Search results for "CD"

showing 10 items of 4072 documents

The PDGFRβ/ERK1/2 pathway regulates CDCP1 expression in triple-negative breast cancer

2018

Background CDCP1, a transmembrane protein with tumor pro-metastatic activity, was recently identified as a prognostic marker in TNBC, the most aggressive breast cancer subtype still lacking an effective molecular targeted therapy. The mechanisms driving CDCP1 over-expression are not fully understood, although several stimuli derived from tumor microenvironment, such as factors present in Wound Healing Fluids (WHFs), reportedly increase CDCP1 levels. Methods The expression of CDCP1, PDGFRβ and ERK1/2cell was tested by Western blot after stimulation of MDA-MB-231 cells with PDGF-BB and, similarly, in presence or not of ERK1/2 inhibitor in a panel of TNBC cell lines. Knock-down of PDGFRβ was e…

0301 basic medicineCancer ResearchMAP Kinase Signaling SystemCDCP1medicine.medical_treatmentPDGFRβPDGF-BBBecaplerminTriple Negative Breast NeoplasmsBiologylcsh:RC254-282Targeted therapyReceptor Platelet-Derived Growth Factor beta03 medical and health sciences0302 clinical medicineFISHDownregulation and upregulationWestern blotAntigens CDAntigens NeoplasmCell Line TumorGeneticsmedicineHumansRNA Small InterferingReceptorTriple-negative breast cancerMitogen-Activated Protein Kinase 1Tumor microenvironmentMitogen-Activated Protein Kinase 3ERK1/2medicine.diagnostic_testMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNeoplasm ProteinsUp-RegulationGene Expression Regulation Neoplastic030104 developmental biologyOncologyGene Knockdown Techniques030220 oncology & carcinogenesisCDCP1Cancer researchImmunohistochemistryFemaleCell Adhesion MoleculesTNBCResearch ArticleIHCBMC Cancer
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Efficacy and epigenetic interactions of novel DNA hypomethylating agent guadecitabine (SGI-110) in preclinical models of hepatocellular carcinoma.

2016

ABSTRACT Hepatocellular carcinoma (HCC) is a deadly malignancy characterized at the epigenetic level by global DNA hypomethylation and focal hypermethylation on the promoter of tumor suppressor genes. In most cases it develops on a background of liver steatohepatitis, fibrosis, and cirrhosis. Guadecitabine (SGI-110) is a second-generation hypomethylating agent, which inhibits DNA methyltransferases. Guadecitabine is formulated as a dinucleotide of decitabine and deoxyguanosine that is resistant to cytidine deaminase (CDA) degradation and results in prolonged in vivo exposure to decitabine following small volume subcutaneous administration of guadecitabine. Here we found that guadecitabine i…

0301 basic medicineCancer ResearchMethyltransferasesteatohepatitisDecitabineBiologyDecitabineDNA methylation Decitabine guadecitabine hepatocellular carcinoma (HCC) histone macroH2A1 steatohepatitishepatocellular carcinoma (HCC)03 medical and health scienceschemistry.chemical_compoundCDKN2AmedicineEpigeneticsMolecular BiologyneoplasmsDNA methylationGuadecitabineguadecitabinehistone macroH2A1steatohepatitidigestive system diseases3. Good healthDemethylating agent030104 developmental biologychemistryHypomethylating agentDNA methylationCancer researchResearch Papermedicine.drug
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Constitutive psgl-1 correlates with cd30 and tcr pathways and represents a potential target for immunotherapy in anaplastic large t-cell lymphoma

2021

Simple Summary P-selectin glycoprotein ligand-1 (PSGL-1), coded by the SELPLG gene, is the major ligand of selectins and plays a pivotal role in tethering, rolling and extravasation of immune cells. PSGL-1 involvement in core molecular programs, such as SYK, PLCγ2, PI3Kγ or MAPK pathways, suggests additional functions beyond the modulation of cell trafficking. Recently, several studies identified a novel mechanism responsible for PSGL-1-mediated immune suppression in the tumor microenvironment and proved a novel concept of PSGL-1 as a critical checkpoint molecule for tumor immunotherapy. The immunotherapeutic approach has gained an ever-growing interest in the treatment of several hematolog…

0301 basic medicineCancer ResearchPTCLCD30medicine.medical_treatmentSykLymphoproliferative disordersBiologyALCL; ALK; CD30; Immunotherapy; PSGL-1; PTCL; TCRArticle03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesmedicineT-cell lymphomaPSGL-1RC254-282integumentary systemT-cell receptorNeoplasms. Tumors. Oncology. Including cancer and carcinogensImmunotherapymedicine.diseaseALCLLymphomaGene expression profiling030104 developmental biologyOncologyALK030220 oncology & carcinogenesisCD30Cancer researchImmunotherapyTCR
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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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Aberrant splicing of the tumor suppressor CYLD promotes the development of chronic lymphocytic leukemia via sustained NF-κB signaling

2017

The pathogenesis of chronic lymphocytic leukemia (CLL) has been linked to constitutive NF-κB activation but the underlying mechanisms are poorly understood. Here we show that alternative splicing of the negative regulator of NF-κB and tumor suppressor gene CYLD regulates the pool of CD5+ B cells through sustained canonical NF-κB signaling. Reinforced canonical NF-κB activity leads to the development of B1 cell-associated tumor formation in aging mice by promoting survival and proliferation of CD5+ B cells, highly reminiscent of human B-CLL. We show that a substantial number of CLL patient samples express sCYLD, strongly implicating a role for it in human B-CLL. We propose that our new CLL-l…

0301 basic medicineCancer ResearchTumor suppressor geneCell SurvivalRNA SplicingChronic lymphocytic leukemia2720 Hematology610 Medicine & healthBiologyCD5 Antigenslaw.inventionPathogenesisMice03 medical and health sciencesimmune system diseaseslawhemic and lymphatic diseasesmedicineAnimalsHumans10239 Institute of Laboratory Animal Science1306 Cancer ResearchGenes Tumor SuppressorGeneCell ProliferationB-LymphocytesAlternative splicingNF-kappa BUbiquitinationHematologymedicine.diseaseLeukemia Lymphocytic Chronic B-CellDeubiquitinating Enzyme CYLDLeukemia030104 developmental biologyOncologyImmunologyCancer research570 Life sciences; biologySuppressor2730 OncologyCD5Signal TransductionLeukemia
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Pattern of Invasion in Human Pancreatic Cancer Organoids Is Associated with Loss of SMAD4 and Clinical Outcome

2020

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy characterized by extensive local invasion and systemic spread. In this study, we employed a three-dimensional organoid model of human pancreatic cancer to characterize the molecular alterations critical for invasion. Time-lapse microscopy was used to observe invasion in organoids from 25 surgically resected human PDAC samples in collagen I. Subsequent lentiviral modification and small-molecule inhibitors were used to investigate the molecular programs underlying invasion in PDAC organoids. When cultured in collagen I, PDAC organoids exhibited two distinct, morphologically defined invasive phenotypes, mesenchymal an…

0301 basic medicineCancer Researchendocrine system diseasesPancreatic ductal adenocarcinoma (PDAC)RAC1CDC42AdenocarcinomaBiologyArticle03 medical and health sciences0302 clinical medicineHuman Pancreatic CancerCell MovementPancreatic cancerBiomarkers TumorTumor Cells CulturedmedicineOrganoidHumansNeoplasm InvasivenessCell ProliferationSmad4 ProteinRegulation of gene expressionCell growthMesenchymal stem cellPrognosismedicine.diseasePhenotypedigestive system diseasesGene Expression Regulation NeoplasticOrganoidsPancreatic NeoplasmsSurvival Rate030104 developmental biologyOncology030220 oncology & carcinogenesisembryonic structuresCancer researchCarcinoma Pancreatic DuctalSignal TransductionCancer Research
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Immunobiology of Uveal Melanoma: State of the Art and Therapeutic Targets

2019

Uveal Melanoma (UM) represents the most common primary intraocular malignant tumor in adults. Although it originates from melanocytes as cutaneous melanoma, it shows significant clinical and biological differences with the latter, including high resistance to immune therapy. Indeed, UM can evade immune surveillance via multiple mechanisms, such as the expression of inhibitory checkpoints (e.g., PD-L1, CD47, CD200) and the production of IDO-1 and soluble FasL, among others. More in-depth understanding of these mechanisms will suggest potential targets for the design of novel and more effective management strategies for UM patients.

0301 basic medicineCancer Researchimmune-escapemedicine.medical_treatmentReviewlcsh:RC254-282Fas ligand03 medical and health sciences0302 clinical medicineImmune privilegemedicinebusiness.industryMelanomaCD47Effective managementImmunotherapyinhibitory checkpointimmune-privilegemedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensImmune surveillanceimmune-escape; immune-privilege; immunotherapy; inhibitory checkpoints; uveal melanomainhibitory checkpoints030104 developmental biologyOncology030220 oncology & carcinogenesisCutaneous melanomaCancer researchimmunotherapyuveal melanomabusiness
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Immunomodulatory activity of microRNAs: potential implications for multiple myeloma treatment

2015

Multiple myeloma (MM) is an incurable plasma cell neoplasm accounting for about 10% of all hematologic malignancies. Recently, emerging evidence is disclosing the complexity of bone marrow interactions between MM cells and infiltrating immune cells, which have been reported to promote proliferation, survival and drug resistance of tumor cells. MicroRNAs (miRNAs) are small non-coding RNA molecules with regulatory functions in the cell, whose expression has predictive and prognostic value in different malignancies. MiRNAs are gaining increasing interest due to their capability to polarize the immune-response through different mechanisms, which include the molecular reprogramming of immune cel…

0301 basic medicineCancer Researchmedicine.medical_treatmentCellOsteoclastsAntineoplastic AgentsCD8-Positive T-LymphocytesBiologyBioinformaticsT-Lymphocytes RegulatoryImmunomodulation03 medical and health sciencesTh2 Cells0302 clinical medicineImmune systemBone MarrowDrug DiscoverymicroRNAmedicineHumansMultiple myelomamiRNAPharmacologyImmune-responseTumor immunology.MacrophagesMicroRNADendritic CellsImmunotherapyTh1 CellsPlasma cell neoplasmmedicine.diseaseGene Expression Regulation NeoplasticKiller Cells NaturalMicroRNAs030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisImmunotherapyBone marrowMultiple MyelomaReprogrammingCurrent Cancer Drug Targets
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Modulation of CD4 T Cell Response According to Tumor Cytokine Microenvironment

2021

Simple Summary It is now accepted that CD4 T lymphocytes play an essential role in the anti-tumor response. CD4 T lymphocytes can activate and regulate several aspects of innate and adaptive immunity and participate in the rejection of tumors. Understanding the impact of the tumor, through cytokines present in the microenvironment, but also the effect of anti-cancer therapies are critical aspects of immunotherapy research aiming at improving the anti-tumor response dependent on CD4 T lymphocytes. Abstract The advancement of knowledge on tumor biology over the past decades has demonstrated a close link between tumor cells and cells of the immune system. In this context, cytokines have a majo…

0301 basic medicineCancer Researchmedicine.medical_treatmentContext (language use)ReviewBiologylcsh:RC254-28203 medical and health sciences0302 clinical medicineImmune systemmedicinecancerTumor microenvironmentImmunotherapyAcquired immune systemlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPhenotypeCD4cytokines030104 developmental biologyCytokineOncology030220 oncology & carcinogenesisCancer researchimmunotherapyHomeostasisCancers
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The Functional Crosstalk between Myeloid-Derived Suppressor Cells and Regulatory T Cells within the Immunosuppressive Tumor Microenvironment

2021

Simple Summary Immunotherapy improved the therapeutic landscape for patients with advanced cancer diseases. However, many patients do not benefit from immunotherapy. The bidirectional crosstalk between myeloid-derived suppressor cells (MDSC) and regulatory T cells (Treg) contributes to immune evasion, limiting the success of immunotherapy by checkpoint inhibitors. This review aims to outline the current knowledge of the role and the immunosuppressive properties of MDSC and Treg within the tumor microenvironment (TME). Furthermore, we will discuss the importance of the functional crosstalk between MDSC and Treg for immunosuppression, issuing particularly the role of cell adhesion molecules. …

0301 basic medicineCancer Researchmedicine.medical_treatmentT cellCellReviewBiologylcsh:RC254-282regulatory T cellscrosstalk03 medical and health sciencestumor immune evasion0302 clinical medicinecell–cell contactmedicinetumor microenvironmentReceptorCD18Tumor microenvironmentCell adhesion moleculeImmunotherapylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmyeloid-derived suppressor cells<b>Keywords: </b>myeloid-derived suppressor cellsCrosstalk (biology)030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisβ2 integrinsMyeloid-derived Suppressor CellCancer researchimmunotherapyCD11Cancers
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