Search results for " Tumor Cells"

showing 10 items of 46 documents

Novel iodoacetamido benzoheterocyclic derivatives with potent antileukemic activity are inhibitors of STAT5 phosphorylation

2016

Signal Transducer and Activator of Transcription 5 (STAT5) protein, a component of the STAT family of signaling proteins, is considered to be an attractive therapeutic target because of its involvement in the progression of acute myeloid leukemia. In an effort to discover potent molecules able to inhibit the phosphorylation-activation of STAT5, twenty-two compounds were synthesized and evaluated on the basis of our knowledge of the activity of 2-(3’,4’,5’-trimethoxybenzoyl)-3-iodoacetamido-6-methoxy benzo[b]furan derivative 1 as a potent STAT5 inhibitor. Most of these molecules, structurally related to compound 1, were characterized by the presence of a common 3’,4’,5’-trimethoxybenzoyl moi…

0301 basic medicineApoptosisAntineoplastic Agentchemistry.chemical_compoundBenzophenone0302 clinical medicinehemic and lymphatic diseasesFuranDrug DiscoverySTAT5 Transcription FactorTumor Cells CulturedThiopheneMoietyPhosphorylationSTAT5Molecular StructurebiologyChemistryBiological activityGeneral MedicineApoptosis; BCR/ABL expressing leukemia; In vitro antiproliferative activity; STAT5 inhibitors; Structure-activity relationship; Drug Discovery3003 Pharmaceutical Science; Organic Chemistry; PharmacologyLeukemia Myeloid Acute030220 oncology & carcinogenesisBCR/ABL expressing leukemiaApoptosis; BCR/ABL expressing leukemia; In vitro antiproliferative activity; STAT5 inhibitors; Structure-activity relationship; Antineoplastic Agents; Apoptosis; Benzofurans; Benzophenones; Cell Proliferation; Dose-Response Relationship Drug; Drug Screening Assays Antitumor; Humans; K562 Cells; Leukemia Myeloid Acute; Molecular Structure; Phosphorylation; STAT5 Transcription Factor; Structure-Activity Relationship; Tumor Cells Cultured; Drug Discovery3003 Pharmaceutical Science; Organic Chemistry; PharmacologyHumanStereochemistryAntineoplastic AgentsArticleNOBenzophenones03 medical and health sciencesK562 CellHumansStructure–activity relationshipBenzofuransCell ProliferationPharmacologyIndole testDose-Response Relationship DrugIn vitro antiproliferative activitySTAT5 inhibitorsDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryApoptosiSTAT5 inhibitorStructure-activity relationshipIn vitro030104 developmental biologybiology.proteinBenzofuranDrug Screening Assays AntitumorK562 Cells
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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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Nicotinamide Phosphoribosyltransferase Acts as a Metabolic Gate for Mobilization of Myeloid-Derived Suppressor Cells

2019

Abstract Cancer induces alteration of hematopoiesis to fuel disease progression. We report that in tumor-bearing mice the macrophage colony-stimulating factor elevates the myeloid cell levels of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD salvage pathway, which acts as negative regulator of the CXCR4 retention axis of hematopoietic cells in the bone marrow. NAMPT inhibits CXCR4 through a NAD/Sirtuin 1–mediated inactivation of HIF1α-driven CXCR4 gene transcription, leading to mobilization of immature myeloid-derived suppressor cells (MDSC) and enhancing their production of suppressive nitric oxide. Pharmacologic inhibition or myeloid-specific ablation …

0301 basic medicineCancer ResearchMyeloidmedicine.medical_treatmentNudeNicotinamide phosphoribosyltransferaseApoptosisColorectal NeoplasmInbred C57BLMicechemistry.chemical_compound0302 clinical medicineTumor Cells CulturedHematopoiesiNicotinamide PhosphoribosyltransferaseInbred BALB CMice Inbred BALB CCulturedbiologySarcomaTumor CellsHaematopoiesismedicine.anatomical_structureOncology030220 oncology & carcinogenesisSirtuinFemaleSarcoma ExperimentalColorectal NeoplasmsAnimals; Apoptosis; Cell Proliferation; Colorectal Neoplasms; Female; Hematopoiesis; Humans; Mammary Neoplasms Experimental; Mice; Mice Inbred BALB C; Mice Inbred C57BL; Mice Nude; Myeloid-Derived Suppressor Cells; NAD; Nicotinamide Phosphoribosyltransferase; Sarcoma Experimental; Signal Transduction; Tumor Cells Cultured; Xenograft Model Antitumor AssaysHumanSignal TransductionMice NudeExperimental03 medical and health sciencesmedicineMyeloid-Derived Suppressor CellAnimalsHumansCell ProliferationAnimalMyeloid-Derived Suppressor CellsMammary NeoplasmsApoptosiMammary Neoplasms ExperimentalImmunotherapyNADXenograft Model Antitumor AssaysHematopoiesisMice Inbred C57BL030104 developmental biologychemistrybiology.proteinCancer researchMyeloid-derived Suppressor CellNAD+ kinaseBone marrowCancer Research
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Preclinical and Clinical Evaluation of Magnetic-Activated Cell Separation Technology for CTC Isolation in Breast Cancer

2020

Circulating tumor cell (CTC) count is an independent prognostic factor in early breast cancer. CTCs can be found in the blood of 20% of patients prior to neoadjuvant therapy. We aimed to assess the suitability of magnetic-activated cell separation (MACS) technology for isolation and cytological characterization of CTCs. In the preclinical part of the study, cell lines were spiked into buffy coat samples derived from healthy donors, and isolated using MACS. Breast cancer cells with preserved cell morphology were successfully isolated. In the clinical part, blood for CTC isolation was drawn from 44 patients with early and locally advanced breast cancer prior to neoadjuvant chemotherapy. Stand…

0301 basic medicineCancer ResearchPathologymedicine.medical_specialtymedicine.medical_treatmentPapanicolaou stainBuffy coatcirculating tumor cellsCell morphologylcsh:RC254-28203 medical and health sciences0302 clinical medicineBreast cancerCirculating tumor cellbreast cancermorphologymedicineLiquid biopsyNeoadjuvant therapyOriginal Researchliquid biopsybusiness.industrylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyOncologyCytopathology030220 oncology & carcinogenesisbusinessmagnetic-activated cell separationFrontiers in Oncology
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Ginkgo biloba induces different gene expression signatures and oncogenic pathways in malignant and non-malignant cells of the liver

2018

Ginkgo biloba (EGb761) is a widely used botanical drug. Several reports indicate that EGb761 confers preventive as well as anti-tumorigenic properties in a variety of tumors, including hepatocellular carcinoma (HCC). We here evaluate functional effects and molecular alterations induced by EGb761 in hepatoma cells and non-malignant hepatocytes. Hepatoma cell lines, primary human HCC cells and immortalized human hepatocytes (IH) were exposed to various concentrations (0-1000 μg/ml) of EGb761. Apoptosis and proliferation were evaluated after 72h of EGb761 exposure. Response to oxidative stress, tumorigenic properties and molecular changes were further investigated. While anti-oxidant effects w…

0301 basic medicineCarcinogenesisApoptosismedicine.disease_causeBiochemistryAntioxidantsTranscriptome0302 clinical medicineCell SignalingAnimal CellsMedicine and Health SciencesCellular Stress ResponsesCultured Tumor CellsMultidisciplinaryCell DeathbiologyGinkgo bilobaTOR Serine-Threonine KinasesLiver NeoplasmsQRLiverOncologyCell Processes030220 oncology & carcinogenesisHepatocellular carcinomaMedicineBiological CulturesCellular TypesAnatomyResearch ArticleSignal TransductionCarcinoma HepatocellularNF-E2-Related Factor 2ScienceResearch and Analysis MethodsCell Line03 medical and health sciencesmedicineHumansCell ProliferationOncogenic SignalingPlant ExtractsBiology and Life SciencesGinkgo bilobaCell BiologyCell Culturesbiology.organism_classificationmedicine.diseaseOxidative Stress030104 developmental biologyCell cultureApoptosisCancer cellHepatocytesCancer researchHepatoma CellsTranscriptomeCarcinogenesisOxidative stressPLOS ONE
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Functional characterization of circulating tumor cells (CTCs) from metastatic ER+/HER2− breast cancer reveals dependence on HER2 and FOXM1 for endocr…

2021

Simple Summary Acquired endocrine resistance and late recurrence in patients with ER+/HER2− breast cancer are complex and not fully understood. Here, we evaluated mechanisms of acquired resistance in circulating tumor cells (CTCs) from an ER+/HER2− breast cancer patient who initially responded but later progressed under endocrine treatment. We found a switch from ERα-dependent to HER2-dependent and ERα-independent expression of FOXM1, which may enable disseminated ER+/HER2− cells to re-initiate tumor cell growth and metastasis formation in the presence of endocrine treatment. We found that NFkB signaling sustains HER2 and FOXM1 expression in CTCs in the presence of ERα inhibitors suggesting…

0301 basic medicineDrugLife sciences; biologyCancer Researchmedia_common.quotation_subjectTumor cellslcsh:RC254-282Article03 medical and health sciencesTherapeutic approach0302 clinical medicineCirculating tumor cellBreast cancerHER2-dependent FOXM1 expressionddc:570ER+/HER2− circulating tumor cellsMedicineEndocrine systemskin and connective tissue diseasesmedia_commonER+/HER2��� circulating tumor cellsbusiness.industryendocrine therapy resistancelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyOncologyApoptosis030220 oncology & carcinogenesisFOXM1Cancer researchbusiness
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Detection of MET Alterations Using Cell Free DNA and Circulating Tumor Cells from Cancer Patients

2020

MET alterations may provide a potential biomarker to evaluate patients who will benefit from treatment with MET inhibitors. Therefore, the purpose of the present study is to investigate the utility of a liquid biopsy-based strategy to assess MET alterations in cancer patients. We analyzed MET amplification in circulating free DNA (cfDNA) from 174 patients with cancer and 49 healthy controls and demonstrated the accuracy of the analysis to detect its alteration in patients. Importantly, a significant correlation between cfDNA concentration and MET copy number (CN) in cancer patients (r = 0.57, p &lt

0301 basic medicineOncologyMale<i>MET</i> copy numbermedicine.medical_treatmentproteínas protooncogénicas c-metdosificación génicahumanosresistencia a medicamentosDrug ResistanceGene Dosagecirculating free DNA (cfDNA)<i>MET</i> amplificationTargeted therapyTargeted therapy0302 clinical medicineCirculating tumor cellestudios prospectivosNeoplasmsantineoplásicosProspective Studieslcsh:QH301-705.5Circulating tumor cells (CTCs)neoplasiasGeneral MedicineProto-Oncogene Proteins c-mettargeted therapyNeoplastic Cells CirculatingErbB ReceptorsCell-free fetal DNA030220 oncology & carcinogenesisinhibidores de proteína cinasasBiomarker (medicine)FemaleMET protein expressionCell-Free Nucleic AcidsMET amplificationmedicine.medical_specialtycirculating tumor cells (CTCs)estudios de casos y controlesMet amplificationCirculating free DNA (cfDNA)Antineoplastic AgentsArticle03 medical and health sciencesInternal medicinemedicineBiomarkers TumorHumansLiquid biopsyProtein Kinase InhibitorsRetrospective Studiesbusiness.industryHead and neck cancerestudios retrospectivosLiquid BiopsyCancermedicine.disease030104 developmental biologylcsh:Biology (General)Drug Resistance NeoplasmCase-Control StudiesMET copy numberbusinessCells
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Phospho-Akt overexpression is prognostic and can be used to tailor the synergistic interaction of Akt inhibitors with gemcitabine in pancreatic cancer

2017

Background There is increasing evidence of a constitutive activation of Akt in pancreatic ductal adenocarcinoma (PDAC), associated with poor prognosis and chemoresistance. Therefore, we evaluated the expression of phospho-Akt in PDAC tissues and cells, and investigated molecular mechanisms influencing the therapeutic potential of Akt inhibition in combination with gemcitabine. Methods Phospho-Akt expression was evaluated by immunohistochemistry in tissue microarrays (TMAs) with specimens tissue from radically-resected patients (n = 100). Data were analyzed by Fisher and log-rank test. In vitro studies were performed in 14 PDAC cells, including seven primary cultures, characterized for their…

0301 basic medicineOncologyMaleCancer ResearchBiopsyAKT1ApoptosisAkt; Gemcitabine; Pancreatic ductal adenocarcinoma; Synergism; Hematology; Molecular Biology; Oncology; Cancer ResearchDeoxycytidinePancreatic ductal adenocarcinoma0302 clinical medicineCell MovementTumor Cells CulturedGlucose Transporter Type 1medicine.diagnostic_testChemistryCell CyclePancreatic NeoplasmDrug Synergismlcsh:Diseases of the blood and blood-forming organsHematologyCell cycleMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisOncologyAkt; Gemcitabine; Pancreatic ductal adenocarcinoma; Synergism; Aged; Apoptosis; Biopsy; Carcinoma Pancreatic Ductal; Cell Cycle; Cell Movement; Deoxycytidine; Drug Synergism; Female; Glucose Transporter Type 1; Humans; Male; Middle Aged; Pancreatic Neoplasms; Phosphoproteins; Prognosis; Proto-Oncogene Proteins c-akt; RNA Messenger; Spheroids Cellular; Tumor Cells Cultured; Hematology; Molecular Biology; Oncology; Cancer Research030220 oncology & carcinogenesisPhosphoproteinFemalemedicine.drugHumanCarcinoma Pancreatic Ductalmedicine.medical_specialtyPrognosilcsh:RC254-282Flow cytometry03 medical and health sciencesInternal medicinePancreatic cancerSpheroids CellularmedicineHumansRNA MessengerProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayAgedlcsh:RC633-647.5ResearchAktSynergismApoptosimedicine.diseasePhosphoproteinsGemcitabineGemcitabinePancreatic Neoplasms030104 developmental biologyCancer cellCancer researchProto-Oncogene Proteins c-akt
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Liquid biopsy as surrogate for tissue for molecular profiling in pancreatic cancer: A meta-analysis towards precision medicine

2019

Liquid biopsy (LB) is a non-invasive approach representing a promising tool for new precision medicine strategies for cancer treatment. However, a comprehensive analysis of its reliability for pancreatic cancer (PC) is lacking. To this aim, we performed the first meta-analysis on this topic. We calculated the pooled sensitivity, specificity, positive (LR+) and negative (LR-) likelihood ratio, and diagnostic odds ratio (DOR). A summary receiver operating characteristic curve (SROC) and area under curve (AUC) were used to evaluate the overall accuracy. We finally assessed the concordance rate of all mutations detected by multi-genes panels. Fourteen eligible studies involving 369 patients wer…

0301 basic medicineOncologymedicine.medical_specialtyCancer ResearchConcordanceprecision medicinepancreatic cancerReviewlcsh:RC254-282Circulating tumor cells (CTC)03 medical and health sciences0302 clinical medicineInternal medicinePancreatic cancermedicineLiquid biopsycfDNALiquid biopsyReceiver operating characteristicliquid biopsybusiness.industryCfDNAPrecision medicinePancreatic cancerPrecision medicinemedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthCancer treatment030104 developmental biologyOncologycirculating tumor cells (CTC)030220 oncology & carcinogenesisMeta-analysisDiagnostic odds ratiobusinesscfDNA; circulating tumor cells (CTC); liquid biopsy; pancreatic cancer; precision medicine
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Epigenomic landscape of human colorectal cancer unveils an aberrant core of pan-cancer enhancers orchestrated by YAP/TAZ

2021

Cancer is characterized by pervasive epigenetic alterations with enhancer dysfunction orchestrating the aberrant cancer transcriptional programs and transcriptional dependencies. Here, we epigenetically characterize human colorectal cancer (CRC) using de novo chromatin state discovery on a library of different patient-derived organoids. By exploring this resource, we unveil a tumor-specific deregulated enhancerome that is cancer cell-intrinsic and independent of interpatient heterogeneity. We show that the transcriptional coactivators YAP/TAZ act as key regulators of the conserved CRC gained enhancers. The same YAP/TAZ-bound enhancers display active chromatin profiles across diverse human t…

0301 basic medicineOrganoidEpigenomicsTranscription FactorGeneral Physics and AstronomyColorectal NeoplasmAdaptor Proteins Signal Transducing; Colorectal Neoplasms; Gene Expression Regulation Neoplastic; Histone Code; Humans; Models Genetic; Organoids; RNA-Seq; Single-Cell Analysis; Trans-Activators; Transcription Factors; Tumor Cells Cultured; Enhancer Elements Genetic; Epigenesis GeneticEpigenesis Genetic0302 clinical medicineModelsAdaptor Proteins Signal Transducing Colorectal Neoplasms Gene Expression Regulation NeoplasticHistone Code Humans Models Genetic Organoids RNA-Seq Single-Cell Analysis Trans-Activators Transcription Factors Tumor Cells Cultured Enhancer Elements Genetic Epigenesis GeneticTumor Cells CulturedCancer genomicsHistone codeRNA-SeqEpigenomicsAdaptor Proteins Signal Transducing; Colorectal Neoplasms; Gene Expression Regulation Neoplastic; Histone Code; Humans; Models Genetic; Organoids; RNA-Seq; Single-Cell Analysis; Trans-Activators; Transcription Factors; Transcriptional Coactivator with PDZ-Binding Motif Proteins; Tumor Cells Cultured; YAP-Signaling Proteins; Enhancer Elements Genetic; Epigenesis GeneticMultidisciplinaryCulturedQAdaptor Proteins3. Good healthChromatinTumor CellsGene Expression Regulation NeoplasticHistone CodeOrganoidsSingle-Cell AnalysiEnhancer Elements GeneticTrans-Activator030220 oncology & carcinogenesisSingle-Cell AnalysisColorectal NeoplasmsHumanEnhancer ElementsScienceTumour heterogeneityBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesGeneticmedicineHumansEpigeneticsEnhancerTranscription factorAdaptor Proteins Signal TransducingNeoplasticModels GeneticSignal TransducingCancerYAP-Signaling ProteinsGeneral Chemistrymedicine.diseaseColorectal cancerdigestive system diseases030104 developmental biologyGene Expression RegulationTranscriptional Coactivator with PDZ-Binding Motif ProteinsCancer cellCancer researchTrans-ActivatorsEpigenesisTranscription Factors
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