Search results for "TUMOR"

showing 10 items of 6365 documents

Molecular, Biological and Structural Features of VL CDR-1 Rb44 Peptide, Which Targets the Microtubule Network in Melanoma Cells

2019

Microtubules are important drug targets in tumor cells, owing to their role in supporting and determining the cell shape, organelle movement and cell division. The complementarity-determining regions (CDRs) of immunoglobulins have been reported to be a source of anti-tumor peptide sequences, independently of the original antibody specificity for a given antigen. We found that, the anti-Lewis B mAb light-chain CDR1 synthetic peptide Rb44, interacted with microtubules and induced depolymerization, with subsequent degradation of actin filaments, leading to depolarization of mitochondrial membrane-potential, increase of ROS, cell cycle arrest at G2/M, cleavage of caspase-9, caspase-3 and PARP, …

0301 basic medicineCancer ResearchCell divisionComplementarity determining regionCleavage (embryo)lcsh:RC254-28203 medical and health sciences0302 clinical medicineDownregulation and upregulationMicrotubulecomplementarity-determining regionActinbiologyChemistryIntrinsic apoptosisapoptosislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenspeptideCell biology030104 developmental biologyTubulintubulinOncology030220 oncology & carcinogenesisbiology.proteinmetastatic melanomamicrotubuleFrontiers in Oncology
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Metabolic Cooperation and Competition in the Tumor Microenvironment: Implications for Therapy

2017

The tumor microenvironment (TME) is an ensemble of non-tumor cells comprising fibroblasts, cells of the immune system, and endothelial cells, besides various soluble secretory factors from all cellular components (including tumor cells). The TME forms a pro-tumorigenic cocoon around the tumor cells where reprogramming of the metabolism occurs in tumor and non-tumor cells that underlies the nature of interactions as well as competitions ensuring steady supply of nutrients and anapleoretic molecules for the tumor cells that fuels its growth even under hypoxic conditions. This metabolic reprogramming also plays a significant role in suppressing the immune attack on the tumor cells and in resis…

0301 basic medicineCancer ResearchCell signalingTumor microenvironmentimmune networkReviewBiologymetabolic cooperationcancer cell metabolismWarburg effectCell biology03 medical and health sciences030104 developmental biologyImmune systemOncologyCancer-Associated Fibroblaststumor microenvironmentmetabolic reprogrammingEpigeneticssense organsWarburg effectTranscription factorReprogrammingcancer-associated fibroblastsFrontiers in Oncology
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Multiple Myeloma-Derived Extracellular Vesicles Induce Osteoclastogenesis through the Activation of the XBP1/IRE1α Axis

2020

Bone disease severely affects the quality of life of over 70% of multiple myeloma (MM) patients, which daily experience pain, pathological fractures, mobility issues and an increased mortality. Recent data have highlighted the crucial role of the endoplasmic reticulum-associated unfolded protein response (UPR) in malignant transformation and tumor progression

0301 basic medicineCancer ResearchCell signalingXBP1Cellular differentiationlcsh:RC254-282Article03 medical and health sciences0302 clinical medicineSettore BIO/13 - Biologia ApplicataTranscription factorChemistryEndoplasmic reticulumextracellular-vesiclesExtracellular vesiclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensCell biologymultiple myelomaUPR-related molecules030104 developmental biologyosteoclastsOncology030220 oncology & carcinogenesisUnfolded protein responsePhosphorylationbone diseaseCancers
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Intratumoral Heterogeneity and Longitudinal Changes in Gene Expression Predict Differential Drug Sensitivity in Newly Diagnosed and Recurrent Gliobla…

2020

Background: Inevitable recurrence after radiochemotherapy is the major problem in the treatment of glioblastoma, the most prevalent type of adult brain malignancy. Glioblastomas are notorious for a high degree of intratumor heterogeneity manifest through a diversity of cell types and molecular patterns. The current paradigm of understanding glioblastoma recurrence is that cytotoxic therapy fails to target effectively glioma stem cells. Recent advances indicate that therapy-driven molecular evolution is a fundamental trait associated with glioblastoma recurrence. There is a growing body of evidence indicating that intratumor heterogeneity, longitudinal changes in molecular biomarkers and spe…

0301 basic medicineCancer ResearchCell typeMalignancylcsh:RC254-282ArticleTranscriptome03 medical and health sciencestranscriptomics0302 clinical medicineGliomaGene expressionmedicineneoplasmsTemozolomideglioblastoma stem cellsbusiness.industryglioblastomaMolecular diagnosticsmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensnervous system diseases030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchgene expressionStem cellbusinesstarget anti-cancer therapymolecular pathwaysmedicine.drugrecurrent glioblastomaCancers
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Common extracellular matrix regulation of myeloid cell activity in the bone marrow and tumor microenvironments

2017

The complex interaction between cells undergoing transformation and the various stromal and immunological cell components of the tumor microenvironment (TME) crucially influences cancer progression and diversification, as well as endowing clinical and prognostic significance. The immunosuppression characterizing the TME depends on the recruitment and activation of different cell types including regulatory T cells, myeloid-derived suppressor cells, and tumor-associated macrophages. Less considered is the non-cellular component of the TME. Here, we focus on the extracellular matrix (ECM) regulatory activities that, within the TME, actively contribute to many aspects of tumor progression, acti…

0301 basic medicineCancer ResearchCell typeStromal cellMyeloidCarcinogenesisImmunologyBiology03 medical and health sciencesBone MarrowNeoplasmsmedicineImmune ToleranceImmunology and AllergyAnimalsHumansMyeloid-Derived Suppressor CellCarcinogenesiTumor microenvironmentAnimalMyeloid-Derived Suppressor CellsHematopoietic stem cellSPARCBone marrow nicheExtracellular matrixCell biology030104 developmental biologymedicine.anatomical_structureRegulatory myeloid suppressor cellOncologyTumor microenvironmentTumor progressionMyeloid-derived Suppressor CellBone marrow niche; Extracellular matrix; Regulatory myeloid suppressor cells; SPARC; Tumor microenvironment; Animals; Bone Marrow; Carcinogenesis; Extracellular Matrix; Humans; Immune Tolerance; Myeloid-Derived Suppressor Cells; Neoplasms; Tumor Escape; Tumor MicroenvironmentNeoplasmTumor Escapesense organsBone marrowHuman
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Context-Dependent Role of NF-κB Signaling in Primary Liver Cancer—from Tumor Development to Therapeutic Implications

2019

Chronic inflammatory cell death is a major risk factor for the development of diverse cancers including liver cancer. Herein, disruption of the hepatic microenvironment as well as the immune cell composition are major determinants of malignant transformation and progression in hepatocellular carcinomas (HCC). Considerable research efforts have focused on the identification of predisposing factors that promote induction of an oncogenic field effect within the inflammatory liver microenvironment. Among the most prominent factors involved in this so-called inflammation-fibrosis-cancer axis is the NF-κB pathway. The dominant role of this pathway for malignant transformation and progression…

0301 basic medicineCancer ResearchCell typechronic inflammationContext (language use)Reviewlcsh:RC254-282Malignant transformation03 medical and health sciences0302 clinical medicineImmune systemMedicinebusiness.industryhepatocarcinogenesishepatocellular carcinomalcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseNf κb signaling030104 developmental biologyOncology030220 oncology & carcinogenesisHepatocellular carcinomaNF-κB signalingCancer researchbusinessLiver cancerPrimary liver cancerCancers
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Establishment and characterization of a highly immunogenic human renal carcinoma cell line.

2015

Renal cell carcinoma (RCC) is the most common kidney cancer, and accounts for ~3% of all adult malignancies. RCC has proven refractory to conventional treatment modalities but appears to be the only histological form that shows any consistent response to immunotherapeutic approaches. The development of a clinically effective vaccine remains a major strategic target for devising active specific immunotherapy in RCC. We aimed to identify a highly immunogenic antigenic format for immunotherapeutic approaches, so as to boost immune responses in RCC patients. We established and cloned an immunogenic cell line, RCC85#21 named Elthem, which was derived from a non-aggressive and non-metastatic clea…

0301 basic medicineCancer ResearchCellClone (cell biology)BiologyImmunophenotyping03 medical and health sciencesimmunogenic antigenic format0302 clinical medicineImmune systemAntigenAntigens NeoplasmCell Line TumormedicineCytotoxic T cellHumansElectrophoresis Gel Two-DimensionalCarcinoma Renal Cellrenal cancer cell lineSystems BiologyArticlesCell cycleMolecular biologyKidney Neoplasms030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisSpectrometry Mass Matrix-Assisted Laser Desorption-Ionizationcell proteomeClear cell carcinomaK562 CellsCD8International journal of oncology
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Extracellular Vesicles Shed by Melanoma Cells Contain a Modified Form of H1.0 Linker Histone and H1.0 mRNA-binding Proteins

2016

Extracellular vesicles (EVs) are shed in the extracellular environment by both prokaryotes and eukaryotes. Although produced from both normal and cancer cells, malignant cells release a much higher amount of EVs, which also contain tumor-specific proteins and RNAs. We previously found that G26/24 oligodendroglioma cells shed EVs that contain the pro-apoptotic factors FasL and TRAIL1-2. Interestingly, G26/24 release, via EVs, extracellular matrix remodelling proteases3, and H1° histone protein4, and mRNA. To shed further light on the role of EVs in discarding proteins and mRNAs otherwise able to counteract proliferative signals, we studied a melanoma cell line (A375). We found that also thes…

0301 basic medicineCancer ResearchCellular differentiationBlotting WesternFluorescent Antibody TechniqueMYEF2ApoptosisRNA-binding proteinexosomesmembrane vesiclesReal-Time Polymerase Chain ReactionChromatography AffinityHistones03 medical and health sciencesH1.0 linker histone; RNA-binding proteins (RBPs); extracellular vesicles (EVs) membrane vesicles (MVs); exosomes; MYEF2Settore BIO/10 - BiochimicaTumor Cells CulturedHumansexosomeSecretionRNA MessengerSettore BIO/06 - Anatomia Comparata E Citologiamelanoma cell line (A375) myelin expression factor-2 (MYEF2)MelanomaTranscription factorCell ProliferationH1.0 linker histonebiologyReverse Transcriptase Polymerase Chain ReactionEXTRACELLULAR VESICLESRNA-Binding ProteinsRNACell DifferentiationArticlesCell biologyBlotCell Transformation Neoplastic030104 developmental biologyHistoneOncologySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationCancer cellbiology.proteinRNA-binding proteins (RBPs)extracellular vesicles (EVs) membrane vesicles (MVs)
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Tumor-Derived Prostaglandin E2 Promotes p50 NF-κB-Dependent Differentiation of Monocytic MDSCs

2020

Abstract Myeloid-derived suppressor cells (MDSC) include immature monocytic (M-MDSC) and granulocytic (PMN-MDSC) cells that share the ability to suppress adaptive immunity and to hinder the effectiveness of anticancer treatments. Of note, in response to IFNγ, M-MDSCs release the tumor-promoting and immunosuppressive molecule nitric oxide (NO), whereas macrophages largely express antitumor properties. Investigating these opposing activities, we found that tumor-derived prostaglandin E2 (PGE2) induces nuclear accumulation of p50 NF-κB in M-MDSCs, diverting their response to IFNγ toward NO-mediated immunosuppression and reducing TNFα expression. At the genome level, p50 NF-κB promoted binding …

0301 basic medicineCancer ResearchCellular differentiationProstaglandin E2 receptormedicine.medical_treatmentMelanoma ExperimentalApoptosisSettore MED/08 - Anatomia PatologicaNitric OxideDinoprostoneMonocytesInterferon-gammaMice03 medical and health sciences0302 clinical medicineImmune systemOxytocicsImmune ToleranceTumor Cells CulturedmedicineAnimalsHumansProstaglandin E2Cell ProliferationChemistryMyeloid-Derived Suppressor CellsNF-kappa B p50 SubunitCell DifferentiationImmunotherapyAcquired immune systemPancreatic Neoplasms030104 developmental biologyOncologyp50 NF-κB differentiation of monocytic MDSC.030220 oncology & carcinogenesisMyeloid-derived Suppressor CellCancer researchTumor necrosis factor alphaColorectal Neoplasmsmedicine.drugCancer Research
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AP2α controls the dynamic balance between miR-126&126* and miR-221&222 during melanoma progression

2016

Accumulating evidences have shown the association between aberrantly expressed microRNAs (miRs) and cancer, where these small regulatory RNAs appear to dictate the cell fate by regulating all the main biological processes. We demonstrated the responsibility of the circuitry connecting the oncomiR-221&222 with the tumor suppressors miR-126&126∗ in melanoma development and progression. According to the inverse correlation between endogenous miR-221&222 and miR-126&126∗, respectively increasing or decreasing with malignancy, their enforced expression or silencing was sufficient for a reciprocal regulation. In line with the opposite roles of these miRs, protein analyses confirmed the reverse ex…

0301 basic medicineCancer ResearchCellular differentiationSettore MED/08 - Anatomia Patologicagrowth-factorCell fate determinationBiologyFatty Acid-Binding ProteinsBioinformaticsap-2 transcription factorlaw.inventioncutaneous melanoma03 medical and health sciencesMolecular Biology; Cancer Research; Genetics0302 clinical medicinelawTranscription (biology)Cell Line TumormicroRNAGeneticsmedicineHumansGene silencingMelanomaMolecular BiologyPsychological repressionsquamous-cell carcinoma; ap-2 transcription factor; cutaneous melanoma; growth-factor; metastatic melanoma; terminal fragment; cancer-cells; tumor-growth; mir-126; methylationMelanomaCell Differentiationsquamous-cell carcinomatumor-growthmedicine.diseaseMicroRNAscancer-cells030104 developmental biologyterminal fragmentmir-126030220 oncology & carcinogenesisDisease ProgressionCancer researchSuppressorOriginal Articlemethylationmetastatic melanomaOncogene
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