about
Molecular pathways: hypoxia response in immune cells fighting or promoting cancerModelling pulmonary microthrombosis coupled to metastasis: distinct effects of thrombogenesis on tumorigenesisIntensive pharmacological immunosuppression allows for repetitive liver gene transfer with recombinant adenovirus in nonhuman primatesHIF transcription factors, inflammation, and immunity.Hypoxia-induced soluble CD137 in malignant cells blocks CD137L-costimulation as an immune escape mechanism.Therapeutic antitumor efficacy of anti-CD137 agonistic monoclonal antibody in mouse models of myelomaS-2-hydroxyglutarate regulates CD8+ T-lymphocyte fate.Lysine 63 polyubiquitination in immunotherapy and in cancer-promoting inflammation.Immune response regulation in the tumor microenvironment by hypoxia.Essential complicity of perforin-granzyme and FAS-L mechanisms to achieve tumor rejection following treatment with anti-CD137 mAbCombined immunostimulatory monoclonal antibodies extend survival in an aggressive transgenic hepatocellular carcinoma mouse model.T cell costimulation with anti-CD137 monoclonal antibodies is mediated by K63-polyubiquitin-dependent signals from endosomes.Constitutive Glycolytic Metabolism Supports CD8(+) T Cell Effector Memory Differentiation during Viral Infection.Agonist anti-CD137 mAb act on tumor endothelial cells to enhance recruitment of activated T lymphocytes.Intratumoral injection of interferon-α and systemic delivery of agonist anti-CD137 monoclonal antibodies synergize for immunotherapy.In vivo depletion of DC impairs the anti-tumor effect of agonistic anti-CD137 mAb.Palettes of vaccines and immunostimulatory monoclonal antibodies for combination.An HIF-1α/VEGF-A Axis in Cytotoxic T Cells Regulates Tumor Progression.Hypoxia-induced soluble CD137 in malignant cells blocks CD137L-costimulation as an immune escape mechanism.Therapeutic activity of a combination of immunostimulatory monoclonal antibodies (anti-B7-H1, CD137 and OX40) on a c-myc-driven spontaneous transgenic model of hepatocellular carcinoma.CD69 is a direct HIF-1α target gene in hypoxia as a mechanism enhancing expression on tumor-infiltrating T lymphocytes.The Factor Inhibiting HIF Asparaginyl Hydroxylase Regulates Oxidative Metabolism and Accelerates Metabolic Adaptation to Hypoxia.CD137 on inflamed lymphatic endothelial cells enhances CCL21-guided migration of dendritic cellsThe HIF-1α Hypoxia Response in Tumor-Infiltrating T Lymphocytes Induces Functional CD137 (4-1BB) for ImmunotherapyDendritic cells adhere to and transmigrate across lymphatic endothelium in response to IFN-αDelivery of immunostimulatory monoclonal antibodies by encapsulated hybridoma cells
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description
researcher
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wetenschapper
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հետազոտող
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name
Asis Palazon
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Asis Palazon
@en
Asis Palazon
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Asis Palazon
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type
label
Asis Palazon
@ast
Asis Palazon
@en
Asis Palazon
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Asis Palazon
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prefLabel
Asis Palazon
@ast
Asis Palazon
@en
Asis Palazon
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Asis Palazon
@nl
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P108
P31
P496
0000-0002-7172-7229