno‐oncological agents targeting checkpoints such as programmed death‐1 (PD‐1) or its ligand, PD‐L1, are very promising new anticancer drugs, while efficacy correlates with PD‐L1 expression in various tumour types. In order to provide a translational basis for the possible use of PD‐1/PD‐L1 inhibitors in cSCC, we examined the expression pattern of PD‐L1 in tumour cells and tumour infiltrating leucocytes (TILs), as well as the proportion of CD8+ T cells and correlated these findings with the clinicopathological characteristics of patients. We therefore performed immunohistochemical dual staining against PD‐L1 (clone E1L3N; Cell Signaling Technology, Danvers, MA, U.S.A.) and CD8 (clone C8/144B; Dako, Hamburg, Germany) (Fig. S1; see Supporting Information) of 75 formalin‐fixed, paraffin‐embedded specimens [68 primary cSCC and seven cutaneous metastases; for details see Appendix S1 (Supporting Information)].

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