Search results for "MT"

showing 10 items of 2759 documents

Combination of the mTOR inhibitor ridaforolimus and the anti-IGF1R monoclonal antibody dalotuzumab: preclinical characterization and phase I clinical…

2014

Abstract Purpose: Mammalian target of rapamycin (mTOR) inhibition activates compensatory insulin–like growth factor receptor (IGFR) signaling. We evaluated the ridaforolimus (mTOR inhibitor) and dalotuzumab (anti-IGF1R antibody) combination. Experimental Design: In vitro and in vivo models, and a phase I study in which patients with advanced cancer received ridaforolimus (10–40 mg/day every day × 5/week) and dalotuzumab (10 mg/kg/week or 7.5 mg/kg/every other week) were explored. Results: Preclinical studies demonstrated enhanced pathway inhibition with ridaforolimus and dalotuzumab. With 87 patients treated in the phase I study, main dose-limiting toxicities (DLT) of the combination were p…

AdultCancer ResearchPhases of clinical researchBreast NeoplasmsPharmacologyAntibodies Monoclonal HumanizedArticleReceptor IGF Type 1Ridaforolimuschemistry.chemical_compoundBreast cancerIn vivoAntineoplastic Combined Chemotherapy ProtocolsMedicineAnimalsHumansPI3K/AKT/mTOR pathwayInsulin-like growth factor 1 receptorAgedSirolimusDalotuzumabbusiness.industryTOR Serine-Threonine KinasesAntibodies MonoclonalReceptors SomatomedinMiddle Agedmedicine.diseaseXenograft Model Antitumor AssaysOncologychemistryMonoclonalbusinessSignal TransductionClinical cancer research : an official journal of the American Association for Cancer Research
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PI3K pathway mutations and PTEN levels in primary and metastatic breast cancer.

2011

Abstract The purpose of this work was to determine whether there are differences in PIK3CA mutation status and PTEN protein expression between primary and matched metastatic breast tumors as this could influence patient management. Paraffin sections of 50 μm were used for DNA extraction and slides of 3 μm for immunohistochemistry (IHC) and FISH. Estrogen receptor, progesterone receptor, and HER2 IHC were repeated in a central laboratory for both primary tumors and metastases. PTEN levels were assessed by IHC and phosphoinositide 3-kinase (PI3K) pathway mutations were detected by a mass spectroscopy–based approach. Median age was 48 years (range: 30–83 years). Tumor subtype included 72% horm…

AdultCancer Researchmedicine.medical_specialtyClass I Phosphatidylinositol 3-KinasesReceptor ErbB-2Breast Neoplasmsmedicine.disease_causeArticleMetastasisMetastasisPhosphatidylinositol 3-KinasesBreast cancerInternal medicineBreast CancermedicinePTENHumansPTEN lossReceptorneoplasmsPI3K/AKT/mTOR pathwayAgedAged 80 and overMutationbiologyPTEN PhosphohydrolaseMiddle Agedmedicine.diseaseMetastatic breast cancerEndocrinologyOncologyReceptors EstrogenMutationbiology.proteinCancer researchImmunohistochemistryFemalePIK3CA mutationsReceptors ProgesteroneSignal TransductionMolecular cancer therapeutics
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RCBF-quantification with 99mTc-HMPAO-SPECT: theory and first results.

1989

The activity concentrations of 99mTc-HMPAO in brain after intravenous injection were evaluated in 25 patients using SPECT. With additional first pass studies of heart and brain with the short lived isotope 195mAu, the cardiac output and the mean cerebral transit times of the patients were measured a short time before the HMPAO injection. The time dependence of 99mTc-HMPAO activity in the brain was registered during the first 5 min after injection over both hemispheres. Using a simplified three compartment model it was possible to calculate the mean retention fraction of HMPAO in brain from the time activity curves. It could be shown that the regional cerebral blood flow in ml/min per 100 g …

AdultCardiac outputCorrelation coefficientAdolescentHemodynamicsGrey matterTechnetium Tc 99m ExametazimeOximesmedicineOrganometallic CompoundsHumansRadiology Nuclear Medicine and imagingChild99mtc hmpao spectAgedmedicine.diagnostic_testbusiness.industryBrainTechnetiumGeneral MedicineMiddle Agedmedicine.anatomical_structureCerebral blood flowPositron emission tomographyCerebrovascular CirculationbusinessNuclear medicineTechnetium-99mTomography Emission-ComputedEuropean journal of nuclear medicine
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Knockdown of NANOG Reduces Cell Proliferation and Induces G0/G1 Cell Cycle Arrest in Human Adipose Stem Cells

2019

The core components of regenerative medicine are stem cells with high self-renewal and tissue regeneration potentials. Adult stem cells can be obtained from many organs and tissues. NANOG, SOX2 and OCT4 represent the core regulatory network that suppresses differentiation-associated genes, maintaining the pluripotency of mesenchymal stem cells. The roles of NANOG in maintaining self-renewal and undifferentiated status of adult stem cells are still not perfectly established. In this study we define the effects of downregulation of NANOG in maintaining self-renewal and undifferentiated state in mesenchymal stem cells (MSCs) derived from subcutaneous adipose tissue (hASCs). hASCs were expanded…

AdultHomeobox protein NANOGDown-RegulationBiologyArticleCatalysisSettore MED/13 - Endocrinologialcsh:ChemistryInorganic ChemistrySOX2human adipose stem cellHumansCell Self RenewalPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologyCells CulturedSpectroscopyCell Proliferationmolecular_biologyCell growthOrganic ChemistryMesenchymal stem cellDNMT1lentiviral transductionCell DifferentiationMesenchymal Stem CellsNanog Homeobox ProteinGeneral MedicineMiddle AgedCell cycleG1 Phase Cell Cycle CheckpointsComputer Science ApplicationsCell biologySettore MED/18 - Chirurgia GeneraleNANOGlcsh:Biology (General)lcsh:QD1-999Gene Knockdown Techniquesembryonic structures<i>NANOG</i>Female<i>DNMT1</i>CDKN1Bbiological phenomena cell phenomena and immunityStem cellcell cycle regulationAdult stem cell
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A First-in-Human Phase I Study of the ATP-Competitive AKT Inhibitor Ipatasertib Demonstrates Robust and Safe Targeting of AKT in Patients with Solid …

2016

Abstract Activation of AKT signaling by PTEN loss or PIK3CA mutations occurs frequently in human cancers, but targeting AKT has been difficult due to the mechanism-based toxicities of inhibitors that target the inactive conformation of AKT. Ipatasertib (GDC-0068) is a novel selective ATP-competitive small-molecule inhibitor of AKT that preferentially targets active phosphorylated AKT (pAKT) and is potent in cell lines with evidence of AKT activation. In this phase I study, ipatasertib was well tolerated; most adverse events were gastrointestinal and grade 1–2 in severity. The exposures of ipatasertib ≥200 mg daily in patients correlated with preclinical TGI90, and pharmacodynamic studies co…

AdultMale0301 basic medicineProto-Oncogene Proteins c-aktAdministration OralPharmacologyIpatasertibDrug Administration SchedulePiperazines03 medical and health sciences0302 clinical medicineCell Line TumorNeoplasmsHumansPTENMedicineProtein Kinase InhibitorsProtein kinase BPI3K/AKT/mTOR pathwayAgedbiologybusiness.industryMiddle AgedXenograft Model Antitumor AssaysSmall moleculePyrimidines030104 developmental biologyOncologyCell culture030220 oncology & carcinogenesisPharmacodynamicsbiology.proteinFemalebusinessProto-Oncogene Proteins c-akt
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Hypoxic macrophages impair autophagy in epithelial cells through Wnt1: relevance in IBD.

2014

A defective induction of epithelial autophagy may have a role in the pathogenesis of inflammatory bowel diseases. This process is regulated mainly by extracellular factors such as nutrients and growth factors and is highly induced by diverse situations of stress. We hypothesized that epithelial autophagy is regulated by the immune response that in turn is modulated by local hypoxia and inflammatory signals present in the inflamed mucosa. Our results reveal that HIF-1 alpha and Wnt1 were co-localized with CD68 in cells of the mucosa of IBD patients. We have observed increased protein levels of beta-catenin, phosphorylated mTOR, and p62 and decreased expression of LC3II in colonic epithelial …

AdultMaleAdolescentImmunologyWnt1 ProteinBiologyYoung AdultImmune systemAutophagyExtracellularHumansImmunology and AllergyIntestinal MucosaWNT1Wnt Signaling PathwayPI3K/AKT/mTOR pathwayRegulation of gene expressionCD68MacrophagesTOR Serine-Threonine KinasesAutophagyWnt signaling pathwayEpithelial CellsMiddle AgedHypoxia-Inducible Factor 1 alpha SubunitInflammatory Bowel DiseasesCell HypoxiaCell biologyGene Expression RegulationFemale
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A phase II study of alemtuzumab, fludarabine, cyclophosphamide, and doxorubicin (Campath-FCD) in peripheral T-cell lymphomas

2010

The clinical course of peripheral T-cell lymphoma (PTCL) is usually aggressive and the prognosis unfavorable. Therefore, there is a need for improvement of treatment options. Patients with newly diagnosed (n = 27) or refractory/relapsed (n = 11) PTCL received a combination of alemtuzumab, fludarabine, cyclophosphamide, and doxorubicin. The overall response rate (ORR) was 61%, with a complete response rate of 39%. In newly diagnosed patients the ORR was 63%, the median overall survival 25.9 months, and progression-free survival 11.8 months. In relapsed/refractory patients the median OS was 6.1 months. The most frequent grade 3/4 toxicities were leukopenia (95% of patients) and thrombocytopen…

AdultMaleCancer Researchmedicine.medical_specialtyCyclophosphamideAntibodies Neoplasmmedicine.medical_treatmentPhases of clinical researchAntibodies Monoclonal HumanizedLymphoma T-CellGastroenterologyDisease-Free SurvivalRefractoryRecurrenceInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansAlemtuzumabCyclophosphamideAgedChemotherapyLeukopeniabusiness.industryAntibodies MonoclonalHematologyMiddle Agedmedicine.diseaseLymphomaFludarabineSurgeryTreatment OutcomeOncologyDoxorubicinAlemtuzumabFemalemedicine.symptombusinessVidarabinemedicine.drugLeukemia &amp; Lymphoma
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Final report of the efficacy and safety of gemtuzumab ozogamicin (Mylotarg) in patients with CD33-positive acute myeloid leukemia in first recurrence

2005

BACKGROUND In this study, the authors analyzed the efficacy and safety of gemtuzumab ozogamicin (GO) (Mylotarg®), an antibody-targeted chemotherapy for CD33-positive acute myeloid leukemia (AML). METHODS Patients with CD33-positive AML in first recurrence were entered in 3 open-label, single-arm, Phase II studies. Patients received monotherapy with GO 9 mg/m2 as a 2-hour intravenous infusion in 2 doses separated by 2 weeks. Patients were evaluated for remission, survival, and treatment-emergent adverse events. RESULTS Two hundred seventy-seven patients (median age, 61 yrs) were treated with GO, and 71 patients (26%) achieved remission, which was defined as ≤ 5% blasts in the bone marrow wit…

AdultMaleCancer Researchmedicine.medical_specialtyMyeloidMaximum Tolerated DoseGemtuzumab ozogamicinmedicine.medical_treatmentCD33Sialic Acid Binding Ig-like Lectin 3Antigens Differentiation MyelomonocyticHematopoietic stem cell transplantationNeutropeniaAntibodies Monoclonal HumanizedGastroenterologyRisk AssessmentSeverity of Illness IndexDrug Administration ScheduleClinical Trials Phase II as TopicAntigens CDRecurrenceInternal medicinemedicineHumansSingle-Blind MethodSurvival rateAgedAged 80 and overChemotherapyDose-Response Relationship Drugbusiness.industryAntibodies MonoclonalMiddle Agedmedicine.diseaseGemtuzumabSurgerySurvival RateLeukemiaLeukemia Myeloid Acutemedicine.anatomical_structureAminoglycosidesTreatment OutcomeOncologyEvaluation Studies as TopicFemalebusinessmedicine.drugFollow-Up StudiesCancer
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Temsirolimus for the treatment of mantle cell lymphoma.

2010

Although recent progress has been made in the treatment of mantle cell lymphoma (MCL) the majority of patients experience relapse and ultimately die of their disease. The translocation t(11;14) is a prerequisite for the diagnosis of MCL and results in overexpression of cyclin D1. Its protein translation is controlled by mTOR, a key element of the PI3K/Akt pathway, and mTOR constitutes an attractive therapeutic target. Temsirolimus, a specific inhibitor of mTOR, has been evaluated in two Phase II trials in patients with relapsed MCL, and promising response rates up to 40% were found. Subsequently, a randomized Phase III trial was initiated, in which superiority in remission induction and pro…

AdultMaleCombination therapyChromosomal translocationAntineoplastic AgentsLymphoma Mantle-CellPharmacologyDisease-Free SurvivalDrug Administration ScheduleCyclin D1hemic and lymphatic diseasesmedicineSecondary PreventionHumansCyclin D1PI3K/AKT/mTOR pathwayAgedAged 80 and overSirolimusClinical Trials as Topicbusiness.industryTOR Serine-Threonine KinasesRemission InductionIntracellular Signaling Peptides and ProteinsHematologyMiddle Agedmedicine.diseaseTemsirolimusNon-Hodgkin's lymphomaRegimenCancer researchMantle cell lymphomaFemalebusinessmedicine.drugExpert review of hematology
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Neddylation inhibition ameliorates steatosis in NAFLD by boosting hepatic fatty acid oxidation via the DEPTOR-mTOR axis

2021

Objective Neddylation is a druggable and reversible ubiquitin-like post-translational modification upregulated in many diseases, including liver fibrosis, hepatocellular carcinoma, and more recently, non-alcoholic fatty liver disease (NAFLD). Herein, we propose to address the effects of neddylation inhibition and the underlying mechanisms in pre-clinical models of NAFLD. Methods Hepatic neddylation measured by immunohistochemical analysis and NEDD8 serum levels measured by ELISA assay were evaluated in NAFLD clinical and pre-clinical samples. The effects of neddylation inhibition by using a pharmacological small inhibitor, MLN4924, or molecular approaches were assessed in isolated mouse hep…

AdultMaleCoronavirus disease 2019 (COVID-19)AdolescentMLN4924[SDV.BC]Life Sciences [q-bio]/Cellular BiologyDiet High-Fat03 medical and health sciencesMiceYoung Adult0302 clinical medicineNon-alcoholic Fatty Liver DiseasePolitical scienceNAFLDmedia_common.cataloged_instanceAnimalsHumansEuropean unionNeddylationMolecular BiologyInternal medicineComputingMilieux_MISCELLANEOUS030304 developmental biologymedia_commonAged0303 health sciencesTOR Serine-Threonine KinasesFatty AcidsIntracellular Signaling Peptides and ProteinsCell BiologyMiddle AgedRC31-12453. Good healthMice Inbred C57BLRare tumorDisease Models AnimalDeptor; Fatty acid oxidation; MLN4924; mTOR; NAFLD; NeddylationDeptorFatty acid oxidationHepatocytesmTOR030211 gastroenterology & hepatologyChristian ministryOriginal ArticleHumanitiesSignal Transduction
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