Search results for "mTOR pathway"

showing 10 items of 226 documents

The MID1 protein is a central player during development and in disease.

2015

Loss-of-function mutations in the MID1 gene cause a rare monogenic disorder, Opitz BBB/G syndrome (OS), which is characterized by malformations of the ventral midline. The MID1 gene encodes the MID1 protein, which assembles a large microtubule-associated protein complex. Intensive research over the past several years has shed light on the function of the MID1 protein as a ubiquitin ligase and regulator of mTOR signalling and translational activator. As a central player in the cell MID1 has been implicated in the pathogenesis of various other disorders in addition to OS including cancer and neurodegenerative diseases. Influencing the activity of the MID1 protein complex is a promising new st…

0301 basic medicinephysiopathology [Huntington Disease]CarcinogenesisUbiquitin-Protein LigasesRegulatorDiseaseBiologyBioinformaticsmedicine.disease_causephysiopathology [Alzheimer Disease]Congenital AbnormalitiesPathogenesis03 medical and health sciencesMiceAlzheimer Diseasephysiology [Nuclear Proteins]medicineAnimalsHumansgenetics [Microtubule Proteins]ddc:610GenePI3K/AKT/mTOR pathwayActivator (genetics)Nuclear Proteinsgenetics [Nuclear Proteins]genetics [Transcription Factors]physiology [Transcription Factors]Ubiquitin ligase030104 developmental biologyHuntington DiseaseMutationbiology.proteinMicrotubule Proteinsphysiology [Microtubule Proteins]CarcinogenesisMid1 protein humanTranscription FactorsFrontiers in bioscience (Landmark edition)
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STRIPAK Members Orchestrate Hippo and Insulin Receptor Signaling to Promote Neural Stem Cell Reactivation

2019

Summary Adult stem cells reactivate from quiescence to maintain tissue homeostasis and in response to injury. How the underlying regulatory signals are integrated is largely unknown. Drosophila neural stem cells (NSCs) also leave quiescence to generate adult neurons and glia, a process that is dependent on Hippo signaling inhibition and activation of the insulin-like receptor (InR)/PI3K/Akt cascade. We performed a transcriptome analysis of individual quiescent and reactivating NSCs harvested directly from Drosophila brains and identified the conserved STRIPAK complex members mob4, cka, and PP2A (microtubule star, mts). We show that PP2A/Mts phosphatase, with its regulatory subunit Widerbors…

0301 basic medicinereactivationendocrine systemMitosisNerve Tissue ProteinsProtein Serine-Threonine KinasesBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyAnimals Genetically ModifiedPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineNeural Stem CellsAnimalsDrosophila ProteinsquiescenceProtein Phosphatase 2lcsh:QH301-705.5Protein kinase BCells CulturedPI3K/AKT/mTOR pathwayTissue homeostasisAdaptor Proteins Signal TransducingCell ProliferationHippo signaling pathwayGene Expression ProfilingHippo signalingInR/PI3K/Akt signalingfungiIntracellular Signaling Peptides and ProteinsBrainSTRIPAK membersProtein phosphatase 2Receptor InsulinNeural stem cellCell biologyDrosophila melanogaster030104 developmental biologylcsh:Biology (General)nervous systemHippo signalingSingle-Cell AnalysisTranscriptomeProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryAdult stem cellCell Reports
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Differential PI3K signal transduction in obesity-associated cardiac hypertrophy and response to ischemia

2014

Objective Elevated insulin and inflammatory cytokine levels in obesity may chronically activate signaling pathways regulating cardiac growth and contractility. Our aim was to examine the effect of obesity on cardiac PI3K isoform and Akt activation during left ventricular (LV) hypertrophy and heart failure. Methods Wild-type mice were fed normal chow or high-fat diet (HFD) for 2, 4, or 6 months. A subset of mice was subjected to chronic myocardial ischemia (MI). Results Echocardiography revealed a progressive increase in LV mass, wall thickness, and diameters in obese mice. Systolic pump function was not impaired. Increased cardiac levels of PI3Kγ, phosphorylated Akt, GSK3β, and Epac were ob…

0303 health sciencesmedicine.medical_specialtyNutrition and DieteticsCardiac fibrosisbusiness.industryEndocrinology Diabetes and MetabolismIschemiaMedicine (miscellaneous)030204 cardiovascular system & hematologymedicine.diseaseMuscle hypertrophyContractility03 medical and health sciences0302 clinical medicineEndocrinologyEndocrinologyInternal medicineHeart failuremedicineCardiologySOCS3businessProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biologyObesity
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Identification of a Novel Pathway in BCR/ABL Signal Transduction Involving Akt-Independent Activation of PLC-gamma/mTOR/p70-S6K.

2006

Abstract In BCR/ABL positive CML, defining new, additional therapeutic targets in the pathways, activated by BCR/ABL is critical for the development of new treatment strategies, especially for patients resistant or refractory to Imatinib. While studying the involvement of PI3K/Akt/mTOR signaling pathway in the development of such resistance we have uncovered the existence of additional, Akt-independent mechanism of activation of mTOR/p70-S6 Kinase pathway. Short term treatment with Imatinib (1μM, 4 hours) of the BCR/ABL-positive cell lines LAMA84, AR320, KCL22, K562, Ba/F3-BCR/ABL caused downregulation of p70-S6K phosphorylation and of S6 ribosomal protein phosphorylation without decreasing…

ABLImmunologybreakpoint cluster regionP70-S6 Kinase 1Cell BiologyHematologyBiologyBiochemistryImatinib mesylatehemic and lymphatic diseasesCancer researchPhosphorylationProtein kinase BPI3K/AKT/mTOR pathwayK562 cellsBlood
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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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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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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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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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