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Atsuko Kasajima Department of Pathology, Technical University Munich, Munich, Germany
Department of Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan

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Yuichi Ishikawa Pathology Department, The Cancer Institute Hospital of JFCR, Tokyo, Japan

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Ayaka Iwata Department of Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan

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Katja Steiger Department of Pathology, Technical University Munich, Munich, Germany

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Naomi Oka Department of Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan
National Hospital Organization, Sendai Medical Center, Sendai, Japan

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Hirotaka Ishida Department of Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan

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Akira Sakurada Department of Thoracic Surgery, Institute of Development, Aging and Cancer, Tohoku University Graduate School of Medicine, Sendai, Japan

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Hiroyoshi Suzuki National Hospital Organization, Sendai Medical Center, Sendai, Japan

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Toru Kameya Division of Pathology, Shizuoka Cancer Center Hospital and Research Institute, Sizuoka, Japan

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Björn Konukiewitz Department of Pathology, Technical University Munich, Munich, Germany

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Günter Klöppel Department of Pathology, Technical University Munich, Munich, Germany

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Yoshinori Okada Department of Thoracic Surgery, Institute of Development, Aging and Cancer, Tohoku University Graduate School of Medicine, Sendai, Japan

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Hironobu Sasano Department of Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan

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Wilko Weichert Department of Pathology, Technical University Munich, Munich, Germany
Member of the German Cancer Consortium (DKTK)

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In the light of novel cancer immune therapies, the status of antitumor inflammatory response and its regulation has gained much attention in patients with lung cancer. Ample datasets exist for non-small-cell lung cancer, but those for pulmonary neuroendocrine tumors are scarce and controversial. Here, tumor-associated inflammation, CD8+ cell infiltration and PD-L1 status were evaluated in a cohort of 57 resected carcinoids and 185 resected neuroendocrine carcinomas of the lung (58 large cell carcinomas and 127 small cell carcinomas). Data were correlated with clinicopathological factors and survival. Moderate or high tumor-associated inflammation was detected in 4 carcinoids (7%) and in 37 neuroendocrine carcinomas (20%). PD-L1 immunoreactivity was seen in immune cells of 73 (39%) neuroendocrine carcinomas, while tumor cells were labeled in 21 (11%) cases. Inflammatory cells and tumor cells in carcinoids lacked any PD-L1 expression. In neuroendocrine carcinomas, PD-L1 positivity in immune cells, but not in tumor cells, was associated with intratumoral CD8+ cell infiltration (P < 0.001), as well as with the severity of tumor-associated inflammation (P < 0.001). In neuroendocrine carcinomas, tumor-associated inflammation and PD-L1 positivity in immune cells correlated with prolonged survival and the latter factor was also an independent prognosticator (P < 0.01, hazard ratio 0.4 for overall survival, P < 0.001 hazard ratio 0.4 for disease-free survival). Taken together, in neuroendocrine tumors, antitumor inflammatory response and PD-L1 expression are largely restricted to neuroendocrine carcinomas, and in this tumor entity, PD-L1 expression in inflammatory cells is positively correlated to patient survival.

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