Search results for " tumor microenvironment"

showing 10 items of 36 documents

HGF/MET Axis Induces Tumor Secretion of Tenascin-C and Promotes Stromal Rewiring in Pancreatic Cancer

2021

Simple Summary It has been previously shown that activation of the MET receptor by its ligand, the hepatocyte growth factor (HGF), modulates the tumor-stroma cross-talk in models of pancreatic cancer. We now wish to cast light on the molecular mechanisms by which this ligand/receptor pair sustains the interaction between cancer cells and the tumor microenviroment. To this end, we compared data obtained by large-scale analysis of gene expression in pancreatic cancer cells grown in the presence of HGF versus cells grown in the presence of HGF and treated with specific inhibitors of HGF/MET signaling. By clustering differentially expressed genes according to functional groups, we identified ca…

0301 basic medicineCancer ResearchStromal cellpancreatic ductal adenocarcinomaArticle03 medical and health sciences0302 clinical medicinePancreatic tumorPancreatic cancerMET oncogenemedicinetumor microenvironmentmetastasisHepatocyte growth factor; MET oncogene; Metastasis; Pancreatic ductal adenocarcinoma; Tenascin C; Tumor microenvironmentRC254-282Tumor microenvironmentbiologyChemistryTenascin Ctenascin CNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyhepatocyte growth factorOncology030220 oncology & carcinogenesisCancer cellHepatic stellate cellbiology.proteinCancer researchHepatocyte growth factormedicine.drugCancers
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Promises and Pitfalls in the Use of PD-1/PD-L1 Inhibitors in Multiple Myeloma

2018

In the biology of multiple myeloma (MM), immune dysregulation has emerged as a critical component for novel therapeutic strategies. This dysfunction is due to a reduced antigen presentation, a reduced effector cell ability and a loss of reactive T cells against myeloma, together with a bone marrow microenvironment that favors immune escape. The Programmed Death-1 (PD-1) pathway is associated with the regulation of T cell activation and with the apoptotic pathways of effector memory T cells. Specifically, the binding with PD-1 ligand (PD-L1) on the surface of tumor plasma cells down-regulates T cell-proliferation, thus contributing to the immune escape of tumor cells. In relapsed and/or refr…

0301 basic medicinePD-L1lcsh:Immunologic diseases. AllergyDurvalumabMini ReviewT-LymphocytesT cellProgrammed Cell Death 1 ReceptorImmunologyAntigen presentationT cellsPembrolizumabmedicine.disease_causeB7-H1 Antigen03 medical and health sciences0302 clinical medicineBone Marrowimmune dysregulationPD-L1PD-1Tumor MicroenvironmentmedicineAnimalsHumansImmunology and AllergyImmune dysregulation; Multiple myeloma; PD-1; PD-L1; T cells; Animals; B7-H1 Antigen; Bone Marrow; Humans; Multiple Myeloma; Programmed Cell Death 1 Receptor; T-Lymphocytes; Tumor MicroenvironmentMultiple myelomabiologybusiness.industryImmune dysregulationmedicine.diseasemultiple myeloma030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisbiology.proteinCancer researchNivolumabbusinesslcsh:RC581-607Frontiers in Immunology
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Anti-angiogenic agents in the age of resistance to immune checkpoint inhibitors: Do they have a role in non-oncogene-addicted non-small cell lung can…

2020

The introduction of licensed front-line immunotherapies has heralded a new era for the treatment of non-oncogene-addicted, advanced non-small cell lung cancer (NSCLC). Yet as with all evolutions in clinical management, changes in practice can outpace the availability of the clinical evidence needed to inform subsequent therapeutic decision making. At the time of writing, there is limited available evidence on the optimum therapeutic options after progression on immunotherapy. Further research is needed to define mechanisms of immunotherapy resistance in patients with advanced NSCLC, and to understand the implications for subsequent treatment response. Pending the availability of robust clin…

0301 basic medicinePulmonary and Respiratory MedicineOncologyCancer Researchmedicine.medical_specialtyLung Neoplasmsmedicine.medical_treatmentNintedanibContext (language use)Angiogenesis InhibitorsAnti-angiogenic drugNon-oncogene-addicted non-small cell lung cancer (NSCLC)03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineCarcinoma Non-Small-Cell LungmedicineTumor MicroenvironmentHumansTumor microenvironment (TME)Lung cancerImmune Checkpoint InhibitorsTumor microenvironmentAnti-angiogenic drug; Immunotherapy resistance; Nintedanib; Non-oncogene-addicted non-small cell lung cancer (NSCLC); Tumor microenvironment (TME); Vascular endothelial growth factor (VEGF)Oncogenebusiness.industryVascular endothelial growth factor (VEGF)ImmunosuppressionImmunotherapymedicine.diseaseImmunotherapy resistance030104 developmental biologyOncologychemistry030220 oncology & carcinogenesisNintedanibNon small cellImmunotherapybusiness
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The Abundance of Tumor-Infiltrating CD8+ Tissue Resident Memory T Lymphocytes Correlates with Patient Survival in Glioblastoma

2022

Glial tumors alone account for 40% of all CNS tumors and present a low survival rate. The tumor microenvironment is a critical regulator of tumor progression and therapeutic effectiveness in glioma. Growing evidence from numerous studies of human solid tumor-infiltrating CD8(+) T cells indicates that tissue-resident memory T cells (TRM) represent a substantial subpopulation of tumor-infiltrating lymphocytes (TILs). Although it is reported that some types of cancer patients with high immune infiltration tend to have better outcomes than patients with low immune infiltration, it seems this does not happen in gliomas. This study aimed to characterize TRMs cells in the glioma tumor microenviron…

Settore MED/04 - Patologia Generaletissue resident memory cellsSettore MED/27 - NeurochirurgiaglioblastomaMedicine (miscellaneous)glioblastoma; tissue resident memory cells; CD8<sup>+</sup> lymphocytes; tumor microenvironmenttumor microenvironmentSettore MED/05 - Patologia ClinicaGeneral Biochemistry Genetics and Molecular BiologyCD8+ lymphocytes
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Mast Cells and Th17 Cells Contribute to the Lymphoma-Associated Pro-Inflammatory Microenvironment of Angioimmunoblastic T-Cell Lymphoma

2010

Reports focusing on the immunological microenvironment of peripheral T-cell lymphomas (PTCL) are rare. Here we studied the reciprocal contribution of regulatory (Treg) and interleukin-17-producing (Th17) T-cells to the composition of the lymphoma-associated microenvironment of angioimmunoblastic T-cell lymphoma (AITL) and PTCL not otherwise specified on tissue microarrays from 30 PTCLs not otherwise specified and 37 AITLs. We found that Th17 but not Treg cells were differently represented in the two lymphomas and correlated with the amount of mast cells (MCs) and granulocytes, which preferentially occurred in the cellular milieu of AITL cases. We observed that MCs directly synthesized inter…

Angioimmunoblastic T-cell lymphomaLymphomaInflammationBiologymedicine.disease_causeCXCR3Lymphoma T-CellCXCR5Pathology and Forensic MedicineAutoimmunityAnimals Chemokine CXCL13; immunology Cytokines; genetics/immu/nology Forkhead Transcription Factors; immunology Gene Expression Profiling Humans Immunoblastic Lymphadenopathy; immunology/pathology Inflammation; immunology Interleukin-17; immunology Interleukin-6; immunology Lymphoma; T-Cell; immunology/pathology Mast Cells; immunology Microarray Analysis Th17 Cells; immunology Tumor MicroenvironmentimmunologymedicineTumor MicroenvironmentAnimalsHumansMast CellsInflammationTumor microenvironmentInterleukin-6Gene Expression ProfilingInterleukin-17Forkhead Transcription FactorsMast cellmedicine.diseaseT-CellMicroarray AnalysisChemokine CXCL13humanitiesgenetics/immu/nologyLymphomamedicine.anatomical_structureImmunoblastic LymphadenopathyImmunologyCytokinesimmunology/pathologyTh17 CellsMast Cell microenvironment angioimmunoblasticmedicine.symptomRegular Articles
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Mutant p53 induces Golgi tubulo-vesiculation driving a prometastatic secretome

2020

TP53 missense mutations leading to the expression of mutant p53 oncoproteins are frequent driver events during tumorigenesis. p53 mutants promote tumor growth, metastasis and chemoresistance by affecting fundamental cellular pathways and functions. Here, we demonstrate that p53 mutants modify structure and function of the Golgi apparatus, culminating in the increased release of a pro-malignant secretome by tumor cells and primary fibroblasts from patients with Li-Fraumeni cancer predisposition syndrome. Mechanistically, interacting with the hypoxia responsive factor HIF1α, mutant p53 induces the expression of miR-30d, which in turn causes tubulo-vesiculation of the Golgi apparatus, leading …

0301 basic medicineBiopsyGeneral Physics and AstronomyGolgi ApparatusAnimals Biopsy Breast Neoplasms Cell Line Tumor Cell Transformation Neoplastic Female Fibroblasts Gene Expression Regulation Neoplastic Golgi Apparatus Humans Hypoxia-Inducible Factor 1 alpha Subunit Li-Fraumeni Syndrome Mice MicroRNAs Microtubules Mutation Primary Cell Culture Secretory Vesicles Signal TransductionSkin Tumor Microenvironment Tumor Suppressor Protein p53 Xenograft Model Antitumor Assays02 engineering and technologymedicine.disease_causeCell TransformationMicrotubulesSettore BIO/09 - FisiologiaMetastasisLi-Fraumeni SyndromeMiceTumor MicroenvironmentGolgisecretory machinerySuper-resolution microscopyAnimals; Biopsy; Breast Neoplasms; Cell Line Tumor; Cell Transformation Neoplastic; Female; Fibroblasts; Gene Expression Regulation Neoplastic; Golgi Apparatus; Humans; Hypoxia-Inducible Factor 1 alpha Subunit; Li-Fraumeni Syndrome; Mice; MicroRNAs; Microtubules; Mutation; Primary Cell Culture; Secretory Vesicles; Signal Transduction; Skin; Tumor Microenvironment; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assayslcsh:ScienceSkinMultidisciplinaryTumorChemistrymutant p53QCell migrationMicroRNASecretomics021001 nanoscience & nanotechnologyCell biologyGene Expression Regulation NeoplasticCell Transformation NeoplasticsymbolsFibroblastmiR-30dFemaleHypoxia-Inducible Factor 10210 nano-technologyBreast NeoplasmHumanSignal TransductionCancer microenvironmentStromal cellSecretory VesicleSciencePrimary Cell CultureBreast NeoplasmsMicrotubuleGolgi ApparatuSettore MED/08 - Anatomia Patologicaalpha SubunitGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencessymbols.namesakeCell Line TumormedicineAnimalsHumansSettore MED/05 - Patologia ClinicaSecretionTumor microenvironmentNeoplasticAnimalSecretory VesiclesGeneral ChemistryOncogenesGolgi apparatusHDAC6FibroblastsMicroreviewHypoxia-Inducible Factor 1 alpha SubunitmicroenvironmentXenograft Model Antitumor AssaysMicroRNAs030104 developmental biologyGene Expression RegulationMutationlcsh:QTumor Suppressor Protein p53Carcinogenesis
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Editorial: The effects of chemotherapy towards the tumor microenvironment

2022

3 p.-1 fig.

Cancer ResearchOncologyTumor microenvironmentImmunogeniccancer chemotherapy tumor microenvironmentChemotherapyTherapyCancer
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Editorial: CAR T-cells: novel therapeutic approaches in the new era of cancer immunotherapy

2023

Immunotherapy has emerged as one of the most effective treatments capable of overcoming tumor resistance mechanisms due to its ability to modulate the patient’s immune response against cancer. Personalized anti-tumor therapy based on T cells engineered to express a cancer-specific chimeric antigen receptor (CAR) acts directly on the immune system of patients. Specifically, this therapy enhances the recognition of cancer cells by T lymphocytes, thus promoting their elimination. In this Research Topic several aspects of CAR T-cell therapy, with particular emphasis on novel findings aimed at ameliorating the effectiveness of CAR T-cell-based immunotherapy and reducing side effects, are describ…

CAR T-cell cancer immunotherapy side effects tumor microenvironmentddc:610
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Messing Up the Cancer Stem Cell Chemoresistance Mechanisms Supported by Tumor Microenvironment

2021

Despite the recent advances in cancer patient management and in the development of targeted therapies, systemic chemotherapy is currently used as a first-line treatment for many cancer types. After an initial partial response, patients become refractory to standard therapy fostering rapid tumor progression. Compelling evidence highlights that the resistance to chemotherapeutic regimens is a peculiarity of a subpopulation of cancer cells within tumor mass, known as cancer stem cells (CSCs). This cellular compartment is endowed with tumor-initiating and metastasis formation capabilities. CSC chemoresistance is sustained by a plethora of grow factors and cytokines released by neighboring tumor…

cancer stem cells0301 basic medicineCancer ResearchDNA repairmedicine.medical_treatmentReviewTargeted therapy03 medical and health sciences0302 clinical medicineImmune systemCancer stem celltumor microenvironmentMedicinecancer stem cells tumor microenvironment anticancer drugs chemoresistance targeted therapyRC254-282Tumor microenvironmentbusiness.industrychemoresistanceNeoplasms. Tumors. Oncology. Including cancer and carcinogensCancertargeted therapymedicine.diseaseanticancer drugs030104 developmental biologyOncologyTumor progression030220 oncology & carcinogenesisCancer cellCancer researchSettore MED/46 - Scienze Tecniche Di Medicina Di Laboratoriobusiness
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C1q–Ha matrix regulates the local synthesis of hyaluronan in malignant pleural mesothelioma by modulating has3 expression

2021

Increased hyaluronic acid (HA) production is often associated with cancer progression. In malignant pleural mesothelioma (MPM), HA is found at elevated levels in pleural effusions and sera of patients, and it has been widely debated whether MPM cells are able to produce HA by themselves or through the release of growth factors stimulating other cells. Another key component of the MPM microenvironment is C1q, which can act as a pro-tumorigenic factor favoring cell adhesion, migration and proliferation. The aim of the current study was to prove that MPM primary cells are able to synthesize HA and to inquire the stimulus given by C1q&ndash

hyaluronan synthaseCancer ResearchComplement systemHyaluronic acidMalignant pleural mesotheliomahyaluronan synthasesMatrix (biology)lcsh:RC254-282Articlechemistry.chemical_compoundImmune systemHyaluronan synthaseHyaluronic acidhyaluronic acidmalignant pleural mesotheliomacancertumor microenvironmentC1q; Cancer; Complement system; HAS3; Hyaluronan synthases; Hyaluronic acid; Immune system; Malignant pleural mesothelioma; Tumor microenvironmenttumor microenvironment.Cell adhesioncomplement systemC1qCancerTumor microenvironmentMessenger RNAChemistrylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensComplement systemimmune systemHAS3Immune systemOncologyTumor microenvironmentCancer researchIntracellular
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