A5070789136- Immune cells in cancer
- Cytokine Signaling Pathways and Interactions
- Inflammatory mediators and NSAID effects
- Cancer Immunotherapy and Biomarkers
- Adipose Tissue and Metabolism
- Immune Cell Function and Interaction
- Cancer, Hypoxia, and Metabolism
- HIV-related health complications and treatments
- interferon and immune responses
- Lymphoma Diagnosis and Treatment
- Vitamin C and Antioxidants Research
- Metabolomics and Mass Spectrometry Studies
- Histone Deacetylase Inhibitors Research
- Peroxisome Proliferator-Activated Receptors
- Immune Response and Inflammation
- NF-κB Signaling Pathways
- Cancer Research and Treatments
- Adenosine and Purinergic Signaling
- Nanoparticle-Based Drug Delivery
- TGF-β signaling in diseases
- Sphingolipid Metabolism and Signaling
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- RNA modifications and cancer
- Immunotherapy and Immune Responses
- Pharmacological Effects of Natural Compounds
Università degli Studi del Piemonte Orientale “Amedeo Avogadro”
2015-2025
IRCCS Humanitas Research Hospital
2023-2024
Humanitas University
2016-2023
Istituti di Ricovero e Cura a Carattere Scientifico
2020-2023
Myeloid-derived suppressor cells (MDSC) include immature monocytic (M-MDSC) and granulocytic (PMN-MDSC) that share the ability to suppress adaptive immunity hinder effectiveness of anticancer treatments. Of note, in response IFNγ, M-MDSCs release tumor-promoting immunosuppressive molecule nitric oxide (NO), whereas macrophages largely express antitumor properties. Investigating these opposing activities, we found tumor-derived prostaglandin E2 (PGE2) induces nuclear accumulation p50 NF-κB...
Abstract Purpose: Tumor-associated macrophages (TAMs) and the hyperactivation of PI3K/AKT pathway are involved in pathogenesis Hodgkin lymphoma affect disease outcome. Because δ γ isoforms PI3K overexpressed Hodgkin/Reed–Sternberg (HRS) cells tumor microenvironment (TME), we propose that PI3Kδ/γ inhibitor RP6530 might both HRS TME, ultimately leading to an enhanced antitumor response. Experimental Design: cell lines (L-540, KM-H2, L-428) primary human were used investigate activity vitro...
Abstract Cancer induces alteration of hematopoiesis to fuel disease progression. We report that in tumor-bearing mice the macrophage colony-stimulating factor elevates myeloid cell levels nicotinamide phosphoribosyltransferase (NAMPT), rate-limiting enzyme NAD salvage pathway, which acts as negative regulator CXCR4 retention axis hematopoietic cells bone marrow. NAMPT inhibits through a NAD/Sirtuin 1–mediated inactivation HIF1α-driven gene transcription, leading mobilization immature...
Myeloid-derived suppressor cells (MDSC) are well-known key negative regulators of the immune response during tumor growth, however scattered is knowledge their capacity to influence and adapt different microenvironments markers that identify those capacities. Here we show secreted protein acidic rich in cysteine (SPARC) identifies both human mouse MDSC with suppressive pro-tumoral activities including induction epithelial-to-mesenchymal transition (EMT) angiogenesis. In mice genetic deletion...
Although tumor-associated macrophages (TAM) display a M2-skewed tumor-promoting phenotype in most cancers, colorectal cancer, both TAM polarization and its impact remain controversial. We investigated the role of M2-polarizing p50 NF-κB subunit orchestrating phenotype, tumor microenvironment composition, cancer progression. first demonstrated, by parallel studies colitis-associated (CAC) genetically driven ApcMin mouse models, that p50-dependent inhibition M1-polarized gut inflammation...
Abstract Despite well-documented metabolic and hematopoietic alterations during tumor development, the mechanisms underlying this crucial immunometabolic intersection remain elusive. Of particular interest is connection between lipid metabolism retinoic-acid-related orphan receptor (RORC1/RORγ), whose transcriptional activity modulates cancer-related emergency myelopoiesis boosted by cholesterol metabolites, while hypercholesterolemia itself associated with dysregulated myelopoiesis. Here,...
Background A bidirectional crosstalk between tumor cells and the surrounding microenvironment contributes to progression response therapy. Our previous studies have demonstrated that bcl-2 affects melanoma regulates microenvironment. The aim of this study was evaluate whether expression in could influence tumor-promoting functions tumor-associated macrophages, a major constituent anticancer immunity favoring progression. Methods THP-1 monocytic cells, monocyte-derived macrophages expressing...
Research Article14 December 2016Open Access Source DataTransparent process VEGF blockade enhances the antitumor effect of BRAFV600E inhibition Valentina Comunanza Department Oncology, University Torino, Candiolo, Italy Candiolo Cancer Institute IRCCS, Search for more papers by this author Davide Corà Center Molecular Systems Biology, Orbassano, Francesca Orso Biotechnology (MBC), and Health Sciences, Maria Consonni Humanitas Clinical Center, Rozzano, Emanuele Middonti Federica Di...
Even though cancer patients are generally considered more susceptible to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, the mechanisms driving their predisposition forms of disease 2019 (COVID-19) have not yet been deciphered. Since metabolic disorders associated with homeostatic frailty, which increases risk infection and cancer, we asked whether could identify immunometabolic pathways intersecting SARS-CoV-2 infection. Thanks a combined flow cytometry multiomics...
<div>Abstract<p>Myeloid-derived suppressor cells (MDSC) include immature monocytic (M-MDSC) and granulocytic (PMN-MDSC) that share the ability to suppress adaptive immunity hinder effectiveness of anticancer treatments. Of note, in response IFNγ, M-MDSCs release tumor-promoting immunosuppressive molecule nitric oxide (NO), whereas macrophages largely express antitumor properties. Investigating these opposing activities, we found tumor-derived prostaglandin E2 (PGE2) induces...
<div>Abstract<p>Cancer induces alteration of hematopoiesis to fuel disease progression. We report that in tumor-bearing mice the macrophage colony-stimulating factor elevates myeloid cell levels nicotinamide phosphoribosyltransferase (NAMPT), rate-limiting enzyme NAD salvage pathway, which acts as negative regulator CXCR4 retention axis hematopoietic cells bone marrow. NAMPT inhibits through a NAD/Sirtuin 1–mediated inactivation HIF1α-driven <i>CXCR4</i> gene...
<p>NAMPT inhibitors reduce both tumor growth and MDSCs expansion</p>
<p>G-CSF and M-CSF control NAMPT-dependent regulation of CXCR4</p>
<p>NAMPT controls the suppressive activity of M-MDSCs</p>