Search results for "MT"

showing 10 items of 2759 documents

Mesenchymal Transition of High-Grade Breast Carcinomas Depends on Extracellular Matrix Control of Myeloid Suppressor Cell Activity

2016

SummaryThe extracellular matrix (ECM) contributes to the biological and clinical heterogeneity of breast cancer, and different prognostic groups can be identified according to specific ECM signatures. In high-grade, but not low-grade, tumors, an ECM signature characterized by high SPARC expression (ECM3) identifies tumors with increased epithelial-to-mesenchymal transition (EMT), reduced treatment response, and poor prognosis. To better understand how this ECM3 signature is contributing to tumorigenesis, we expressed SPARC in isogenic cell lines and found that SPARC overexpression in tumor cells reduces their growth rate and induces EMT. SPARC expression also results in the formation of a h…

0301 basic medicineMyeloidMDSCGene Expressionmedicine.disease_causeT-Lymphocytes RegulatoryPolyethylene GlycolsExtracellular matrixMiceBreast cancerMyeloid CellsOsteonectinMast Cellslcsh:QH301-705.5Mice KnockoutAntigen PresentationMice Inbred BALB CEMTepithelial to mesenchymal transitionBreast cancer; COX-2; CXCL12; ECM; EMT; G-CSF; GM-CSF; MDSC; SPARC; aminobisphosphonates; cyclooxygenase-2; epithelial to mesenchymal transition; extracellular matrix; granulocyte colony-stimulating factor; granulocyte-macrophage colony-stimulating factor; myeloid-derived suppressor cellsCXCL12Granulocyte macrophage colony-stimulating factormedicine.anatomical_structurecyclooxygenase-2granulocyte-macrophage colony-stimulating factorFemalegranulocyte colony-stimulating factormedicine.drugEpithelial-Mesenchymal Transitionextracellular matrixAntineoplastic AgentsBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaG-CSFGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpithelial–mesenchymal transitionECMMesenchymal stem cellSPARCGM-CSFCOX-2myeloid-derived suppressor cellsXenograft Model Antitumor AssaysIsogenic human disease modelsaminobisphosphonates030104 developmental biologylcsh:Biology (General)CelecoxibDoxorubicinImmunologyCancer researchMyeloid-derived Suppressor CellaminobisphosphonateNeoplasm GradingCarcinogenesisCell Reports
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Nrf2 expression driven by Foxp3 specific deletion of Keap1 results in loss of immune tolerance in mice

2020

European journal of immunology 50(4), 515-524 (2020). doi:10.1002/eji.201948285

0301 basic medicineNF-E2-Related Factor 2T cellImmunologyAutoimmunitychemical and pharmacologic phenomenaBiologyLymphocyte ActivationT-Lymphocytes Regulatorydigestive systemenvironment and public healthImmune toleranceImmunomodulationMice03 medical and health sciences0302 clinical medicineImmune systemImmune TolerancemedicineAnimalsHomeostasisImmunology and AllergyTranscription factorPI3K/AKT/mTOR pathwayInflammationMice KnockoutKelch-Like ECH-Associated Protein 1ChimeraEffectorTOR Serine-Threonine KinasesPeripheral toleranceFOXP3Forkhead Transcription Factorshemic and immune systemsrespiratory systemCell biologyMice Inbred C57BLOxidative Stress030104 developmental biologymedicine.anatomical_structure030215 immunology
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Levosimendan protects human hepatocytes from ischemia-reperfusion injury.

2017

Background Ischemia-reperfusion injury (IRI) is a major challenge in liver transplantation. The mitochondrial pathway plays a pivotal role in hepatic IRI. Levosimendan, a calcium channel sensitizer, was shown to attenuate apoptosis after IRI in animal livers. The aim of this study was to investigate the effect of levosimendan on apoptosis in human hepatocytes. Methods Primary human hepatocytes were either exposed to hypoxia or cultured under normoxic conditions. After the hypoxic phase, reoxygenation was implemented and cells were treated with different concentrations of levosimendan (10ng/ml, 100ng/ml, 1000ng/ml). The overall metabolic activity of the cells was measured using 3-(4,5-dimeth…

0301 basic medicineNecrosisCritical Care and Emergency Medicinelcsh:MedicineApoptosis030204 cardiovascular system & hematologyBiochemistry0302 clinical medicineAnimal CellsMedicine and Health SciencesEnzyme assaysColorimetric assayslcsh:ScienceBioassays and physiological analysisCells CulturedEnergy-Producing Organellesbcl-2-Associated X ProteinMultidisciplinaryMTT assaybiologyCell DeathMitochondriaPyridazinesLiverCell ProcessesReperfusion Injurymedicine.symptomCellular TypesAnatomyCellular Structures and Organellesmedicine.drugResearch Articlemedicine.medical_specialtyCell PhysiologyIschemiaCardiologySurgical and Invasive Medical ProceduresBioenergetics03 medical and health sciencesDigestive System ProceduresBcl-2-associated X proteinInternal medicinemedicineHumansMTT assayddc:610SimendanHeart FailureTransplantationbusiness.industrylcsh:RHydrazonesBiology and Life SciencesLevosimendanCell BiologyOrgan TransplantationHypoxia (medical)medicine.diseaseLiver TransplantationCell MetabolismResearch and analysis methods030104 developmental biologyEndocrinologyApoptosisReperfusionBiochemical analysisbiology.proteinHepatocyteslcsh:QbusinessReperfusion injuryPloS one
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Binge-like ethanol treatment in adolescence impairs autophagy and hinders synaptic maturation: Role of TLR4.

2018

Abstract Adolescence is a developmental period of brain maturation in which remodeling and changes in synaptic plasticity and neural connectivity take place in some brain regions. A different mechanism participates in adolescent brain maturation, including autophagy processes that play a role in synaptic development and plasticity. Alcohol is a neurotoxic compound whose abuse in adolescence causes TLR4 response activation by triggering neuroinflammation, neural damage and behavioral alterations. However, the potential participation of autophagy in long-term neurochemical and cognitive dysfunctions induced by binge ethanol drinking in adolescence is uncertain. We therefore evaluated whether …

0301 basic medicineNeurogenesisImmune receptorBiologyBinge Drinking03 medical and health sciencesMice0302 clinical medicineNeurochemicalAutophagyAnimalsTLR4PI3K/AKT/mTOR pathwayNeuroinflammationMice KnockoutBinge ethanol treatmentEthanolGeneral NeuroscienceAutophagyAge FactorsAdolescenceMice Inbred C57BLToll-Like Receptor 4030104 developmental biologyStructural synaptic plasticitySynaptic plasticitySynapsesExcitatory postsynaptic potentialTLR4FemaleNeuroscience030217 neurology & neurosurgeryNeuroscience letters
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Transcriptomic and Genetic Associations between Alzheimer's Disease, Parkinson's Disease, and Cancer.

2021

Simple Summary Epidemiological studies have identified a link between neurodegenerative disorders and a reduced risk of overall cancer. Increases and decreases in the risk of site-specific cancers have also been reported. However, it is still unknown whether these associations arise due to shared genetic and molecular factors or are explained by other phenomena (e.g., biases in epidemiological studies or the use of medication). In this study, we aimed to investigate the potential molecular, genetic, and pharmacological links between Alzheimer’s and Parkinson’s diseases and a large panel of 22 cancer types. To examine the overlapping involvement of genes and pathways, we obtained differentia…

0301 basic medicineOncologyCancer ResearchParkinson's diseaseGenetic correlationsGenome-wide association studyDiseaseComorbidityParkinson Enfermedad de - Aspectos genéticos.chemistry.chemical_compound0302 clinical medicineExemestaneParkinson's disease - Genetic aspects.MedicineParkinsonCáncer - Aspectos genéticos.Càncer -- Aspectes genèticsRC254-282Alzheimer's disease - Genetic aspects.NeurodegenerationNeoplasms. Tumors. Oncology. Including cancer and carcinogensCódigo genético.comorbidityOncology:Informàtica::Aplicacions de la informàtica::Bioinformàtica [Àrees temàtiques de la UPC]medicine.medical_specialtyGenetic code.Alzheimer Enfermedad de - Aspectos genéticos.Article03 medical and health sciencesInternal medicineParkinson Malaltia dePI3K/AKT/mTOR pathwaygenetic correlationsCancer - Genetic aspects.business.industryCancertranscriptomicmedicine.diseaseComorbidityAlzheimer Malaltia d'030104 developmental biologychemistryTranscriptomicmeta-analysesMeta-analysesNeurodegenerative disordersAlzheimerGene expressionbusiness030217 neurology & neurosurgeryCancers
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Loss of HER2 and decreased T-DM1 efficacy in HER2 positive advanced breast cancer treated with dual HER2 blockade: the SePHER Study

2020

AbstractBackgroundHER2-targeting agents have dramatically changed the therapeutic landscape of HER2+ advanced breast cancer (ABC). Within a short time frame, the rapid introduction of new therapeutics has led to the approval of pertuzumab combined with trastuzumab and a taxane in first-line, and trastuzumab emtansine (T-DM1) in second-line. Thereby, evidence of T-DM1 efficacy following trastuzumab/pertuzumab combination is limited, with data from some retrospective reports suggesting lower activity. The purpose of the present study is to investigate T-DM1 efficacy in pertuzumab-pretreated and pertuzumab naïve HER2 positive ABC patients. We also aimed to provide evidence on the exposure to d…

0301 basic medicineOncologyCancer ResearchReceptor ErbB-2ApoptosisAdo-Trastuzumab EmtansineSettore MED/06chemistry.chemical_compound0302 clinical medicineTrastuzumabAntineoplastic Combined Chemotherapy ProtocolsTumor Cells Culturedskin and connective tissue diseasesAged 80 and overMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisGene Expression Regulation NeoplasticSurvival RateOncology030220 oncology & carcinogenesisFemalePertuzumabmedicine.drugT-DM1 efficacymusculoskeletal diseasesAdultmedicine.medical_specialtyHER2+ breast cancer; Trastuzumab/pertuzumab blockade; T-DM1 efficacyBreast NeoplasmsAntibodies Monoclonal Humanizedlcsh:RC254-28203 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALEInternal medicinemedicineBiomarkers TumorHumansneoplasmsAgedCell ProliferationRetrospective StudiesHER2+ breast cancer; T-DM1 efficacy; Trastuzumab/pertuzumab blockadeTaxanebusiness.industryResearchCancerHER2+ breast cancerTrastuzumabmedicine.diseaseTrastuzumab/pertuzumab blockadeBlockadeLog-rank test030104 developmental biologychemistryTrastuzumab emtansineCancer cellbusiness
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Predictive factors of response to mTOR inhibitors in neuroendocrine tumours

2016

Medical treatment of neuroendocrine tumours (NETs) has drawn a lot of attention due to the recent demonstration of efficacy of several drugs on progression-free survival, including somatostatin analogs, small tyrosine kinase inhibitors and mTOR inhibitors (or rapalogs). The latter are approved as therapeutic agents in advanced pancreatic NETs and have been demonstrated to be effective in different types of NETs, with variable efficacy due to the development of resistance to treatment. Early detection of patients that may benefit from rapalogs treatment is of paramount importance in order to select the better treatment and avoid ineffective and expensive treatments. Predictive markers for th…

0301 basic medicineOncologyCancer ResearchmTOR inhibitorEndocrinology Diabetes and MetabolismNeuroendocrine tumorsAntineoplastic Agent0302 clinical medicineEndocrinologyNeuroendocrine tumoursneuroendocrine tumourTreatment resistanceMTOR inhibitorsTumorMedical treatmentTOR Serine-Threonine KinasesDiscovery and development of mTOR inhibitorsResponse to treatmentPatient managementDiabetes and MetabolismNeuroendocrine TumorsOncology030220 oncology & carcinogenesisResponse to treatmentNeuroendocrine TumorHumanMTOR inhibitors; Neuroendocrine tumours; Predictors; Response to treatment; Animals; Antineoplastic Agents; Biomarkers Tumor; Diagnostic Imaging; Humans; Neuroendocrine Tumors; Protein Kinase Inhibitors; TOR Serine-Threonine Kinases; Endocrinology Diabetes and Metabolism; Oncology; Endocrinology; Cancer ResearchDiagnostic Imagingmedicine.medical_specialtyProtein Kinase InhibitorEarly detectionpredictorAntineoplastic AgentsMTOR inhibitors; Neuroendocrine tumours; Predictors; Response to treatment; Endocrinology; Oncology; Cancer Research; Endocrinology Diabetes and MetabolismBiologyNO03 medical and health sciencesmTOR inhibitors; neuroendocrine tumours; predictors; response to treatment; Animals; Antineoplastic Agents; Biomarkers Tumor; Diagnostic Imaging; Humans; Neuroendocrine Tumors; Protein Kinase Inhibitors; TOR Serine-Threonine KinasesInternal medicineBiomarkers TumormedicineAnimalsHumansmTOR inhibitorsneuroendocrine tumourspredictorsresponse to treatmentProtein Kinase InhibitorsmTOR inhibitors neuroendocrine tumours predictors response to treatmentAnimalPredictorsmedicine.disease030104 developmental biologyImmunologyBiomarkersResource utilizationEndocrine-Related Cancer
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Prognostic Role of High-Grade Tumor Budding in Pancreatic Ductal Adenocarcinoma: A Systematic Review and Meta-Analysis with a Focus on Epithelial to …

2019

This study aims at clarifying the prognostic role of high-grade tumor budding (TB) in pancreatic ductal adenocarcinoma (PDAC) with the first systematic review and meta-analysis on this topic. Furthermore, we analyzed with a systematic review the relationship between TB and a recently suggested TB-associated mechanism: the epithelial to mesenchymal transition (EMT). Analyzing a total of 613 patients, 251 of them (40.9%) with high grade-TB, we found an increased risk of all-cause mortality (RR, 1.46; 95% CI, 1.13-1.88, p = 0.004; HR, 2.65; 95% CI, 1.79-3.91; p < 0.0001) and of recurrence (RR, 1.61; 95% CI, 1.05-2.47, p = 0.03) for PDAC patients with high-grade TB. Moreover, we found that E…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyPancreatic ductal adenocarcinomapancreatic cancerHigh grade tumorReviewEMT; budding; buds; epithelial to mesenchymal transition; pancreatic cancerbuddinglcsh:RC254-28203 medical and health sciences0302 clinical medicineTumor buddingPancreatic cancerInternal medicineMedicineClinical significanceEpithelial–mesenchymal transitionbusiness.industryEMTepithelial to mesenchymal transitionbudslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasebud3. Good health030104 developmental biologyIncreased riskOncology030220 oncology & carcinogenesisMeta-analysisbusinessCancers
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The prognostic relevance of HER2-positivity gain in metastatic breast cancer in the ChangeHER trial

2021

Breast cancer (BC) heterogeneity is composite in nature, with a wide variety of factors concurring to define several pathological entities, which differ by clinical presentation, pathologic features, therapy administered, and inherent outcomes1. Additional sources of breast cancer heterogeneity may raise during the disease course. In BC patients whose disease was initially diagnosed in the early stage and subsequently progressed with metastatic involvement of one single or multiple site/s, the molecular characteristics of metastatic lesions do not necessary mimic those of the disease initially diagnosed. A well-depicted molecular landscape is crucial for subtype definition, prognostic evalu…

0301 basic medicineOncologyCancer therapyReceptor ErbB-2medicine.medical_treatmentAdo-Trastuzumab Emtansineprogesterone receptorSettore MED/060302 clinical medicinehuman epidermal growth factor receptor 2 (HER2)Antineoplastic Combined Chemotherapy ProtocolsestrogenNeoplasm Metastasisskin and connective tissue diseasesMultidisciplinaryBrain NeoplasmsQRMiddle AgedPrognosisMetastatic breast cancerNeoplasm Metastasi030220 oncology & carcinogenesisMedicineFemalePertuzumabmetastatic breast cancerReceptors ProgesteroneBreast NeoplasmHER2 positivitymedicine.drugHumanAdultmedicine.medical_specialtymedicine.drug_classSciencetrastuzumab-emtansineBreast Neoplasmsmetastatic breast cancer; HER2 positivity; cancerArticleDisease-Free SurvivalBrain Neoplasm03 medical and health sciencesBreast cancerbreast cancerSettore MED/04 - PATOLOGIA GENERALEpertuzumabInternal medicineProgesterone receptormedicineHumanscancerbreast cancer; human epidermal growth factor receptor 2 (HER2); pertuzumab; trastuzumab-emtansine; estrogen; progesterone receptorneoplasmsAgedChemotherapyAntineoplastic Combined Chemotherapy Protocolbusiness.industryCancermedicine.diseaseHER2-positiveBreast cancer; oncology; radiotherapy; chemotherapy; HER2Radiation therapy030104 developmental biologyEstrogenbusinessprognostic relevance
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Compassionate use of everolimus for refractory epilepsy in a patient with MTOR mosaic mutation

2020

Abstract The MTOR gene encodes the mechanistic target of rapamycin (mTOR), which is a core component of the PI3K-AKT-mTOR signaling pathway. Postzygotic MTOR variants result in various mosaic phenotypes, referred to in OMIM as Smith-Kinsgmore syndrome or focal cortical dysplasia. We report here the case of a patient, with an MTOR mosaic gain-of-function variant (p.Glu2419Lys) in the DNA of 41% skin cells, who received compassionate off-label treatment with everolimus for refractory epilepsy. This 12-year-old-girl presented with psychomotor regression, intractable seizures, hypopigmentation along Blaschko's lines (hypomelanosis of Ito), asymmetric regional body overgrowth, and ocular anomali…

0301 basic medicineOncologyCompassionate Use Trialsmedicine.medical_specialty[SDV]Life Sciences [q-bio]030105 genetics & heredityMuscle hypertrophyCraniofacial Abnormalities03 medical and health sciencesInternal medicineGeneticsmedicineHumansEverolimusChildMechanistic target of rapamycinProtein Kinase InhibitorsGenetics (clinical)PI3K/AKT/mTOR pathwayHypopigmentationEverolimusbiologybusiness.industryMosaicismTOR Serine-Threonine KinasesNeuropsychologyGeneral MedicineCortical dysplasiamedicine.disease3. Good healthClinical trialMalformations of Cortical Development[SDV] Life Sciences [q-bio]030104 developmental biologyPhenotypeGain of Function Mutationbiology.proteinFemaleEpilepsies Partialmedicine.symptombusinessmedicine.drug
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