PD-1 and PD-L1 expression in pulmonary carcinoid tumors and their association to tumor spread
Vesterinen, T., Kuopio, T., Ahtiainen, M., Knuuttila, A., Mustonen, H., Salmenkivi, K., Arola, J., & Haglund, C. (2019). PD-1 and PD-L1 expression in pulmonary carcinoid tumors and their association to tumor spread. Endocrine Connections, 8(9), 1168-1175. https://doi.org/10.1530/EC-19-0308
Published inEndocrine Connections
© 2019 The authors. Published by Bioscientifica Ltd
Pulmonary carcinoid (PC) tumors are rare tumors that account for approximately 1% of all lung cancers. The primary treatment option is surgery, while there is no standard treatment for metastatic disease. As the number of PCs diagnosed yearly is increasing, there is a need to establish novel therapeutic options. This study aimed to investigate programmed death protein 1 (PD-1) and programmed death ligand 1 (PD-L1) expression in PC tumors since blocking of the PD-1/PD-L1 pathway is a promising therapeutic option in various other malignancies. A total of 168 PC patients treated between 1990 and 2013 were collected from the Finnish biobanks. After re-evaluation of the tumors, 131 (78%) were classified as typical carcinoid (TC) and 37 (22%) as atypical carcinoid (AC) tumors. Primary tumor samples were immunohistochemically labeled for PD-1, PD-L1 and CD8. High PD-1 expression was detected in 16% of the tumors. PD-L1 expression was detected in 7% of TC tumors; all AC tumors were PD-L1 negative. PD-L1 expression was associated with mediastinal lymph-node metastasis at the time of diagnosis (P = 0.021) as well as overall metastatic potential of the tumor (P = 0.010). Neither PD-1 expression, PD-L1 expression nor CD8+ T cell density was associated with survival. In conclusion, PD-1 and PD-L1 were expressed in a small proportion of PC tumors and PD-L1 expression was associated with metastatic disease. Targeting of the PD-1/PD-L1 pathway with immune checkpoint inhibitors may thus offer a treatment option for a subset of PC patients. ...
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Additional information about fundingThis work was supported by the Finnish Cancer Foundation (no grant number) and the Helsinki University Hospital Research Fund (grant number TYH2017204).
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