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Programmed cell death (PD)-1/PD-1 ligand-1 (PD-L1)-targeted therapy has emerged as a promising therapeutic strategy for lung cancer. However, whether EML4-ALK regulates PD-L1 expression in lung cancer remains unknown. A total of 532 pulmonary adenocarcinomas (pADCs), including 58 ALK-translocated tumors, were immunohistochemically evaluated for PD-L1 and PD-1. H23 (EGFRWild-typeEML4-ALK−PD-L1Low) and H2228 (EGFRWild-typeEML4-ALK+PD-L1High) cells were transfected with EML4-ALK or ALK short interf

AIMS: To investigate the clinicopathological characteristics of programmed cell death ligand 1 (PD-L1) and programmed cell death 1 (PD-1) expression in the tumour microenvironments of diffuse large B cell lymphoma (DLBCL). METHODS AND RESULTS: Tumour tissues from 126 DLBCL patients were immunostained for PD-L1 and PD-1. The expression of PD-L1 by tumour cells and/or tumour-infiltrating immune cells (mainly macrophages) was evaluated, and the number of tumour-infiltrating PD-1(+) cells was assess

Tumor-associated macrophages (TAMs) and regulatory T-cells (Tregs) play an important role in the tumor microenvironment. Here, we investigated the prognostic implications of TAMs and Tregs in 165 diffuse large B-cell lymphomas (DLBCLs) using immunohistochemistry. Survival analysis was performed among 109 DLBCLs treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP). An increase in CD68 (+) cells was related to improved overall survival (OS) (p = 0.033). By con

Abstract Background We investigated the role of PD-L1 in the metabolic reprogramming of non-small cell lung cancer (NSCLC). Methods Changes in glycolysis-related molecules and glycolytic activity were evaluated in PD-L1 low and PD-L1 high NSCLC cells after transfection or knockdown of PD-L1 , respectively. Jurkat T-cell activation was assessed after co-culture with NSCLC cells. The association between PD-L1 and immune response-related molecules or glycolysis were analyzed in patients with NSCLC

Pellino-1 is an E3 ubiquitin ligase acting as a critical mediator for a variety of immune receptor signaling pathways, including Toll-like receptors, interleukin-1 receptor and T-cell receptors. We recently showed that the Pellino-1-transgenic (Tg) mice developed multiple tumors with different subtypes in hematolymphoid and solid organs. However, the molecular mechanism underlying the oncogenic role of Pellino-1 in solid tumors remains unknown. Pellino-1-Tg mice developed adenocarcinoma in the l