0000000000815735

AUTHOR

Emma Di Carlo

0000-0001-7778-1042

showing 6 related works from this author

Interleukin-17A promotes the growth of human germinal center derived non-Hodgkin B cell lymphoma

2015

Interleukin (IL)-17A belongs to IL-17 superfamily and binds the heterodimeric IL-17 receptor (R)(IL-17RA/IL-17RC). IL-17A promotes germinal center (GC) formation in mouse models of autoimmune or infectious diseases, but the role of IL-17A/IL-17AR complex in human neoplastic GC is unknown. In this study, we investigated expression and function of IL-17A/IL-17AR in the microenvironments of 44 B cell non-Hodgkin lymphomas (B-NHL) of GC origin (15 follicular lymphomas, 17 diffuse large B cells lymphomas and 12 Burkitt lymphomas) and 12 human tonsil GC. Furthermore, we investigated the role of IL-17A in two in vivo models of GC B cell lymphoma, generated by s.c. injection of SU-DHL-4 and OCI-Ly8…

Cell typeImmunologySettore MED/08 - Anatomia PatologicaangiogenesisB non-Hodgkin lymphomahemic and lymphatic diseasesmedicineIL-17AImmunology and Allergytumor immunologyCXCL13B-cell lymphomaangiogenesis; B non-Hodgkin lymphoma; GC B cells; IL-17A; IL-17A receptor; tumor immunology; Immunology and Allergy; Oncology; ImmunologyB cellOriginal ResearchSevere combined immunodeficiencybusiness.industryIL-17A receptorGerminal centerInterleukinangiogenesimedicine.diseaseMolecular biologyGC B cellmedicine.anatomical_structureOncologyCell cultureImmunologyGC B cellsbusiness
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Genetic deletion of osteopontin in TRAMP mice skews prostate carcinogenesis from adenocarcinoma to aggressive human-like neuroendocrine cancers

2015

// Giorgio Mauri 1 , Elena Jachetti 1 , Barbara Comuzzi 1 , Matteo Dugo 2 , Ivano Arioli 1 , Silvia Miotti 1 , Sabina Sangaletti 1 , Emma Di Carlo 3, 4 , Claudio Tripodo 5 , Mario P. Colombo 1 1 Molecular Immunology Unit, Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale Tumori, 20133, Milano, Italy 2 Functional Genomics and Bioinformatics, Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale Tumori, 20133, Milano, Italy 3 Department of Medicine and Science of Aging, Section of Anatomic Pathology and Molecular Medicine, “G. d’Annunzio” University, 66100, Chieti, Italy 4 Ce.S.I. Aging Research Center, “G…

0301 basic medicineMalePathologyFluorescent Antibody Techniquemedicine.disease_causeImmunoenzyme TechniquesProstate cancerMice0302 clinical medicineOsteopontinProstate cancerbiologyReverse Transcriptase Polymerase Chain ReactionExtracellular matrixNeuroendocrine TumorsCell Transformation NeoplasticNeuroendocrineOncology030220 oncology & carcinogenesisDisease ProgressionAdenocarcinomaTrampResearch Papermedicine.medical_specialtyBlotting WesternMice TransgenicAdenocarcinomaSettore MED/08 - Anatomia PatologicaReal-Time Polymerase Chain Reaction03 medical and health sciencesstomatognathic systemmedicineAnimalsHumansExtracellular matrix; Neuroendocrine; Osteopontin; Prostate cancer; OncologyRNA Messengerbusiness.industryGene Expression ProfilingCancerProstatic Neoplasmsmedicine.diseaseMolecular medicineMice Inbred C57BLDisease Models Animal030104 developmental biologyTumor progressionbiology.proteinOsteopontinCarcinogenesisbusinessGene Deletion
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Interleukin-30 feeds breast cancer stem cells via CXCL10 and IL23 autocrine loops and shapes immune contexture and host outcome

2021

BackgroundBreast cancer (BC) progression to metastatic disease is the leading cause of death in women worldwide. Metastasis is driven by cancer stem cells (CSCs) and signals from their microenvironment. Interleukin (IL) 30 promotes BC progression, and its expression correlates with disease recurrence and mortality. Whether it acts by regulating BCSCs is unknown and could have significant therapeutic implications.MethodsHuman (h) and murine (m) BCSCs were tested for their production of and response to IL30 by using flow cytometry, confocal microscopy, proliferation and sphere-formation assays, and PCR array. Immunocompetent mice were used to investigate the role of BCSC-derived IL30 on tumor…

Cancer Research2434ImmunologyTriple Negative Breast NeoplasmsBiologyInterleukin-23Paracrine signallingMiceCancer stem cellCell Line Tumorbreast neoplasmsImmunology and Allergytumor microenvironmentAnimalsHumans1506Autocrine signallingRC254-282PharmacologyTumor microenvironmentbreast neoplasms cytokines tumor microenvironmentInterleukinsInnate lymphoid cellNeoplasms. Tumors. Oncology. Including cancer and carcinogensFOXP3Basic Tumor ImmunologyDendritic cellcytokinesChemokine CXCL10Autocrine CommunicationOncologyKLF4Cancer researchNeoplastic Stem CellsMolecular MedicineFemaleJournal for Immunotherapy of Cancer
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Coexpression of IL-6 and soluble IL-6R causes nodular regenerative hyperplasia and adenomas of the liver

1998

Studies with tumor necrosis factor p55 receptor- and interleukin-6 (IL-6)-deficient mice have shown that IL-6 is required for hepatocyte proliferation and reconstitution of the liver mass after partial hepatectomy. The biological activities of IL-6 are potentiated when this cytokine binds soluble forms of its specific receptor subunit (sIL-6R) and the resulting complex interacts with the transmembrane signaling chain gp130. We show here that double transgenic mice expressing high levels of both human IL-6 and sIL-6R under the control of liver-specific promoters spontaneously develop nodules of hepatocellular hyperplasia around periportal spaces and present signs of sustained hepatocyte prol…

AdenomaSTAT3 Transcription FactorAdenomail-6; liver adenomas; nodular hyperplasia; soluble il-6rMice TransgenicBiologyGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins c-mycMiceMyeloproliferative Disordersil-6medicineAnimalsnodular hyperplasiaReceptorMolecular BiologyHyperplasialiver adenomasHaptoglobinsGeneral Immunology and MicrobiologyInterleukin-6General NeuroscienceLiver NeoplasmsHyperplasiaGlycoprotein 130medicine.diseaseReceptors Interleukin-6Liver regenerationLiver RegenerationDNA-Binding Proteinsmedicine.anatomical_structureGene Expression RegulationLiverSolubilityHepatocyteTrans-ActivatorsCancer researchEndothelium Vascularsoluble il-6rNodular regenerative hyperplasiaResearch ArticleThe EMBO Journal
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IL-25 dampens the growth of human germinal center-derived B-cell non Hodgkin Lymphoma by curtailing neoangiogenesis

2018

Interleukin (IL)-25, a member of the IL-17 cytokine superfamily, is produced by immune and non-immune cells and exerts type 2 pro-inflammatory effects in vitro and in vivo. The IL-25 receptor(R) is composed of the IL-17RA/IL-17RB subunits. Previous work showed that germinal centre (GC)-derived B-cell non Hodgkin lymphomas (B-NHL) expressed IL-17AR, formed by IL-17RA and IL-17RC subunits, and IL-17A/IL-17AR axis promoted B-NHL growth by stimulating neoangiogenesis. Here, we have investigated expression and function of IL-25/IL-25R axis in lymph nodes from human GC-derived B-NHL, i.e. Follicular Lymphoma (FL,10 cases), Diffuse Large B Cell Lymphoma (6 cases) and Burkitt Lymphoma (3 cases). Tu…

0301 basic medicinelcsh:Immunologic diseases. AllergyPathologymedicine.medical_specialtyAngiogenesismedicine.medical_treatmentImmunologyFollicular lymphomalcsh:RC254-282Angiogenesis; B lymphocytes; B-NHL; Cytokines; IL-25; Tumor immunology; Immunology and Allergy; Immunology; Oncology03 medical and health sciencesangiogenesisIL-25immune system diseaseshemic and lymphatic diseasesmedicineImmunology and AllergyCytokineOriginal ResearchB lymphocyteChemistryGerminal centerInterleukinmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenscytokinesLymphomaAngiogenesi030104 developmental biologyCytokineOncologyCancer researchB-Cell Non-Hodgkin LymphomaTumor immunologyB-NHLb lymphocyteslcsh:RC581-607Diffuse large B-cell lymphoma
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The C-X-C Motif Chemokine Ligand 1 Sustains Breast Cancer Stem Cell Self-Renewal and Promotes Tumor Progression and Immune Escape Programs

2021

Breast cancer (BC) mortality is mainly due to metastatic disease, which is primarily driven by cancer stem cells (CSC). The chemokine C-X-C motif ligand-1 (CXCL1) is involved in BC metastasis, but the question of whether it regulates breast cancer stem cell (BCSC) behavior is yet to be explored. Here, we demonstrate that BCSCs express CXCR2 and produce CXCL1, which stimulates their proliferation and self-renewal, and that CXCL1 blockade inhibits both BCSC proliferation and mammosphere formation efficiency. CXCL1 amplifies its own production and remarkably induces both tumor-promoting and immunosuppressive factors, includingSPP1/OPN,ACKR3/CXCR7,TLR4,TNFSF10/TRAILandCCL18and, to a lesser exte…

breast cancer stem cellsQH301-705.5animal diseasesSettore MED/50 - Scienze Tecniche Mediche ApplicatechemokinesBiologyCXCR4MetastasisCell and Developmental Biologyimmunity geneCancer stem cellmedicinetumor microenvironmentCXC chemokine receptorsBiology (General)immunity genesTriple-negative breast cancerTumor microenvironmentbreast cancer stem cellchemokineCell BiologyBrief Research Reportrespiratory systemmedicine.diseaseCXCL1Tumor progressiontriple-negative breast cancerCancer researchCCL28Settore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioDevelopmental BiologyFrontiers in Cell and Developmental Biology
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