Search results for "breast neoplasms"

showing 10 items of 804 documents

Characteristics and Clinical Outcome of Breast Cancer Patients with Asymptomatic Brain Metastases

2020

Background: Brain metastases (BM) have become a major challenge in patients with metastatic breast cancer. Methods: The aim of this analysis was to characterize patients with asymptomatic BM (n = 580) in the overall cohort of 2589 patients with BM from our Brain Metastases in Breast Cancer Network Germany (BMBC) registry. Results: Compared to symptomatic patients, asymptomatic patients were slightly younger at diagnosis (median age: 55.5 vs. 57.0 years, p = 0.01), had a better performance status at diagnosis (Karnofsky index 80&ndash

0301 basic medicineCancer Researchmedicine.medical_specialtyNeoplasm metastasisMetastasePrognoseContext (language use)lcsh:RC254-282AsymptomaticGastroenterologyArticle03 medical and health sciencesbreast cancer0302 clinical medicineBreast cancerbrain metastasesInternal medicineBrustkrebsasymptomaticMedicineClinical significanceddc:610Treatment outcomeHirnmetastasePerformance statusbusiness.industrylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseMetastatic breast cancer030104 developmental biologyRisk factorsOncologyLead time bias030220 oncology & carcinogenesisCohortBreast neoplasmsmedicine.symptombusinessDDC 610 / Medicine & healthCancers
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MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state

2018

Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways. Overexpression of MYC induces transcriptional repression of lineage-specifying transcription factors, causing decommissioning of luminal-specific enhancers. MYC-driven dedifferentiation supports the onset of a stem cell-like state by inducing the activation of de novo enhancers, which drive the transcriptional activation of oncogenic pathways. Furthermo…

0301 basic medicineCarcinogenesisScienceGeneral Physics and AstronomyBreast NeoplasmsMice SCIDTumor initiationBiologyBreast cancer MYC Tumorigenesismedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticProto-Oncogene Proteins c-mycMice03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpigeneticslcsh:ScienceEnhancerTranscription factorRegulation of gene expressionMultidisciplinaryQGeneral ChemistryCellular ReprogrammingCell biologyGene Expression Regulation NeoplasticEnhancer Elements Genetic030104 developmental biologyNeoplastic Stem CellsFemalelcsh:QStem cellCarcinogenesisReprogramming
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WNT signaling modulates PD-L1 expression in the stem cell compartment of triple-negative breast cancer

2019

Triple-negative breast cancers (TNBCs) are characterized by a poor prognosis and lack of targeted treatments, and thus, new therapeutic strategies are urgently needed. Inhibitors against programmed death-1 (PD-1)/PD-1 ligand (PD-L1) have shown significant efficacy in various solid cancers, but their activity against TNBCs remains limited. Here, we report that human TNBCs molecularly stratified for high levels of PD-L1 (PD-L1High) showed significantly enriched expression of immune and cancer stemness pathways compared with those with low PD-L1 expression (PD-L1Low). In addition, the PD-L1High cases were significantly associated with a high stemness score (SSHigh) signature. TNBC cell lines g…

0301 basic medicineCell biologyCancer ResearchTriple Negative Breast NeoplasmImmunologyDown-RegulationTriple Negative Breast NeoplasmsArticleB7-H1 Antigen03 medical and health sciences0302 clinical medicineImmune systemStem CellCell Line TumorBiomarkers TumorGeneticsmedicineAnimalsHumansWnt Signaling PathwayMolecular BiologyTriple-negative breast cancerMice Inbred BALB CbiologyAnimalStem CellsCD44Wnt signaling pathwayCancerAldehyde Dehydrogenasemedicine.diseaseHyaluronan ReceptorUp-RegulationALDH1A1Hyaluronan Receptors030104 developmental biology030220 oncology & carcinogenesisbiology.proteinCancer researchFemaleStem cellB7-H1 AntigenHumanOncogene
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PTP1B phosphatase as a novel target of oleuropein activity in MCF-7 breast cancer model.

2019

Phosphatase PTP1B has become a therapeutic target for the treatment of type 2-diabetes, whereas recent studies have revealed that PTP1B plays a pivotal role in pathophysiology and development of breast cancer. Oleuropein is a natural, phenolic compound with anticancer activity. The aim of this study was to address the question whether PTP1B constitutes a target for oleuropein in breast cancer MCF-7 cells. The cellular MCF-7 breast cancer model was used in the study. The experiments were performed using cellular viability tests, Elisa assays, immunoprecipitation, flow cytometry analyses and computer modelling. Herein, we evidenced that the reduced activity of phosphatase PTP1B after treatmen…

0301 basic medicineCell cycle checkpointImmunoprecipitationCell Survivalmedicine.medical_treatmentPhosphataseIridoid GlucosidesAntineoplastic AgentsBreast NeoplasmsAdenocarcinomaMolecular Dynamics SimulationToxicologyFlow cytometry03 medical and health scienceschemistry.chemical_compoundbreast cancer0302 clinical medicineBreast cancerOleuropeinmedicineHumansPTP1B phosphataseIridoidsskin and connective tissue diseasesSettore CHIM/02 - Chimica FisicaCell ProliferationOleuropeinProtein Tyrosine Phosphatase Non-Receptor Type 1MCF-7 cellmedicine.diagnostic_testAnticancer therapyGeneral Medicinemedicine.disease030104 developmental biologychemistryMCF-7Settore CHIM/03 - Chimica Generale E Inorganica030220 oncology & carcinogenesisSettore BIO/14 - FarmacologiaCancer researchMCF-7 CellsAdjuvanthormones hormone substitutes and hormone antagonistsToxicology in vitro : an international journal published in association with BIBRA
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Direct estrogen receptor (ER) / HER family crosstalk mediating sensitivity to lumretuzumab and pertuzumab in ER+ breast cancer.

2017

Bidirectional cross talk between members of the human epidermal growth factor family of receptors (HER) and the estrogen receptor (ER) is believed to underlie resistance mechanisms that develop in response to treatment with anti-HER agents and endocrine therapy. We investigated the interaction between HER2, HER3 and the ER in vitro using human embryonic kidney cells transfected with human HER2, HER3, and ERα. We also investigated the additive efficacy of combination regimens consisting of anti-HER3 (lumretuzumab), anti-HER2 (pertuzumab), and endocrine (fulvestrant) therapy in vivo. Our data show that both HER2 and HER3 can directly complex with the ER and can mediate phosphorylation of the …

0301 basic medicineCell signalingReceptor ErbB-3Receptor ErbB-2Cancer TreatmentEstrogen receptorlcsh:MedicineSignal transductionBiochemistryMice0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsBreast TumorsMedicine and Health SciencesReceptorlcsh:Scienceskin and connective tissue diseasesMultidisciplinaryRemission InductionEndocrine TherapySignaling cascadesPrecipitation TechniquesTreatment OutcomeReceptors EstrogenOncology030220 oncology & carcinogenesisMonoclonalCell linesFemalePertuzumabBiological culturesmedicine.drugResearch ArticleAdultCell biologyMAPK signaling cascadesPaclitaxelBreast NeoplasmsAntibodies Monoclonal Humanized03 medical and health sciencesBreast cancerCell Line TumorBreast CancermedicineEndocrine systemAnimalsHumansImmunoprecipitationFulvestrantbusiness.industrylcsh:RHEK 293 cellsCancers and NeoplasmsBiology and Life SciencesEstrogensReceptor Cross-TalkLumretuzumabmedicine.diseaseXenograft Model Antitumor AssaysHormonesResearch and analysis methods030104 developmental biologyCancer researchlcsh:QbusinessPloS one
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Resveratrol-Induced Temporal Variation in the Mechanical Properties of MCF-7 Breast Cancer Cells Investigated by Atomic Force Microscopy

2019

Atomic force microscopy (AFM) combined with fluorescence microscopy has been used to quantify cytomechanical modifications induced by resveratrol (at a fixed concentration of 50 &micro

0301 basic medicineCellMotilityBreast Neoplasmsforce spectroscopyResveratrolresveratrolMicroscopy Atomic Forcefluorescence microscopyCatalysisArticleInorganic Chemistrylcsh:Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicinebreast cancerCell MovementElastic ModulusmedicineFluorescence microscopeCell AdhesionHumansPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5SpectroscopyMechanical Phenomenaatomic force microscopyChemistryOrganic ChemistryForce spectroscopytechnology industry and agricultureGeneral MedicineAdhesioncytomechanicsComputer Science Applications030104 developmental biologymedicine.anatomical_structureMCF-7lcsh:Biology (General)lcsh:QD1-999030220 oncology & carcinogenesisCancer cellBiophysicsMCF-7 CellsFemaleMCF-7International Journal of Molecular Sciences
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NF-κB Is a Potential Molecular Drug Target in Triple-Negative Breast Cancers.

2017

Breast cancer continues to cause significant burden in global health morbidity and mortality. Triple-negative breast cancers (TNBCs) are highly aggressive with poor prognosis and are characterized by lack of expression of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor (Her-2). TNBCs are often resistant to cytotoxic chemotherapy and pose major difficulty in achieving personalized medicine due to their molecular heterogeneity. There is increasing evidence that the aberrant activation of nuclear factor (NF)-κB signaling is a frequent characteristic of TNBCs. We evaluated the effects of different potential NF-κB inhibitors, such as bisindolylmaleimide I (BI…

0301 basic medicineCurcuminEstrogen receptorTriple Negative Breast NeoplasmsPharmacologydiagnostics drug targets NF-kB signaling personalized medicine triple-negative breast cancerBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBreast cancerCell Line TumorMG132Progesterone receptorGeneticsmedicineGene silencingHumansPrecision MedicineMolecular BiologyTriple-negative breast cancerbusiness.industryCyclohexanonesNF-kappa BCancermedicine.disease030104 developmental biologychemistry030220 oncology & carcinogenesisBenzamidesProteasome inhibitorCancer researchMolecular MedicineFemalebusinessBiotechnologymedicine.drugSignal TransductionOmics : a journal of integrative biology
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Circadian Rhythm and Concentration of Melatonin in Breast Cancer Patients

2020

Background: Melatonin is a biomarker of the central circadian clock and its chronobiotic actions entraining circadian rhythms to the light-dark cycle are well known. Reduction in melatonin levels and altered circadian rhythms have been associated with a high risk of breast cancer. Melatonin has also shown to display anti-proliferative effects on breast cancer growth and proliferation. Evaluation of melatonin circadian rhythm alterations in patients bearing breast cancer may have interesting prognostic and therapeutic applications. Objective: To review studies evaluating the circadian rhythm of melatonin in breast cancer patients. The effects of surgery and chemotherapy on melatonin secreti…

0301 basic medicineEndocrinology Diabetes and MetabolismBreast surgerymedicine.medical_treatmentChronobioticCircadian clockEstrogen receptorPhysiologyBreast Neoplasms030209 endocrinology & metabolismHistory 21st CenturyAntioxidantsMelatonin03 medical and health sciences0302 clinical medicineBreast cancermedicineHumansImmunology and AllergyCircadian rhythmMelatoninbusiness.industrymedicine.diseaseCircadian RhythmSleep Quality030104 developmental biologyQuality of LifeBiomarker (medicine)FemaleSleepbusinesshormones hormone substitutes and hormone antagonistsmedicine.drugEndocrine, Metabolic & Immune Disorders - Drug Targets
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Integrative analysis of structural variations using short-reads and linked-reads yields highly specific and sensitive predictions.

2020

Genetic diseases are driven by aberrations of the human genome. Identification of such aberrations including structural variations (SVs) is key to our understanding. Conventional short-reads whole genome sequencing (cWGS) can identify SVs to base-pair resolution, but utilizes only short-range information and suffers from high false discovery rate (FDR). Linked-reads sequencing (10XWGS) utilizes long-range information by linkage of short-reads originating from the same large DNA molecule. This can mitigate alignment-based artefacts especially in repetitive regions and should enable better prediction of SVs. However, an unbiased evaluation of this technology is not available. In this study, w…

0301 basic medicineFalse discovery rateComputer scienceArtificial Gene Amplification and ExtensionPolymerase Chain ReactionDatabase and Informatics MethodsSequencing techniques0302 clinical medicineBreast TumorsBasic Cancer ResearchMedicine and Health SciencesDNA sequencingBiology (General)EcologyHigh-Throughput Nucleotide SequencingGenomicsDNA Neoplasm3. Good healthIdentification (information)OncologyComputational Theory and MathematicsModeling and SimulationMCF-7 CellsFemaleSequence AnalysisResearch ArticleBioinformaticsQH301-705.5Breast NeoplasmsGenomicsComputational biologyResearch and Analysis MethodsHuman Genomics03 medical and health sciencesCellular and Molecular NeuroscienceCancer GenomicsGenomic MedicineBreast CancerGeneticsDNA Barcoding TaxonomicHumansMolecular Biology TechniquesMolecular BiologyEcology Evolution Behavior and SystematicsWhole genome sequencingLinkage (software)Whole Genome SequencingGenome HumanDideoxy DNA sequencingGenetic Diseases InbornCancers and NeoplasmsBiology and Life SciencesComputational BiologyStatistical modelSequence Analysis DNARepetitive RegionsLogistic Models030104 developmental biologyGenomic Structural VariationHuman genomeSequence Alignment030217 neurology & neurosurgeryPLoS Computational Biology
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ΔNp63 drives metastasis in breast cancer cells via PI3K/CD44v6 axis

2016

P63 is a transcription factor belonging to the family of p53, essential for the development and differentiation of epithelia. In recent years, it has become clear that altered expression of the different isoforms of this gene can play an important role in carcinogenesis. The p63 gene encodes for two main isoforms known as TA and ΔN p63 with different functions. The role of these different isoforms in sustaining tumor progression and metastatic spreading however has not entirely been clarified. Here we show that breast cancer initiating cells express ΔNp63 isoform that supports a more mesenchymal phenotype associated with a higher tumorigenic and metastatic potential. On the contrary, the ma…

0301 basic medicineGene isoformEpithelial-Mesenchymal TransitionBreast Neoplasmsmedicine.disease_causeMetastasisMicePhosphatidylinositol 3-Kinases03 medical and health sciencesBreast cancerTumor MicroenvironmentmedicineAnimalsHumansmetastasisEpithelial–mesenchymal transitionNeoplasm MetastasisPI3K/AKT/mTOR pathwayAgedAged 80 and overTumor microenvironmentp63breast cancer initiating cellsbusiness.industryMembrane ProteinsCD44v6Middle Agedmedicine.diseasePI3K/AKT pathwayHyaluronan Receptors030104 developmental biologyOncologyDrug Resistance NeoplasmTumor progressionImmunologyCancer researchFemalebreast cancer initiating cellmetastasibusinessCarcinogenesisProto-Oncogene Proteins c-aktSignal TransductionPriority Research Paper
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