Search results for " Neoplasm"

showing 10 items of 6604 documents

Marine Actinomycetes-Derived Secondary Metabolites Overcome TRAIL-Resistance via the Intrinsic Pathway through Downregulation of Survivin and XIAP

2020

Resistance of cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis represents the major hurdle to the clinical use of TRAIL or its derivatives. The discovery and development of lead compounds able to sensitize tumor cells to TRAIL-induced cell death is thus likely to overcome this limitation. We recently reported that marine actinomycetes&rsquo

0301 basic medicineAquatic OrganismsProgrammed cell deathCell SurvivalSurvivinDown-RegulationSecondary MetabolismX-Linked Inhibitor of Apoptosis ProteinTRAILJurkat cellsArticleTNF-Related Apoptosis-Inducing LigandJurkat Cells03 medical and health sciences0302 clinical medicinemarine actinomycetesDownregulation and upregulationDrug DiscoveryOxazinesSurvivinHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyFADDBenzopyreneslcsh:QH301-705.5ComputingMilieux_MISCELLANEOUSCaspase 8therapybiologyChemistryProdigiosinQuinonesapoptosisGeneral MedicineHCT116 Cells3. Good healthXIAPActinobacteria030104 developmental biologylcsh:Biology (General)Drug Resistance NeoplasmApoptosis030220 oncology & carcinogenesisCancer cellbiology.proteinCancer researchGene DeletionCells
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Virus-encoded microRNA contributes to the molecular profile of EBV-positive Burkitt lymphomas

2015

Burkitt lymphoma (BL) is an aggressive neoplasm characterized by consistent morphology and phenotype, typical clinical behavior and distinctive molecular profile. The latter is mostly driven by the MYC over-expression associated with the characteristic translocation (8;14) (q24; q32) or with variant lesions. Additional genetic events can contribute to Burkitt Lymphoma pathobiology and retain clinical significance. A pathogenetic role for Epstein-Barr virus infection in Burkitt lymphomagenesis has been suggested; however, the exact function of the virus is largely unknown. In this study, we investigated the molecular profiles (genes and microRNAs) of Epstein-Barr virus-positive and -negative…

0301 basic medicineBART6; Burkitt lymphoma; EBV; miRNA; pathogenesisEpstein-Barr Virus InfectionsHerpesvirus 4 HumanpathogenesiRNA-binding proteinRNA-Binding ProteinEpstein-Barr Virus Infectionhemic and lymphatic diseasesCluster AnalysisViralOligonucleotide Array Sequence AnalysisGeneticsBART6; Burkitt lymphoma; EBV; miRNA; pathogenesis; Burkitt Lymphoma; Cluster Analysis; Cytoskeletal Proteins; Epstein-Barr Virus Infections; Gene Expression Profiling; Gene Expression Regulation Neoplastic; Gene Expression Regulation Viral; Herpesvirus 4 Human; Host-Pathogen Interactions; Humans; Immunohistochemistry; MicroRNAs; Neoplasm Proteins; Oligonucleotide Array Sequence Analysis; Phospholipase C delta; RNA Viral; RNA-Binding Proteins; Reverse Transcriptase Polymerase Chain Reaction; ras Proteins; OncologyReverse Transcriptase Polymerase Chain ReactionpathogenesisMicrofilament ProteinsIntracellular Signaling Peptides and ProteinsBurkitt lymphomaRNA-Binding ProteinsMicroRNAPhenotypeImmunohistochemistryNeoplasm ProteinsHost-Pathogen InteractionGene Expression Regulation NeoplasticOncologyHost-Pathogen InteractionsRNA ViralHumanResearch PaperGene Expression Regulation ViralBART6BiologySettore MED/08 - Anatomia PatologicaVirusNeoplasm Protein03 medical and health sciencesEBVmicroRNACytoskeletal ProteinmedicineHumansEpstein–Barr virus infectionGenemiRNANeoplasticCluster AnalysiOligonucleotide Array Sequence AnalysiGene Expression ProfilingHerpesvirus 4ras Proteinmedicine.diseaseLymphomaGene expression profilingCytoskeletal ProteinsMicroRNAs030104 developmental biologyGene Expression Regulationras ProteinsRNABART6; EBV; burkitt lymphoma; miRNA; pathogenesisPhospholipase C deltaOncotarget
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Dynamics and predicted drug response of a gene network linking dedifferentiation with β-catenin dysfunction in hepatocellular carcinoma

2019

Background & Aims Alterations of individual genes variably affect the development of hepatocellular carcinoma (HCC). Thus, we aimed to characterize the function of tumor-promoting genes in the context of gene regulatory networks (GRNs). Methods Using data from The Cancer Genome Atlas, from the LIRI-JP (Liver Cancer – RIKEN, JP project), and from our transcriptomic, transfection and mouse transgenic experiments, we identify a GRN which functionally links LIN28B-dependent dedifferentiation with dysfunction of β-catenin (CTNNB1). We further generated and validated a quantitative mathematical model of the GRN using human cell lines and in vivo expression data. Results We found that LIN28B and C…

0301 basic medicineBeta-cateninCarcinoma HepatocellularHepatocellular carcinomaLIN28BCellGene regulatory networkPrincipal component analysisMice TransgenicBiologyTransfectionTranscriptomeCohort Studies03 medical and health sciencesMice0302 clinical medicineMathematical modelmicroRNAmedicineAnimalsHumansGene Regulatory NetworksCTNNB1Genebeta CateninHepatologySequence Analysis RNALiver NeoplasmsGene regulatory networkRNA-Binding ProteinsHGF/MET pathwayMicroRNAHep G2 CellsHCCSModels TheoreticalPrognosisPersonalized medicinedigestive system diseases030104 developmental biologymedicine.anatomical_structureCancer researchSMARCA4biology.protein030211 gastroenterology & hepatologyTranscriptome
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Skin-derived mesenchymal stem cells as quantum dot vehicles to tumors

2017

Dominyka Dapkute,1,2 Simona Steponkiene,1 Danute Bulotiene,1 Liga Saulite,3 Una Riekstina,3 Ricardas Rotomskis1,4 1Biomedical Physics Laboratory, National Cancer Institute, Vilnius, Lithuania; 2Institute of Biosciences, Vilnius University, Vilnius, Lithuania; 3Faculty of Medicine, University of Latvia, Riga, Latvia; 4Biophotonics Group of Laser Research Center, Faculty of Physics, Vilnius University, Vilnius, Lithuania Purpose: Cell-mediated delivery of nanoparticles is emerging as a new method of cancer diagnostics and treatment. Due to their inherent regenerative properties, adult mesenchymal stem cells (MSCs) are naturally attracted to wounds and sites of inflammation, as well as tumors.…

0301 basic medicineBiophysicsPharmaceutical ScienceConnective tissueBioengineeringBreast Neoplasmsquantum dotsMice SCIDFlow cytometryBiomaterialsCell therapy03 medical and health sciencesIn vivoCell MovementInternational Journal of NanomedicineCell Line TumorDrug DiscoverymedicineAnimalsHumansViability assayParticle SizeCytotoxicityCell ShapeSkinOriginal Researchmesenchymal stem cellsMigration Assaymedicine.diagnostic_testCell DeathChemistryOrganic ChemistryMesenchymal stem cellGeneral MedicineDynamic Light ScatteringEndocytosis030104 developmental biologymedicine.anatomical_structureimmunodeficient miceCancer researchNanoparticlesFemaletumor tropismtumor-specific deliveryInternational Journal of Nanomedicine
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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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Five-year follow-up results of aerobic and impact training on bone mineral density in early breast cancer patients

2021

Summary A 12-month exercise program reversibly prevented hip bone loss in premenopausal women with early breast cancer. The bone-protective effect was maintained for 2 years after the end of the program but was lost thereafter. Purpose Breast cancer survivors are at an increased risk for osteoporosis and fracture. This 5-year follow-up of a randomized impact exercise intervention trial evaluated the maintenance of training effects on bone among breast cancer patients. Methods Five hundred seventy-three early breast cancer patients aged 35–68 years and treated with adjuvant therapy were allocated into a 12-month exercise program or a control group. Four hundred forty-four patients (77%) were…

0301 basic medicineBone densityEndocrinology Diabetes and MetabolismOsteoporosisphysical activityliikuntaweight-bearing impact aerobic exerciseMetabolic equivalent0302 clinical medicineAbsorptiometry PhotonBreast cancerBone DensityMedicineharjoitteluSURVIVORSRISKBone mineraltrainingrintasyöpäFemur Neckbone densityCHEMOTHERAPYMiddle Aged3. Good healthmedicine.anatomical_structurePOSTMENOPAUSAL WOMENTRIALFemaleOriginal ArticleHEALTHfyysinen aktiivisuusAdultmedicine.medical_specialtyBODY-COMPOSITIONgovernment.form_of_governmentosteoporoosi3122 CancersluuntiheysEXERCISE030209 endocrinology & metabolismBreast NeoplasmsMASSStep aerobics03 medical and health sciencesBreast cancerbreast cancerInternal medicineAdjuvant therapyHumansTrainingFemoral neckAgedbusiness.industryPhysical activitymedicine.diseaseaerobinen harjoitteluosteoporosisgovernmentOsteoporosisWeight-bearing impact aerobic exercise030101 anatomy & morphologyPHYSICAL PERFORMANCEbusinessFollow-Up Studies
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The mycotoxin zearalenone enhances cell proliferation, colony formation and promotes cell migration in the human colon carcinoma cell line HCT116.

2016

IF 3.522; International audience; Zearalenone (ZEN) and Aflatoxin B1 (AFB1) are fungal secondary metabolites produced by Fusarium and Aspergillus genera, respectively. These mycotoxins are found world-wide as corn and wheat contaminants. AFB1 is probably the most toxic and carcinogenic mycotoxin. It has been demonstrated to be mutagenic, genotoxic, and hepatocarcinogenic. ZEN is a non-steroidal estrogenic mycotoxin that displays hepatotoxicity, immunotoxicity and genotoxicity. Its mutagenic and carcinogenic properties have so far remained controversial and questionable. Using the colon carcinoma cell line HCT116, we will show here that ZEN, at low concentrations, enhances cell proliferation…

0301 basic medicineBone-Marrow-CellsAflatoxinAflatoxin B1Time Factors[ SDV.TOX ] Life Sciences [q-bio]/ToxicologyToxicologymedicine.disease_causeInductionchemistry.chemical_compound0302 clinical medicineProliferation assayCell MovementZearalenonebiologyfood and beveragesCell migrationGeneral MedicineMigration assayDna-Damage030220 oncology & carcinogenesis[SDV.TOX]Life Sciences [q-bio]/ToxicologyColonic NeoplasmsZearalenoneChromosome-AberrationsBalb/C MiceFusariumendocrine systemPreventive Role03 medical and health sciencesBotanymedicineHumansNeoplasm InvasivenessMycotoxinCarcinogenCell ProliferationWound HealingDose-Response Relationship DrugCell growthfungiClonogenic assaybiology.organism_classificationHCT116 CellsMolecular biology030104 developmental biologychemistryMcf-7 CellsFusarium ToxinsIn-VitroVitamin-ECarcinogensGenotoxicityToxicology letters
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The potential of cystatin C as a predictive biomarker in breast cancer

2020

Breast cancer (BCa) is the leading cause of cancer-related deaths among women. Numerous efforts are being directed toward identifying novel tissue and/or circulating molecular markers that may help clinicians in detecting early-stage BCa patients and in providing an accurate estimation of the prognosis and prediction of response to clinical treatments. In this setting, emerging evidence has indicated Cystatin C (Cyst C), as the most potent endogenous inhibitor of cysteine cathepsins, as a possible useful marker in the clinical management of BCa patients.This review analyzes the results of emerging studies underpinning a potential clinical role of Cyst C, as additional marker in BCa.Cyst C e…

0301 basic medicineBreast NeoplasmsMetastasiCysteine proteinaseMetastasisCathepsin03 medical and health sciences0302 clinical medicineBreast cancerBreast cancerBiomarkers Tumorproteinase inhibitorMedicineAnimalsHumansPharmacology (medical)Cystatin Cskin and connective tissue diseasesPredictive biomarkerNeoplasm StagingCathepsinbiologybusiness.industryTumor progressionjCystatin C CystatinCysteine proteinasesmedicine.diseasePrognosis030104 developmental biologyOncologyCystatin CTumor progression030220 oncology & carcinogenesistumor markerCancer researchbiology.proteinDisease ProgressionFemalebusiness
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A headlight on liquid biopsies: a challenging tool for breast cancer management

2016

Breast cancer is the most frequent carcinoma and second most common cause of cancer-related mortality in postmenopausal women. The acquisition of somatic mutations represents the main mechanism through which cancer cells overcome physiological cellular signaling pathways (e.g., PI3K/Akt/mTOR, PTEN, TP53). To date, diagnosis and metastasis monitoring is mainly carried out through tissue biopsy and/or re-biopsy, a very invasive procedure limited only to certain locations and not always feasible in clinical practice. In order to improve disease monitoring over time and to avoid painful procedure such as tissue biopsy, liquid biopsy may represent a new precious tool. Indeed, it represents a bas…

0301 basic medicineCA15-3OncologyCancer Researchmedicine.medical_specialtyPathologyBiopsyBreast NeoplasmsMetastasis03 medical and health sciencesBreast cancer0302 clinical medicineBreast cancerCirculating tumor cellInternal medicineBiopsyBiomarkers TumormedicineCarcinomaHumansPTENNeoplasm MetastasisLiquid biopsyBreast cancer; Circulating tumor cells; Circulating tumor DNA; CTCs; ctDNA; Liquid biopsy; Cancer ResearchCirculating tumor DNALiquid biopsybiologymedicine.diagnostic_testbusiness.industryCirculating tumor cellctDNADNA NeoplasmGeneral MedicineNeoplastic Cells Circulatingmedicine.diseaseCTC030104 developmental biology030220 oncology & carcinogenesisbiology.proteinFemalebusinessTumor Biology
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Critical Roles of EGFR family members in breast cancer and breast cancer stem cells: Targets for therapy

2016

The roles of the epidermal growth factor receptor (EGFR) signaling pathway in various cancers including breast, bladder, brain, colorectal, esophageal, gastric, head and neck, hepatocellular, lung, neuroblastoma, ovarian, pancreatic, prostate, renal and other cancers have been keenly investigated since the 1980's. While the receptors and many downstream signaling molecules have been identified and characterized, there is still much to learn about this pathway and how its deregulation can lead to cancer and how it may be differentially regulated in various cell types. Multiple inhibitors to EGFR family members have been developed and many are in clinical use. Current research often focuses o…

0301 basic medicineCA15-3OncologyEGFR HER2 mIRs Cancer Stem Cells Drug Resistance Metastasismedicine.medical_specialtyEGFRDrug ResistancemIRCancer Stem CellBreast NeoplasmsNOMetastasisMetastasis03 medical and health sciences0302 clinical medicineBreast cancerCancer stem cellInternal medicineCancer Stem CellsHER2Drug DiscoverymicroRNAmedicineCancer Stem Cells; Drug Resistance; EGFR; HER2; Metastasis; mIRs; Pharmacology; Drug Discovery3003 Pharmaceutical ScienceAnimalsHumansEpidermal growth factor receptorPharmacologyCancer Stem Cells; Drug Resistance; EGFR; HER2; Metastasis; mIRsmIRsbiologybusiness.industryEGFR HER2 mIRs Cancer Stem Cells Drug Resistance Metastasis.Drug Discovery3003 Pharmaceutical ScienceCancermedicine.disease3. Good healthErbB Receptors030104 developmental biology030220 oncology & carcinogenesisbiology.proteinNeoplastic Stem CellsFemaleStem cellbusinessSignal Transduction
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