Search results for "TUMOR CELLS"

showing 10 items of 663 documents

Transcriptional Profiles and Stromal Changes Reveal Bone Marrow Adaptation to Early Breast Cancer in Association with Deregulated Circulating microRN…

2020

Abstract The presence of a growing tumor establishes a chronic state of inflammation that acts locally and systemically. Bone marrow responds to stress signals by expanding myeloid cells endowed with immunosuppressive functions, further fostering tumor growth and dissemination. How early in transformation the cross-talk with the bone marrow begins and becomes detectable in blood is unknown. Here, gene expression profiling of the bone marrow along disease progression in a spontaneous model of mammary carcinogenesis demonstrates that transcriptional modifications in the hematopoietic compartment occurred as early as preinvasive disease stages. The transcriptional profile showed downregulation…

0301 basic medicineCancer ResearchMyeloidStromal cellInflammationApoptosisBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaCXCR403 medical and health sciencesMice0302 clinical medicineBone MarrowmedicineBiomarkers TumorTumor Cells CulturedAnimalsHumansCirculating MicroRNACell ProliferationMice Inbred BALB CInnate immune systemGene Expression ProfilingAcquired immune systemAdaptation PhysiologicalXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticHaematopoiesis030104 developmental biologymedicine.anatomical_structureOncologyTrascriptional profiles early brest cancer microRNAs030220 oncology & carcinogenesisCancer researchFemaleBone marrowmedicine.symptomStromal CellsTranscriptomeCancer research
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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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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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Ligand-dependent Hedgehog pathway activation in Rhabdomyosarcoma : the oncogenic role of the ligands

2017

Altres ajuts: This work was supported by grants from Institut Català d'Oncologia (ICO), Instituto de Salud Carlos III (RTICC-RD12/0036/0016, /0020, /0035, /0057; and PI14/00647), Fundació A BOSCH, Fundació Amics Joan Petit, ajuts predoctorals del VHIR and RIS3CAT grants COMRDI15-1-0014 (ACCIÓ and FEDER). Altres ajuts: FEDER/COMRDI15-1-0014 Rhabdomyosarcoma (RMS) is the most common type of soft tissue sarcoma in children. The Hedgehog (HH) pathway is known to develop an oncogenic role in RMS. However, the molecular mechanism that drives activation of the pathway in RMS is not well understood. The expression of HH ligands was studied by qPCR, western blot and immunohistochemistry. Functional …

0301 basic medicineCancer ResearchsarcomaCarcinogenesisVismodegibRhabdomyosarcoma; Hedgehog; vismodegib; UPR; TRIB3; sarcoma; cancerVismodegib610ApoptosisMice SCIDUPRLigandsMice03 medical and health sciences0302 clinical medicineCell MovementvismodegibRhabdomyosarcomaTumor Cells CulturedmedicinecancerAnimalsHumansHedgehog ProteinsAutocrine signallingRhabdomyosarcomaHedgehogCell ProliferationCancerChemistryTRIB3Sarcomamedicine.diseaseXenograft Model Antitumor AssaysHedgehog signaling pathway3. Good health030104 developmental biologyOncology030220 oncology & carcinogenesisUnfolded protein responseCancer researchFemaleSignal transductionTranslational TherapeuticsSmoothenedHedgehogSignal TransductionTranscription Factorsmedicine.drug
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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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Production Conditions Affect the In Vitro Anti-Tumoral Effects of a High Concentration Multi-Strain Probiotic Preparation.

2016

A careful selection of the probiotic agent, standardization of the dose and detailed characterization of the beneficial effects are essential when considering use of a probiotic for the dietary management of serious diseases. However, changes in the manufacturing processes, equipment or facilities can result in differences in the product itself due to the live nature of probiotics. The need to reconfirm safety and/or efficacy for any probiotic product made at a different factory is therefore mandatory. Recently, under the brand VSL#3®, a formulation produced by a manufacturer different from the previous one, has been commercialized in some European countries (the UK and Holland). VSL#3 is a…

0301 basic medicineGenetics and Molecular Biology (all)Cell LinesCancer Treatmentlcsh:MedicineApoptosisMedicine (all); Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)Biochemistrylaw.inventionProbiotic0302 clinical medicinelawMedicine and Health SciencesMedicineCell Cycle and Cell DivisionEnzyme-Linked Immunoassayslcsh:ScienceStainingMultidisciplinaryCell DeathMedicine (all)Inflammatory Bowel DiseasesCell StainingApoptotic deathProbiotic agentOncologyCell Processes030211 gastroenterology & hepatologyBiological CulturesResearch ArticleTumor cellsAffect (psychology)Research and Analysis MethodsMicrobiology03 medical and health sciencesImmunoassaysBeneficial effectsBacteriabusiness.industryProbioticslcsh:ROrganismsBiology and Life SciencesCell BiologyIn vitroBiotechnology030104 developmental biologyAgricultural and Biological Sciences (all)Specimen Preparation and TreatmentImmunologyImmunologic Techniqueslcsh:QCaco-2 CellsbusinessPLoS ONE
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miR-22 suppresses DNA ligase III addiction in multiple myeloma

2019

Multiple myeloma (MM) is a hematologic malignancy characterized by high genomic instability. Here we provide evidence that hyper-activation of DNA ligase III (LIG3) is crucial for genomic instability and survival of MM cells. LIG3 mRNA expression in MM patients correlates with shorter survival and even increases with more advanced stage of disease. Knockdown of LIG3 impairs MM cells viability in vitro and in vivo, suggesting that neoplastic plasmacells are dependent on LIG3-driven repair. To investigate the mechanisms involved in LIG3 expression, we investigated the post-transcriptional regulation. We identified miR-22-3p as effective negative regulator of LIG3 in MM. Enforced expression of…

0301 basic medicineGenome instabilityCancer ResearchmiR-22 LIG3DNA repairDNA damageDNA repairApoptosisLIG3ArticleDNA Ligase ATP03 medical and health sciences0302 clinical medicinemicroRNABiomarkers TumorTumor Cells CulturedHumansPoly-ADP-Ribose Binding ProteinsCell ProliferationmiRNAchemistry.chemical_classificationRegulation of gene expressionGene knockdownDNA ligaseLeukemiamicroRNAChemistryHematologyPrognosisXenograft Model Antitumor AssaysGene Expression Regulation Neoplasticmultiple myelomaMicroRNAs030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchpharmacologyDNA DamageLeukemia
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HSP110 sustains chronic NF-κB signaling in activated B cell diffuse large B cell lymphoma through MyD88 stabilization

2018

International audience; Activated B cell diffuse large B cell lymphoma (ABC-DLBCL) is an aggressive lymphoproliferative disorder involving chronic NF-κB activation. Several mutations in the BCR and the MyD88 signaling pathway components, such as MyD88 L265P, are implicated in this aberrant activation. Among heat-shock proteins, HSP110 has recently been identified as a pro- survival and/or proliferation factor in many cancers but its role in ABC-DLBCL survival mechanisms remained to be established. We observed that shRNA-mediated HSP110 silencing decreased the survival of several ABC-DLBCL cell lines, decreased IgM-MyD88 co-localization and subsequent NF-κB signaling. Conversely, over-expres…

0301 basic medicineImmunology[SDV.CAN]Life Sciences [q-bio]/CancerBiochemistry[ SDV.CAN ] Life Sciences [q-bio]/CancerCohort Studies03 medical and health sciencesimmune system diseaseshemic and lymphatic diseasesmedicineTumor Cells CulturedGene silencingHumansHSP110 Heat-Shock ProteinsB cellChemistryProtein StabilityWild typebreakpoint cluster regionNF-kappa BCell BiologyHematologymedicine.disease3. Good healthLymphoma030104 developmental biologymedicine.anatomical_structureCell cultureMyeloid Differentiation Factor 88Cancer researchLymphoma Large B-Cell DiffuseSignal transductionDiffuse large B-cell lymphomaSignal Transduction
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