Search results for " breast cancer"

showing 10 items of 427 documents

Loss of MCL1 function sensitizes the MDA-MB-231 breast cancer cells to rh-TRAIL by increasing DR4 levels.

2019

Triple-negative breast cancer (TNBC) is a form of BC characterized by high aggressiveness and therapy resistance probably determined by cancer stem cells. MCL1 is an antiapoptotic Bcl-2 family member that could limit the efficacy of anticancer agents as recombinant human tumor necrosis factor related apoptosis-inducing ligand (rh-TRAIL). Here, we investigated MCL1 expression in TNBC tissues and cells. We found MCL1 differentially expressed (upregulated or downregulated) in TNBC tissues. Furthermore, in comparison to the human mammary epithelial cells, we found that MDA-MB-231 cells show similar messenger RNA levels but higher MCL1 protein levels, whereas it resulted downregulated in MDA-MB-…

0301 basic medicinecancer stem cellIndolesPhysiologyCell SurvivalClinical BiochemistryCellPopulationApoptosisTNF-Related Apoptosis-Inducing Ligand03 medical and health sciences0302 clinical medicineCancer stem cellSettore BIO/10 - BiochimicaCell Line Tumormedicinerh-TRAILBiomarkers TumorGene silencingHumansViability assayGene SilencingeducationCell ShapeCell ProliferationMembrane Potential Mitochondrialeducation.field_of_studySulfonamidesChemistryCell growthCell CycleCell BiologyCell cycleRecombinant ProteinsGene Expression Regulation NeoplasticReceptors TNF-Related Apoptosis-Inducing Ligand030104 developmental biologymedicine.anatomical_structureMCL1ApoptosisDR4 receptor030220 oncology & carcinogenesisCancer researchtriple-negative breast cancerMyeloid Cell Leukemia Sequence 1 ProteinJournal of cellular physiology
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MiR-24 induces chemotherapy resistance and hypoxic advantage in breast cancer

2017

// Giuseppina Roscigno 1, 2, * , Ilaria Puoti 1, 2, * , Immacolata Giordano 1 , Elvira Donnarumma 3 , Valentina Russo 1 , Alessandra Affinito 1 , Assunta Adamo 1 , Cristina Quintavalle 1, 2 , Matilde Todaro 4 , Maria dM Vivanco 5 , Gerolama Condorelli 1, 2 1 Department of Molecular Medicine and Medical Biotechnology, “Federico II” University of Naples, Naples, Italy 2 IEOS, CNR, Naples, Italy 3 IRCCS-SDN, Naples, Italy 4 Department of Pathobiology and Medical Biotechnology, University of Palermo, Palermo, Italy 5 CIC bioGUNE, Centre for Cooperative Research in Biosciences, Derio, Spain * These authors have contributed equally to the paper as first authors Correspondence to: Gerolama Condore…

0301 basic medicinecancer stem cellsApoptosisStem cell markermedicine.disease_causemicroRNAs Breast cancer Cancer stem cells BimL FIH1Mixed Function OxygenasesAntineoplastic Agent0302 clinical medicineCell MovementTumor Cells CulturedCell Self RenewalMixed Function OxygenaseBimLmicroRNACell HypoxiamicroRNAsGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesisNeoplastic Stem CellsFemaleBreast NeoplasmAdult stem cellHumanResearch PaperFIH1BimL; FIH1; breast cancer; cancer stem cells; microRNAsAntineoplastic AgentsBreast Neoplasms03 medical and health sciencesBreast cancerbreast cancerDownregulation and upregulationCancer stem cellmicroRNAmedicineBiomarkers TumorHumansCell Proliferationbusiness.industryCancer stem cellApoptosiRepressor Proteinmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitMolecular medicineRepressor Proteins030104 developmental biologyDrug Resistance NeoplasmImmunologyCancer researchNeoplastic Stem CellCisplatinCarcinogenesisbusiness
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Aberrantly Expressed Embryonic Protein NODAL Alters Breast Cancer Cell Susceptibility to γδ T Cell Cytotoxicity

2020

Gamma delta (γδ) T cells kill transformed cells, and increased circulating γδ T cells levels correlate with improved outcome in cancer patients; however, their function within the breast tumor microenvironment (TME) remains controversial. As tumors progress, they begin to express stem-cell associated proteins, concomitant with the emergence of therapy resistant metastatic disease. For example, invasive breast cancers often secrete the embryonic morphogen, NODAL. NODAL has been shown to promote angiogenesis, therapy resistance and metastasis in breast cancers. However, to date, little is known about how this secreted protein may interact with cells in the TME. Herein we explore how NODAL in …

0301 basic medicinelcsh:Immunologic diseases. AllergyNodal ProteinAngiogenesisT cellImmunologytumor evasionTriple Negative Breast NeoplasmsBiologyMetastasis03 medical and health sciences0302 clinical medicineTumor Microenvironmentmedicineinvasive ductal carcinomaHumansImmunology and Allergygamma delta T cellsIntraepithelial LymphocytesTriple-negative breast cancerOriginal ResearchAgedAged 80 and overT-cell receptorCancerReceptors Antigen T-Cell gamma-deltaMiddle Agedmedicine.diseasegammadelta030104 developmental biologymedicine.anatomical_structureCell culturetriple negative breast cancerMICACancer researchFemaleTumor EscapeNODALNODALlcsh:RC581-607030215 immunologyFrontiers in Immunology
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Molecular Signatures Associated with Treatment of Triple-Negative MDA-MB231 Breast Cancer Cells with Histone Deacetylase Inhibitors JAHA and SAHA

2017

Jay Amin Hydroxamic Acid (JAHA; N8-ferrocenylN1-hydroxy-octanediamide) is a ferrocene-containing analogue of the histone deacetylase inhibitor (HDACi) suberoylanilide hydroxamic acid (SAHA). JAHA’s cytotoxic activity on MDA-MB231 triple negative breast cancer (TNBC) cells at 72 h has been previously demonstrated with an IC50 of 8.45 M. JAHA’s lethal effect was found linked to perturbations of cell cycle, mitochondrial activity, signal transduction and autophagy mechanisms. In order to glean novel insights on how MDA-MB231 breast cancer cells respond to the cytotoxic effect induced by JAHA, and to compare the biological effect with the related compound SAHA, we have employed a combination of…

0301 basic medicinemedicine.drug_classAntineoplastic AgentsTriple Negative Breast NeoplasmsBiologyHydroxamic AcidsToxicologyStructure-Activity Relationship03 medical and health sciences0302 clinical medicineCell Line TumormedicineHumansCytotoxic T cellFerrous CompoundsSettore BIO/06 - Anatomia Comparata E Citologiaskin and connective tissue diseasesVorinostatTriple-negative breast cancerVorinostatDose-Response Relationship DrugHistone deacetylase inhibitorComputational BiologyGeneral MedicineTriple Negative Breast NeoplasmsCell cycleHistone Deacetylase InhibitorsSettore BIO/18 - Genetica030104 developmental biologyBiochemistryCell culture030220 oncology & carcinogenesisCancer researchHistone deacetylaseJAHA Comet assay MDA-MB231 Histone Deacetylase InhibitorsDrug Screening Assays Antitumormedicine.drug
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New tricyclic systems as photosensitizers towards triple negative breast cancer cells.

2022

AbstractNineteen pyrrolo[1,2-h][1,7]naphthyridinones and pyrido[2,3-c]pyrrolo[1,2-a]azepinones were synthesized as new tricyclic systems in which the pyridine ring is annelated to the 6,7-dihydroindolizin-8(5H)-one and 5,6,7,8-tetrahydro-9H-pyrrole[1,2-a]azepine-9-one moieties to obtain potential photosensitizing agents. They were tested for their photoantiproliferative activity on a triple-negative breast cancer cell line, MDA-MB-231, in the dark and under UVA light (2.0 J/cm2). We demonstrated that their toxicity, only when exposed to light, was primarily due to the generation of reactive oxygen species while their photodegradation products were not responsible for their activity. The mos…

7]naphthyridinonePhotosensitizing AgentsPyrrolo[12-h][17]naphthyridinoneCell DeathMDA-MB-231Organic ChemistryPhototoxic activityTriple Negative Breast NeoplasmsApoptosisPyrido[23-c]pyrrolo[12-a]azepinoneTriple-negative breast cancerPyrrolo[1Drug DiscoveryMolecular MedicineHumans2-h][1Pyrido[23-c]pyrrolo[12-a]azepinoneMDA-MB-231; Photosensitizing agents; Phototoxic activity; Pyrido[23-c]pyrrolo[12-a]azepinone; Pyrrolo[12-h][17]naphthyridinone; Triple-negative breast cancerReactive Oxygen SpeciesArchives of pharmacal research
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The HERBA Study: A Retrospective Multi-Institutional Italian Study on Patients With Brain Metastases From HER2-Positive Breast Cancer

2019

There is no sufficient evidence to establish a standard of care for patients with brain metastases (BM) from HER2Data of 154 patients were retrospectively collected at 14 Italian institutions through a specifically designed database.Median overall survival (OS) was 24.5 months. Patients receiving surgery/stereotactic radiosurgery experienced longer OS compared to those receiving whole-brain radiotherapy or no treatment (33.5 vs. 11.4 months; hazard ratio = 0.34; 95% confidence interval, 0.22-0.52; P .001). Interestingly, whole-brain radiotherapy did not improve OS compared to no treatment (11.4 vs. 9.8 months; hazard ratio = 0.99; 95% confidence interval, 0.62-1.62; P = .99). HER2-targeted …

Adult0301 basic medicineCancer Researchmedicine.medical_specialtymedicine.medical_treatmentSocio-culturaleBreast NeoplasmsLapatinibTreatment experiencedRadiosurgerySRS03 medical and health sciences0302 clinical medicineBreast cancerTrastuzumabInternal medicineHER2 Positive Breast CancerBiomarkers TumormedicineHumansAgedRetrospective Studiesbusiness.industryLapatinibTrastuzumabMiddle AgedWBRTPrognosismedicine.diseaseCombined Modality TherapyConfidence intervalSurvival RateRadiation therapyLapatinib SRS Surgery Trastuzumab WBRT030104 developmental biologyReceptors EstrogenOncology030220 oncology & carcinogenesisLapatinib; SRS; Surgery; Trastuzumab; WBRTSurgeryFemaleNeoplasm Recurrence LocalbusinessFollow-Up Studiesmedicine.drugClinical Breast Cancer
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Multicenter Phase II Study of Lurbinectedin in BRCA-Mutated and Unselected Metastatic Advanced Breast Cancer and Biomarker Assessment Substudy

2018

Purpose This multicenter phase II trial evaluated lurbinectedin (PM01183), a selective inhibitor of active transcription of protein-coding genes, in patients with metastatic breast cancer. A unicenter translational substudy assessed potential mechanisms of lurbinectedin resistance. Patients and Methods Two arms were evaluated according to germline BRCA1/2 status: BRCA1/2 mutated (arm A; n = 54) and unselected ( BRCA1/2 wild-type or unknown status; arm B; n = 35). Lurbinectedin starting dose was a 7-mg flat dose and later, 3.5 mg/m2 in arm A. The primary end point was objective response rate (ORR) per Response Evaluation Criteria in Solid Tumors (RECIST). The translational substudy of resist…

Adult0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyGenes BRCA2Genes BRCA1Phases of clinical researchAntineoplastic AgentsBreast NeoplasmsHeterocyclic Compounds 4 or More RingsMice03 medical and health sciences0302 clinical medicineGermline mutationInternal medicineBiomarkers TumorClinical endpointAnimalsHumansMedicineProgression-free survivalGerm-Line MutationAgedDose-Response Relationship DrugErratabusiness.industryMiddle Agedmedicine.diseaseXenograft Model Antitumor AssaysMetastatic breast cancerProgression-Free SurvivalClinical trial030104 developmental biologyOncologyResponse Evaluation Criteria in Solid Tumors030220 oncology & carcinogenesisBiomarker (medicine)FemalebusinessCarbolinesJournal of Clinical Oncology
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Triple negative breast cancer: shedding light onto the role of pi3k/akt/mtor pathway

2016

// Daniela Massihnia 1,* , Antonio Galvano 1,* , Daniele Fanale 1 , Alessandro Perez 1 , Marta Castiglia 1 , Lorena Incorvaia 1 , Angela Listi 1 , Sergio Rizzo 1 , Giuseppe Cicero 1 , Viviana Bazan 1 , Sergio Castorina 2,3,** and Antonio Russo 1,** 1 Department of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo, Italy 2 Fondazione Mediterranea “G.B. Morgagni”, Catania, Italy 3 Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy * These authors have contributed equally to this work ** Both the authors are last name Correspondence to: Antonio Russo, email: // Keywords : ER, HER2, PI3K/AKT/mTOR inhib…

Adult0301 basic medicineOncologymedicine.medical_specialtyPathologyAntineoplastic AgentsTriple Negative Breast NeoplasmsReviewTarget therapyPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineBreast cancerHER2Internal medicineDrug DiscoverymedicineCarcinomaHumansTriple negative breast cancerTarget therapyER; HER2; PI3K/AKT/mTOR inhibitor; Target therapy; Triple negative breast cancer; OncologySurvival rateProtein kinase BPI3K/AKT/mTOR pathwayTriple-negative breast cancerAgedClinical Trials as Topicbusiness.industryTOR Serine-Threonine KinasesAge FactorsMiddle Agedmedicine.diseaseOncogene Protein v-aktClinical trial030104 developmental biologyEROncology030220 oncology & carcinogenesisFemalePI3K/AKT/mTOR inhibitorbusinessSignal TransductionOncotarget
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Phase III Trial of Adjuvant Capecitabine After Standard Neo-/Adjuvant Chemotherapy in Patients With Early Triple-Negative Breast Cancer (GEICAM/2003-…

2019

Altres ajuts: Agustí Barnadas: Honoraria: Pfizer. Consulting or Advisory Role: Pfizer, Novartis, Eli Lilly. Speakers'Bureau: Roche, Pfizer, Novartis, Genomic Health International. Travel, Accommodations, Expenses: Roche, Pfizer; Miguel A. Seguí: Consulting or Advisory Role: Roche, Pfizer, Novartis, Amgen, Eisai, Eli Lilly. Speakers' Bureau: Roche, Pfizer, Amgen. Research Funding: Roche (Inst), Novartis (Inst). Travel, Accommodations, Expenses: Roche, Pfizer, Novartis, Amgen. Operable triple-negative breast cancers (TNBCs) have a higher risk of relapse than non-TNBCs with standard therapy. The GEICAM/2003-11_CIBOMA/2004-01 trial explored extended adjuvant capecitabine after completion of sta…

Adult0301 basic medicineSubset AnalysisOncologyAntimetabolites AntineoplasticCancer Researchmedicine.medical_specialtyAxillary lymph nodesmedicine.medical_treatmentTriple Negative Breast NeoplasmsDisease-Free SurvivalCapecitabineYoung Adult03 medical and health sciences0302 clinical medicineInternal medicineHumansMedicineCapecitabineNeoadjuvant therapyTriple-negative breast cancerAgedChemotherapyTaxanebusiness.industryHazard ratioMiddle AgedNeoadjuvant Therapy030104 developmental biologymedicine.anatomical_structureOncologyChemotherapy Adjuvant030220 oncology & carcinogenesisFemalebusinessmedicine.drug
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Cyclophosphamide plus Epidoxorubicin and 5-Fluorouracil with Folinic Acid as a Novel Treatment in Metastatic Breast Cancer: Preliminary Results of a …

1991

Twenty consecutive patients with advanced breast cancer were treated with a combination of cyclophosphamide 600 mg/m2 i.v. on day 1, epidoxorubicin 75 mg/m2 on day 1, and 5-fluorouracil 375 mg/m2 i.v. with folinic acid 200 mg/m2 i.v. on days 1----3. The overall response rate was 60%, with 10% of patients showing a complete response with a mean duration of 11.1 + months, and 50% of patients a partial response of 7.4 + months. A stabilization of 5.2 + months was obtained in 20% of cases, while 20% of patients progressed. The most frequently observed toxicity was leukopenia, while expected mucosal toxicities were rather mild.

Adult0301 basic medicinemedicine.medical_specialtyCyclophosphamide030106 microbiologyLeucovorinPhases of clinical researchBreast NeoplasmsGastroenterologyMetastasis03 medical and health sciencesFolinic acid0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansPharmacology (medical)Neoplasm MetastasisInfusions IntravenousCyclophosphamideEpirubicinPharmacologyLeukopeniabusiness.industryRemission InductionCancerMiddle Agedmedicine.diseaseMetastatic breast cancerSurgeryInfectious DiseasesOncologyFluorouracil030220 oncology & carcinogenesisDrug EvaluationFemaleFluorouracilmedicine.symptombusinessmedicine.drugJournal of Chemotherapy
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