Search results for " Cell"

showing 10 items of 14074 documents

Primary and metastatic brain cancer genomics and emerging biomarkers for immunomodulatory cancer treatment

2018

Abstract: Recent studies with immunomodulatory agents targeting both cytotoxic T-lymphocyte protein 4 (CTLA4) and programmed cell death 1 (PD1)/programmed cell death ligand 1 (PDL1) have shown to be very effective in several cancers revealing an unexpected great activity in patients with both primary and metastatic brain tumors. Combining anti-CTLA4 and anti-PD1 agents as upfront systemic therapy has revealed to further increase the clinical benefit observed with single agent, even at cost of higher toxicity. Since the brain is an immunological specialized area it's crucial to establish the specific composition of the brain tumors' micro environment in order to predict the potential activit…

0301 basic medicineCancer ResearchSettore MED/06 - Oncologia Medicamedicine.medical_treatmentBiomarkers; Brain; CTLA4; Immunotherapy; Metastasis; PD1/PDL1GenomicsMetastasiMetastasisMetastasisImmunomodulation03 medical and health sciences0302 clinical medicinemedicineBiomarkers TumorCytotoxic T cellAnimalsHumansCTLA4Primary (chemistry)business.industryPD1/PDL1Brain NeoplasmsImmunogenicityBrainBiomarkerImmunotherapyGenomicsmedicine.diseaseCancer treatment030104 developmental biology030220 oncology & carcinogenesisToxicityCancer researchImmunotherapyHuman medicinebusinessBiomarkersSeminars in cancer biology
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Abilities of berberine and chemically modified berberines to interact with metformin and inhibit proliferation of pancreatic cancer cells.

2019

Abstract Pancreatic cancer is devastating cancer worldwide with few if any truly effective therapies. Pancreatic cancer has an increasing incidence and may become the second leading cause of death from cancer. Novel, more effective therapeutic approaches are needed as pancreatic cancer patients usually survive for less than a year after being diagnosed. Control of blood sugar levels by the prescription drug metformin in diseases such as diabetes mellitus has been examined in association with pancreatic cancer. While the clinical trials remain inconclusive, there is hope that certain diets and medications may affect positively the outcomes of patients with pancreatic and other cancers. Other…

0301 basic medicineCancer ResearchSettore MED/09 - Medicina Internaendocrine system diseasesBerberineSignal transduction inhibitorsBlood sugarPharmacologyAMP-Activated Protein KinasesBerberine; PDAC; Signal transduction inhibitors; TP5303 medical and health scienceschemistry.chemical_compound0302 clinical medicineBerberineMETFORMINAPancreatic cancerDiabetes mellitusGeneticsmedicineHumansTP53Signal transduction inhibitorMolecular BiologyCell Proliferationbusiness.industryPDACCancerAMPKmedicine.diseaseMetforminMetforminNeoplasm ProteinsPancreatic Neoplasms030104 developmental biologychemistry030220 oncology & carcinogenesisCancer cellMolecular Medicinebusinessmedicine.drugAdvances in biological regulation
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Parthenolide prevents resistance of MDA-MB231 cells to doxorubicin and mitoxantrone: the role of Nrf2.

2017

Triple-negative breast cancer is a group of aggressive cancers with poor prognosis owing to chemoresistance, recurrence and metastasis. New strategies are required that could reduce chemoresistance and increases the effectiveness of chemotherapy. The results presented in this paper, showing that parthenolide (PN) prevents drug resistance in MDA-MB231 cells, represent a contribution to one of these possible strategies. MDA-MB231 cells, the most studied line of TNBC cells, were submitted to selection treatment with mitoxantrone (Mitox) and doxorubicin (DOX). The presence of resistant cells was confirmed through the measurement of the resistance index. Cells submitted to this treatment exhibit…

0301 basic medicineCancer ResearchSmall interfering RNATriple-negative breast cancer resistance parthenolideImmunologyStimulationCancer -- TreatmentArticle03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineDownregulation and upregulationSettore BIO/10 - BiochimicamedicineChemotherapyDoxorubicinParthenolideBreast -- CancerDrug resistance in cancer cellsMitoxantroneChemistryCell BiologyTransfectionHsp70030104 developmental biology030220 oncology & carcinogenesisCancer researchmedicine.drugCell death discovery
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The tumour microenvironment as an integrated framework to understand cancer biology

2019

Cancer cells all share the feature of being immersed in a complex environment with altered cell-cell/cell-extracellular element communication, physicochemical information, and tissue functions. The so-called tumour microenvironment (TME) is becoming recognised as a key factor in the genesis, progression and treatment of cancer lesions. Beyond genetic mutations, the existence of a malignant microenvironment forms the basis for a new perspective in cancer biology where connections at the system level are fundamental. From this standpoint, different aspects of tumour lesions such as morphology, aggressiveness, prognosis and treatment response can be considered under an integrated vision, givin…

0301 basic medicineCancer ResearchStromal cellBiophysicsDiseaseBiologyExtracellular matrix03 medical and health sciences0302 clinical medicineGermline mutationImmune systemNeoplasmsTumor MicroenvironmentmedicineStromal classificationAnimalsHumansCompartment (development)CancerExtracellular matrixmedicine.diseaseBioelectricExtracellular MatrixMetabolism030104 developmental biologyOncologyCancer treatment030220 oncology & carcinogenesisCancer cellStromal CellsNeuroscienceCancer Letters
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Cancer-associated fibroblasts as abettors of tumor progression at the crossroads of EMT and therapy resistance

2019

Abstract In the last decades, the role of the microenvironment in tumor progression and therapeutic outcome has gained increasing attention. Cancer-associated fibroblasts (CAFs) have emerged as key players among stromal cells, owing to their abundance in most solid tumors and their diverse tumor-restraining/promoting roles. The interplay between tumor cells and neighboring CAFs takes place by both paracrine signals (cytokines, exosomes and metabolites) or by the multifaceted functions of the surrounding extracellular matrix. Here, we dissect the most recent identified mechanisms underlying CAF-mediated control of tumor progression and therapy resistance, which include induction of the epith…

0301 basic medicineCancer ResearchStromal cellEpithelial-Mesenchymal TransitionParacrine CommunicationAntineoplastic AgentsReviewBiologylcsh:RC254-28203 medical and health sciences0302 clinical medicineCancer-Associated FibroblastsCancer stem cellSettore MED/04 - PATOLOGIA GENERALENeoplasmsParacrine CommunicationTumor MicroenvironmentHumansEpithelial–mesenchymal transitionTumor microenvironmentCancer associated fibroblasts cancer stem cells extracellular matrix exosomes epithelial-to-mesenchymal transition.lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMicrovesiclesGene Expression Regulation Neoplastic030104 developmental biologyOncologyTumor progressionDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchDisease ProgressionMolecular MedicineCancer-Associated FibroblastsSignal Transduction
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Persistent immune stimulation exacerbates genetically driven myeloproliferative disorders via stromal remodeling

2017

Abstract Systemic immune stimulation has been associated with increased risk of myeloid malignancies, but the pathogenic link is unknown. We demonstrate in animal models that experimental systemic immune activation alters the bone marrow stromal microenvironment, disarranging extracellular matrix (ECM) microarchitecture, with downregulation of secreted protein acidic and rich in cysteine (SPARC) and collagen-I and induction of complement activation. These changes were accompanied by a decrease in Treg frequency and by an increase in activated effector T cells. Under these conditions, hematopoietic precursors harboring nucleophosmin-1 (NPM1) mutation generated myeloid cells unfit for normal …

0301 basic medicineCancer ResearchStromal cellMyeloidMice TransgenicVascular RemodelingBiologyInbred C57BLTransgenicMice03 medical and health sciencesMyelogenousMyeloproliferative DisordersmedicineAnimalsHumansMyeloproliferative DisorderAnimals; Cell Proliferation; Humans; Mice; Mice Inbred C57BL; Mice Inbred CBA; Mice Transgenic; Myeloproliferative Disorders; Stromal Cells; Vascular Remodeling; Oncology; Cancer ResearchCell ProliferationMyeloproliferative DisordersAnimalStromal CellInbred CBANeutrophil extracellular trapsmedicine.diseaseMice Inbred C57BLHaematopoiesisLeukemia030104 developmental biologymedicine.anatomical_structureOncologyImmunologyMice Inbred CBABone marrowStromal CellsNucleophosminHuman
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Differential distribution and enrichment of non-coding RNAs in exosomes from normal and Cancer-associated fibroblasts in colorectal cancer.

2018

Exosome production from cancer-associated fibroblasts seems to be an important driver of tumor progression. We report the first in-depth biotype characterization of ncRNAs, analyzed by Next Generation Sequencing and Bioinformatics, expressed in established primary human normal and cancer-associated fibroblasts (CAFs) from cancer and normal mucosa tissues from 9 colorectal cancer patients, and/or packaged in their derived exosomes. Differential representation and enrichment analyses based on these ncRNAs revealed a significant number of differences between the ncRNA content of exosomes and the expression patterns of the normal and cancer-associated fibroblast cells. ncRNA regulatory elements…

0301 basic medicineCancer ResearchStromal cellRNA UntranslatedColorectal cancerBiologyExosomeslcsh:RC254-282Non-coding RNAs03 medical and health sciencesCancer-Associated FibroblastsCell MovementNext generation sequencingmedicineBiomarkers TumorHumansLiquid biopsyLetter to the EditorCells CulturedCell ProliferationTumor microenvironmentColon CancerLiquid biopsySequence Analysis RNACancerHigh-Throughput Nucleotide SequencingFibroblastsmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisMicrovesiclesGene Expression Regulation Neoplastic030104 developmental biologyOncologyTumor microenvironmentTumor progressionCancer researchMolecular MedicineCancer-Associated FibroblastsColorectal Neoplasms
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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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Melanoma Lesions Independently Acquire T-cell Resistance during Metastatic Latency

2016

Abstract Melanoma often recurs after a latency period of several years, presenting a T cell–edited phenotype that reflects a role for CD8+ T cells in maintaining metastatic latency. Here, we report an investigation of a patient with multiple recurrent lesions, where poorly immunogenic melanoma phenotypes were found to evolve in the presence of autologous tumor antigen–specific CD8+ T cells. Melanoma cells from two of three late recurrent metastases, developing within a 6-year latency period, lacked HLA class I expression. CD8+ T cell–resistant, HLA class I–negative tumor cells became clinically apparent 1.5 and 6 years into stage IV disease. Genome profiling by SNP arrays revealed that HLA …

0301 basic medicineCancer ResearchT cellmedicine.medical_treatmentMedizinHuman leukocyte antigenCD8-Positive T-LymphocytesBiology03 medical and health sciencesAntigens NeoplasmmedicineHumansNeoplasm MetastasisMelanomaMelanomaCancerImmunosuppressionmedicine.diseasePhenotypeNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureOncologyLatency stageImmunologyCD8Cancer Research
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Lack of a peroxiredoxin suppresses the lethality of cells devoid of electron donors by channelling electrons to oxidized ribonucleotide reductase

2017

The thioredoxin and glutaredoxin pathways are responsible of recycling several enzymes which undergo intramolecular disulfide bond formation as part of their catalytic cycles such as the peroxide scavengers peroxiredoxins or the enzyme ribonucleotide reductase (RNR). RNR, the rate-limiting enzyme of deoxyribonucleotide synthesis, is an essential enzyme relying on these electron flow cascades for recycling. RNR is tightly regulated in a cell cycle-dependent manner at different levels, but little is known about the participation of electron donors in such regulation. Here, we show that cytosolic thioredoxins Trx1 and Trx3 are the primary electron donors for RNR in fission yeast. Unexpectedly,…

0301 basic medicineCancer ResearchThioredoxin reductaseSynthesis PhaseYeast and Fungal ModelsBiochemistryElectron DonorsSchizosaccharomyces PombeThioredoxinsGlutaredoxinCell Cycle and Cell DivisionGenetics (clinical)Chemical ReactionsOxidesPeroxidesNucleic acidsChemistryRibonucleotide reductaseBiochemistryExperimental Organism SystemsCell ProcessesSchizosaccharomyces pombePhysical SciencesSynthesis phaseThioredoxinOxidation-ReductionResearch ArticleDNA Replicationlcsh:QH426-470DNA transcriptionElectron donorsBiologyDNA replicationResearch and Analysis MethodsCatalysisElectron Transport03 medical and health sciencesModel OrganismsSchizosaccharomycesRibonucleotide ReductasesOxidationGeneticsMolecular BiologyEcology Evolution Behavior and SystematicsGlutaredoxinsCell growthDNA replicationChemical CompoundsOrganismsFungiBiology and Life SciencesCell BiologyDNAPeroxiredoxinsbiology.organism_classificationYeastCell cycle and cell divisionCheckpoint Kinase 2lcsh:Genetics030104 developmental biologySchizosaccharomyces pombeGene expressionSchizosaccharomyces pombe ProteinsPeroxiredoxin
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