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Transcription factors gene expression in chronic rhinosinusitis with and without nasal polyps

Similarly, Th17 were reported to have a potentially protective immune homeostatic role in CRSwNP and to be a part of the normal homeostatic immune response in healthy nasal mucosa by IL-17 production. 15 Regulatory T cells (Treg) control the CRS inflammation; the regulatory cells deficiency or dysfunction can lead to exaggerated inflammation; on the other hand, an elevated Treg number might be a sign of an unsuccessful inflammation control by immune system. 16 Current therapeutic approaches still fail in a portion of patients with severe persistent CRS symptoms and

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LncRNA NEAT1 promotes endometrial cancer cell proliferation, migration and invasion by regulating the miR-144-3p/EZH2 axis

.1016/j.cancergen.2017.06.003 10.1016/j.cancergen.2017.06.003 29025584 Sun W Yang Y Xu C Guo J Regulatory mechanisms of long noncoding RNAs on gene expression in cancers Cancer Genet 2017 216-217 105 10 10.1016/j.cancergen.2017.06.003 6 Jing N, Huang T, Guo H, Yang J, Li M, Chen Z, et al. LncRNA CASC15 promotes colon cancer cell proliferation and metastasis by regulating the miR4310/LGR5/Wnt/betacatenin signaling pathway. Mol Med Rep 2018; 18: 2269-76. doi: 10.3892/mmr.2018.9191 29956772 Jing N Huang T Guo H Yang J Li

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Dusp6 inhibits epithelial-mesenchymal transition in endometrial adenocarcinoma via ERK signaling pathway

lines. Both overexpression and knockdown of DUSP6 were constructed to evaluate the functions on regulating the expressions of EMT- markers, cell growth, invasion and migration abilities. The protein levels of ERK and phosphorylated ERK were also analyzed to determine the regulatory role of DUSP6 on the ERK signaling. Our results suggest DUSP6 inhibits EMT process in endometrial adenocarcinoma in vitro via suppressing the ERK signaling pathway. Materials and methods Tissue samples, cell culture Tumor and the corresponding adjacent tumor tissues (more than 5

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Cytokine CCL5 and receptor CCR5 axis in glioblastoma multiforme

-1 glioma growth Neoplasia 2015 17 776 88 10.1016/j.neo.2015.10.002 72 Chakraborty R, Rooney C, Dotti G, Savoldo B. Changes in chemokine receptor expression of regulatory T cells after ex vivo culture. J Immunother 2012; 35: 329-36. doi: 10.1097/CJI.0b013e318255adcc 22495390 10.1097/CJI.0b013e318255adcc Chakraborty R Rooney C Dotti G Savoldo B Changes in chemokine receptor expression of regulatory T cells after ex vivo culture J Immunother 2012 35 329 36 10.1097/CJI.0b013e318255adcc 73 Wang SW, Liu SC, Sun HL, Huang

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Radiological findings of porcine liver after electrochemotherapy with bleomycin

E, Sersa G, Jesenko T, Pelofy S, Teissié, et al. Increased permeability of blood vessels after reversible electroporation is facilitated by alterations in endothelial cell-to-cell junctions. J Control Release 2018; 276: 30-41. doi: 10.1016/j.jconrel.2018.02.032 29476881 10.1016/j.jconrel.2018.02.032 Markelc B Bellard E Sersa G Jesenko T Pelofy S Teissié, et al Increased permeability of blood vessels after reversible electroporation is facilitated by alterations in endothelial cell-to-cell junctions J Control Release 2018 276 30

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Mobilization with cyclophosphamide reduces the number of lymphocyte subpopulations in the leukapheresis product and delays their reconstitution after autologous hematopoietic stem cell transplantation in patients with multiple myeloma

marrow aplasia followed by delayed reconstitution of lymphocytes resulting in partial recovery on collection day. 11 As a consequence lower doses of lymphocytes are col lected and reinfused. There is accumulating evidence that the dose of infused lymphocytes and their recovery on day 15 and 30 after AHSCT are independent prognostic factors for overall survival in patients with non-Hodgkin lymphomas and myeloma. 12 - 15 Among lymphocyte subpopulations the CD16+/56+ natural killer (NK) cells are particularly strong independent predictors of survival. 12 T regulatory

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The expanding new era of cancer immunotherapy

processed. Using dendritic cells, it is possible to present antigens in a way that stimulates T regulatory cells, which would opposean antitumor response. APCs require a maturation signal in order to promote immunity. Partial maturation may be induced through toll-like receptor signaling from necrotic tumor cells. The successful use of checkpoint inhibitors led to a breakthrough in the development of cancer immunotherapy. The anti-CTLA-4 monoclonal antibody Ipilimumab was the first checkpoint inhibitor that achieved durable objective responses in metastatic melanoma

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Reinstating endogenous antitumor immunity: The concept of therapeutic management of cancer

biology of tumour cells, making them less immunogenic, highly suppressive, with a high angiogenic output. This may seriously impact the balance between the effector and regulatory cell compartments by favouring the infiltration and accumulation of regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSC) within tumours. In this way, the effector T cells that do infiltrate the tumour will be negatively controlled by these regulatory cellular subsets and inhibitory molecules. The outcome of this dysregulated balance between effector and regulatory cells is

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Targeting the PD-1/PD-L1 axis in the treatment of lung cancer

can be traced as far back as the late 19th century, in recent years the exponential advances in the understanding of tumour–host interplay have led to important breakthroughs in the treatment of solid tumours, especially melanoma and NSCLC. The recognition by the T-cells of antigens bound to specific major histocompatibility complex (MHC) molecules and presented by the antigen-presenting cells (APCs), is the decisive first step in the process of immune recognition. This recognition is regulated by several inhibitory molecules such as the cytotoxic T

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Diagnosis and management of complications of chronic lymphocytic leukemia/small lymphocytic lymphoma

therapies resulting in longer survival. Immune dysfunction effecting both the adaptive and innate immune responses occurs early in the course of CLL and high-count monoclonal B-cell lymphocytosis (MBL) [ 6 , 7 , 8 ]. The mechanism by which CLL induces immune dysfunction is poorly understood. T cell dysfunction in CLL is characterized by abnormal CD4:CD8 effector ratios, skewed helper T cell profiles (e.g., increased Th2:Th1), impaired immune synapse formation, and reduced proliferative and cytotoxic activities characteristic of T cell exhaustion [ 8 , 9 , 10 , 11

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