Search results for "TUMOR"

showing 10 items of 6365 documents

Comment on “Endothelial Protein C Receptor (EPCR), Protease Activated Receptor-1 (PAR-1) and Their Interplay in Cancer Growth and Metastatic Dissemin…

2019

Although the interplay between tumor progression and blood coagulation has been recognized [...]

0301 basic medicineCancer ResearchEndothelial protein C receptorChemistryCancermedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-28203 medical and health sciences030104 developmental biology0302 clinical medicineProtease-Activated Receptor 1n/aOncologyCoagulationTumor progression030220 oncology & carcinogenesisCancer researchmedicineCancers
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Melanoma in the liver: Oxidative stress and the mechanisms of metastatic cell survival.

2020

Abstract Metastatic melanoma is a fatal disease with a rapid systemic dissemination. The most frequent target sites are the liver, bone, and brain. Melanoma metastases represent a heterogeneous cell population, which associates with genomic instability and resistance to therapy. Interaction of melanoma cells with the hepatic sinusoidal endothelium initiates a signaling cascade involving cytokines, growth factors, bioactive lipids, and reactive oxygen and nitrogen species produced by the cancer cell, the endothelium, and also by different immune cells. Endothelial cell-derived NO and H2O2 and the action of immune cells cause the death of most melanoma cells that reach the hepatic microvascul…

0301 basic medicineCancer ResearchEndotheliumCell SurvivalPopulationCellmedicine.disease_cause03 medical and health sciences0302 clinical medicineImmune systemDownregulation and upregulationTumor MicroenvironmentMedicineAnimalsHumansEndotheliumeducationMelanomaeducation.field_of_studybusiness.industryMelanomaLiver Neoplasmsmedicine.diseaseCarcinoma NeuroendocrineOxidative Stress030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer cellCancer researchbusinessOxidation-ReductionOxidative stressSeminars in cancer biology
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PHD3 Controls Lung Cancer Metastasis and Resistance to EGFR Inhibitors through TGFα.

2018

Abstract Lung cancer is the leading cause of cancer-related death worldwide, in large part due to its high propensity to metastasize and to develop therapy resistance. Adaptive responses to hypoxia and epithelial–mesenchymal transition (EMT) are linked to tumor metastasis and drug resistance, but little is known about how oxygen sensing and EMT intersect to control these hallmarks of cancer. Here, we show that the oxygen sensor PHD3 links hypoxic signaling and EMT regulation in the lung tumor microenvironment. PHD3 was repressed by signals that induce EMT and acted as a negative regulator of EMT, metastasis, and therapeutic resistance. PHD3 depletion in tumors, which can be caused by the EM…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionLung NeoplasmsMice NudeAntineoplastic AgentsSMADDrug resistanceMetastasisHypoxia-Inducible Factor-Proline DioxygenasesMitochondrial Proteins03 medical and health sciencesErlotinib HydrochlorideMice0302 clinical medicineDownregulation and upregulationCell Line TumorTumor MicroenvironmentMedicineAnimalsHumansNeoplasm MetastasisLung cancerProtein Kinase InhibitorsEGFR inhibitorsbusiness.industryIntracellular Signaling Peptides and ProteinsCancerTransforming Growth Factor alphamedicine.diseaseHCT116 CellsXenograft Model Antitumor AssaysCell HypoxiaErbB Receptors030104 developmental biologyOncologyA549 CellsDrug Resistance Neoplasm030220 oncology & carcinogenesisembryonic structuresCancer researchFemaleErlotinibbusinessApoptosis Regulatory Proteinsmedicine.drugCancer research
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Transcriptional profiling of circulating tumor cells in multiple myeloma: a new model to understand disease dissemination

2020

The reason why a few myeloma cells egress from the bone marrow (BM) into peripheral blood (PB) remains unknown. Here, we investigated molecular hallmarks of circulating tumor cells (CTCs) to identify the events leading to myeloma trafficking into the bloodstream. After using next-generation flow to isolate matched CTCs and BM tumor cells from 32 patients, we found high correlation in gene expression at single-cell and bulk levels (r ≥ 0.94, P = 10−16), with only 55 genes differentially expressed between CTCs and BM tumor cells. CTCs overexpressed genes involved in inflammation, hypoxia, or epithelial–mesenchymal transition, whereas genes related with proliferation were downregulated in CTCs…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionTranscription GeneticGene ExpressionBiologycirculating tumor cell03 medical and health sciences0302 clinical medicineCirculating tumor cellBone MarrowCell MovementCancer stem cellCell Line TumorTumor MicroenvironmentmedicineHumansHypoxiaMultiple myelomaCell ProliferationInflammationGene knockdownliquid biopsyCD44CENPFHematologyNeoplastic Cells CirculatingPrognosismedicine.disease3. Good healthmultiple myeloma030104 developmental biologymedicine.anatomical_structureOncologyCell culture030220 oncology & carcinogenesisNeoplastic Stem CellsCancer researchbiology.proteinBone marrow
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MiR-205-5p inhibition by locked nucleic acids impairs metastatic potential of breast cancer cells.

2018

AbstractMir-205 plays an important role in epithelial biogenesis and in mammary gland development but its role in cancer still remains controversial depending on the specific cellular context and target genes. We have previously reported that miR-205-5p is upregulated in breast cancer stem cells targeting ERBB pathway and leading to targeted therapy resistance. Here we show that miR-205-5p regulates tumorigenic properties of breast cancer cells, as well as epithelial to mesenchymal transition. Silencing this miRNA in breast cancer results in reduced tumor growth and metastatic spreading in mouse models. Moreover, we show that miR-205-5p knock-down can be obtained with the use of specific lo…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal Transitionmedicine.medical_treatmentAntagomirSettore MED/50 - Scienze Tecniche Mediche ApplicateImmunologyTransplantation HeterologousOligonucleotidesBreast NeoplasmsBiologyArticleTargeted therapy03 medical and health sciencesCellular and Molecular NeuroscienceMiceBreast cancerErbBCell MovementMice Inbred NODOligonucleotideCell Line TumormicroRNAmedicineGene silencingAnimalsHumansEpithelial–mesenchymal transitionlcsh:QH573-671Neoplasm MetastasisCell ProliferationAnimallcsh:CytologyCancerAntagomirsMicroRNACell Biologymedicine.diseaseNeoplasm MetastasiMicroRNAs030104 developmental biologyCancer researchFemaleStem cellBreast NeoplasmHumanCell deathdisease
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Long Pentraxin 3-Mediated Fibroblast Growth Factor Trapping Impairs Fibrosarcoma Growth

2018

Fibrosarcomas are soft tissue mesenchymal tumors originating from transformed fibroblasts. Fibroblast growth factor-2 (FGF2) and its tyrosine-kinase receptors (FGFRs) play pivotal roles in fibrosarcoma onset and progression, FGF2 being actively produced by fibroblasts in all stages along their malignant transformation to the fibrosarcoma stage. The soluble pattern recognition receptor long pentraxin-3 (PTX3) is an extrinsic oncosuppressor whose expression is reduced in different tumor types, including soft tissue sarcomas, via hypermethylation of its gene promoter. PTX3 interacts with FGF2 and other FGF family members, thus acting as a multi-FGF antagonist able to inhibit FGF-dependent neov…

0301 basic medicineCancer ResearchFGF; FGF-trap; FGFR; fibrosarcoma; long pentraxin-3Fibroblast growth factorlcsh:RC254-282Malignant transformation03 medical and health sciences0302 clinical medicinemedicineFGFFibrosarcomaFibroblastReceptorneoplasmsOriginal ResearchFGF-trapintegumentary systemChemistryFGFRMesenchymal stem cellPTX3medicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologymedicine.anatomical_structurelong pentraxin-3OncologyFibroblast growth factor receptor030220 oncology & carcinogenesisCancer researchfibrosarcomaFrontiers in Oncology
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Clinical Impact of Cystatin C/Cathepsin L and Follistatin/Activin A Systems in Breast Cancer Progression: A Preliminary Report.

2016

This study was directed to assess the clinical impact of the circulating cathepsin L, cystatin C, activin A, and follistatin in breast cancer patients. The serum concentrations of these molecules were determined by immunoenzymatic assays, and their association with some clinico-pathological parameters of breast cancer progression was evaluated. Our results identified cystatin C and activin A as predictive markers for the presence of breast cancer and bone metastasis, respectively. Therefore, these proteins may have a clinical role as circulating biomarkers in the diagnosis and therapeutic monitoring of breast cancer patients.

0301 basic medicineCancer ResearchFollistatinCathepsin LBone NeoplasmsBreast NeoplasmsActivinCathepsin L03 medical and health sciencesbreast cancer0302 clinical medicineBreast cancerPreliminary reportmedicineBiomarkers TumorHumansbone metastasiCystatin CNeoplasm Metastasisskin and connective tissue diseasesAgedNeoplasm Stagingbiologybusiness.industryBone metastasisGeneral MedicineMiddle Agedmedicine.diseaseTherapeutic monitoringActivinsActivin a030104 developmental biologyOncologyCystatin CROC Curvetumor markers030220 oncology & carcinogenesisSettore BIO/14 - Farmacologiabiology.proteinCancer researchDisease ProgressionbiomarkerOsteoporosisFemaleNeoplasm Gradingbusinesshormones hormone substitutes and hormone antagonistsFollistatinCancer investigation
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Growth differentiation factor 15 as a radiation-induced marker in oral carcinoma increasing radiation resistance.

2015

Background Growth differentiation factor 15 (GDF15) is involved in tumor pathogenesis of oral squamous cell carcinoma (OSCC). The aim of this study was an investigation of the potential influence of GDF15 on radioresistance of OSCC cells in vitro. Methods Oral squamous cell carcinoma cell lines were irradiated with 0, 2, or 6 Gy, and GDF15 expression in the supernatant per survived cell colony was examined with ELISA. Non-irradiated and OSCC cell lines irradiated with 6 Gy were evaluated for GDF15 expression using immunofluorescent staining. For further investigation of GDF15 effects on radioresistance, a GDF15 knockdown model in a human OSCC cell line was established, and apoptotic activit…

0301 basic medicineCancer ResearchGrowth Differentiation Factor 15CellApoptosisEnzyme-Linked Immunosorbent AssayBiologymedicine.disease_causeReal-Time Polymerase Chain ReactionTransfectionPathology and Forensic Medicine03 medical and health sciences0302 clinical medicineRadioresistanceCell Line TumormedicineCarcinomaBiomarkers TumorHumansRNA Small InterferingMouth neoplasmSquamous Cell Carcinoma of Head and Neckmedicine.diseaseMolecular biologyNeoplasm Proteinsstomatognathic diseases030104 developmental biologymedicine.anatomical_structureOtorhinolaryngologyApoptosisCell cultureTumor progressionHead and Neck Neoplasms030220 oncology & carcinogenesisCaspasesGene Knockdown TechniquesCarcinoma Squamous CellPeriodonticsMouth NeoplasmsOral SurgeryCarcinogenesisJournal of oral pathologymedicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
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Targeting the chromosomal passenger complex subunit INCENP induces polyploidization, apoptosis and senescence in neuroblastoma

2019

Abstract Chromosomal passenger complex (CPC) has been demonstrated to be a potential target of cancer therapy by inhibiting Aurora B or survivin in different types of cancer including neuroblastoma. However, chemical inhibition of either Aurora B or survivin does not target CPC specifically due to off-target effects or CPC-independent activities of these two components. In a previous chromatin-focused siRNA screen, we found that neuroblastoma cells were particularly vulnerable to loss of INCENP, a gene encoding a key scaffolding component of the CPC. In this study, INCENP was highly expressed by neuroblastoma cells, and its expression decreased following retinoic acid–induced neuroblastoma …

0301 basic medicineCancer ResearchINCENP/CPC/Polyploidy/DNA damage/Apoptosis/SenescenceCarcinogenesisChromosomal Proteins Non-HistoneAurora B kinaseApoptosisBiologymedicine.disease_causeArticlePolyploidy03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineNeuroblastomaSurvivinmedicineGene silencingAnimalsHumansneoplasmsCellular SenescenceINCENPmedicine.disease030104 developmental biologyOncologyApoptosisTumor progression030220 oncology & carcinogenesisCancer researchHeterograftsCarcinogenesis
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Tumour mutational burden as a biomarker for immunotherapy: Current data and emerging concepts

2020

International audience; Treatment with immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) or its ligand (PD-L1) can generate durable responses in various cancer types, but only in a subset of patients. The use of predictive biomarkers for response to PD-1/PD-L1 inhibitors is critical for patient selection. Expression of PD-L1 has demonstrated utility in patient selection. Tumour mutational burden (TMB) is an emerging biomarker for response to PD-1/PD-L1 inhibitors. The evaluation of this biomarker is based on the hypothesis that a high number of mutations in somatic exonic regions will lead to an increase in neoantigen production, which could then be recognised by…

0301 basic medicineCancer ResearchImmune checkpoint inhibitorsmedicine.medical_treatment[SDV]Life Sciences [q-bio]DNA Mutational AnalysisProgrammed Cell Death 1 ReceptorTumour mutational burdenBioinformaticsArticleB7-H1 Antigen03 medical and health sciencesAntineoplastic Agents Immunological0302 clinical medicineImmune systemNeoplasmsBiomarkers TumorHumansMedicineIn patientGenetic TestingPredictive biomarkerbusiness.industryPatient SelectionCancerBiomarkerImmunotherapymedicine.disease3. Good healthBiomarker (cell)[SDV] Life Sciences [q-bio]030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisMutationImmunotherapybusinessCD8
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