Search results for " mtor"

showing 10 items of 30 documents

Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR inhibitors: Rationale and importance to inhibiting these pathways in human health

2011

William H. Chappell 1 , Linda S. Steelman 1,2 , Jacquelyn M. Long 2 , Ruth C. Kempf 2 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Jorg Basecke 3 , Franca Stivala 4 , Marco Donia 4 , Paolo Fagone 4 , Graziella Malaponte 4 , Maria C. Mazzarino 4 , Ferdinando Nicoletti 4 , Massimo Libra 4 , Danijela Maksimovic-Ivanic 5 , Sanja Mijatovic 5 , Giuseppe Montalto 6 , Melchiorre Cervello 7 , Piotr Laidler 8 , Michele Milella 9 , Agostino Tafuri 10 , Antonio Bonati 11 , Camilla Evangelisti 12 , Lucio Cocco 12 , Alberto M. Martelli 12,13 , and James A. McCubrey 1 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University 2 Department of Physics, Greenville, N…

MAPK/ERK pathwayAgingmedicine.medical_treatmentDrug ResistancerafPI3KTargeted therapycombination therapyPhosphatidylinositol 3-Kinases0302 clinical medicineTARGETED THERAPYCANCER STEM CELLSNeoplasmsCancer Stem CellsMedicineExtracellular Signal-Regulated MAP Kinases0303 health sciencesCombination TherapybiologyTOR Serine-Threonine KinasesMTORHuman health Ras inhibitors MEK ERKTargeted TherapyDiscovery and development of mTOR inhibitors3. Good healthDRUG RESISTANCECell Transformation NeoplasticOncology030220 oncology & carcinogenesismTORraf KinasesPremature agingMAP Kinase Signaling SystemReviewsSenescence03 medical and health sciencesCell Line TumorHumansPTENProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biologyMitogen-Activated Protein Kinase Kinasesbusiness.industryAKTAktagingPTEN PhosphohydrolaseRafTransplantationSENESCENCEImmunologyras Proteinsbiology.proteinCancer researchaging; akt; cancer stem cells; combination therapy; drug resistance; mtor; pi3k; raf; senescence; targeted therapybusinessProto-Oncogene Proteins c-akt
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Mutations and Deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascades Which Alter Therapy Response.

2012

The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Certain components of these pathways, RAS, NF1, BRAF, MEK1, DUSP5, PP2A, PIK3CA, PIK3R1, PIK3R4, PIK3R5, IRS4, AKT, NFKB1, MTOR, PTEN, TSC1, and TSC2 may also be activated/inactivated by mutations or epigenetic silencing. Upstream mutations in one signaling pathway or even in downstream components of the same pathway can alter the sensitivity of the cells to certain small molecule inhibitors. These pathways have profound effects on proliferative, apoptotic and differentiation pathways. Dysregulation of components of these cas…

MAPK/ERK pathwayPremature agingMAP Kinase Signaling SystemTargeted Therapy Therapy Resistance Mutations Raf Akt PI3K mTORMtorReviewsPi3kPI3KReceptor tyrosine kinaseAkt; Mtor; Mutations; Pi3k; Raf; Targeted therapy; Therapy resistance;Targeted therapyPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineAnimalsHumansPTENExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesbiologyChemistryTOR Serine-Threonine KinasesAktTherapy resistancePTEN PhosphohydrolaseTargeted TherapyTherapy ResistanceRafProtein phosphatase 2MAP Kinase Kinase Kinases3. Good healthCell biologyOncology030220 oncology & carcinogenesisMutationras ProteinsmTORCancer researchbiology.proteinraf KinasesMitogen-Activated Protein KinasesSignal transductionProto-Oncogene Proteins c-aktMutationsSignal TransductionOncotarget
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Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: How mutations can result in therapy resistance and how to overcome resistance

2012

// James A. McCubrey 1 , Linda S. Steelman 1 , William H. Chappell 1 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Giuseppe Montalto 2 , Melchiorre Cervello 3 , Massimo Libra 4 , Saverio Candido 4 , Grazia Malaponte 4 , Maria C. Mazzarino 4 , Paolo Fagone 4 , Ferdinando Nicoletti 4 , Jorg Basecke 5 , Sanja Mijatovic 6 , Danijela Maksimovic-Ivanic 6 , Michele Milella 7 , Agostino Tafuri 8 , Francesca Chiarini 9 , Camilla Evangelisti 9 , Lucio Cocco 10 , Alberto M. Martelli 9,10 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC, USA 2 Department of Internal Medicine and Specialties, University of Palermo, Palermo, Italy 3 Consi…

MAPK/ERK pathwaymedicine.medical_treatmentPI3KTargeted therapyTargeted therapyPhosphatidylinositol 3-Kinases0302 clinical medicineNeoplasmsTreatment resistanceExtracellular Signal-Regulated MAP KinasesPhosphoinositide-3 Kinase InhibitorsGenetics0303 health sciencesbiologyCancer stem cellsTOR Serine-Threonine KinasesMAP Kinase Kinase KinasesDiscovery and development of mTOR inhibitorshumanities3. Good healthOncology030220 oncology & carcinogenesismTORSignal TransductionProto-Oncogene Proteins B-rafReviewsAntineoplastic Agents03 medical and health sciencesCell Line TumormedicineHumansPTENProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biologybusiness.industryAkt; Cancer stem cells; mTOR; PI3K; Raf; Targeted therapy; Therapy resistanceAktPTEN PhosphohydrolaseTherapy resistanceRafProtein phosphatase 2Targeted Therapy Therapy Resistance Cancer Stem Cells Raf Akt PI3K mTORDrug Resistance NeoplasmMutationras ProteinsCancer researchbiology.proteinbusinessProto-Oncogene Proteins c-akt
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The landscape of epilepsy-related GATOR1 variants

2019

Purpose:\ud \ud To define the phenotypic and mutational spectrum of epilepsies related to DEPDC5, NPRL2 and NPRL3 genes encoding the GATOR1 complex, a negative regulator of the mTORC1 pathway.\ud \ud Methods:\ud \ud We analyzed clinical and genetic data of 73 novel probands (familial and sporadic) with epilepsy-related variants in GATOR1-encoding genes and proposed new guidelines for clinical interpretation of GATOR1 variants.\ud \ud Results:\ud \ud The GATOR1 seizure phenotype consisted mostly in focal seizures (e.g., hypermotor or frontal lobe seizures in 50%), with a mean age at onset of 4.4 years, often sleep-related and drug-resistant (54%), and associated with focal cortical dysplasia…

Male0301 basic medicineProbandDEPDC5SUDEP030105 genetics & heredityBioinformaticsLoss of Function Mutation/geneticsEpilepsyINDEL MutationLoss of Function MutationmTORC1 pathwayGenetics(clinical)ChildGenetics (clinical)Multiprotein Complexes/geneticsBrugada SyndromeDNA Copy Number VariationBrugada syndromeINDEL Mutation/geneticsGTPase-Activating ProteinsNPRL3SeizureDEPDC5PhenotypePedigree3. Good healthBrugada Syndrome/geneticsChild PreschoolFemaleHumanSignal TransductionDNA Copy Number VariationsAdolescentSeizures/complicationsMechanistic Target of Rapamycin Complex 1/geneticsDNA Copy Number Variations/geneticsMechanistic Target of Rapamycin Complex 1Tumor Suppressor Proteins/geneticsArticleFocal cortical dysplasia03 medical and health sciencesSeizuresGTPase-Activating Proteins/geneticsmedicineHumansGenetic Predisposition to DiseaseDEPDC5; Focal cortical dysplasia; Genetic focal epilepsy; mTORC1 pathway; SUDEPGenetic focal epilepsyEpilepsy/complicationsRepressor Proteins/geneticsEpilepsybusiness.industryGTPase-Activating ProteinTumor Suppressor ProteinsInfant NewbornCorrectionInfantRepressor ProteinCortical dysplasiamedicine.diseaseddc:616.8Repressor Proteins030104 developmental biologyFrontal lobe seizures[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMultiprotein ComplexesMultiprotein ComplexeSignal Transduction/geneticsHuman medicinebusiness
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Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mtor pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

2011

Dysregulated signaling through the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways is often the result of genetic alterations in critical components in these pathways or upstream activators. Unrestricted cellular proliferation and decreased sensitivity to apoptotic-inducing agents are typically associated with activation of these pro-survival pathways. This review discusses the functions these pathways have in normal and neoplastic tissue growth and how they contribute to resistance to apoptotic stimuli. Crosstalk and commonly identified mutations that occur within these pathways that contribute to abnormal activation and cancer growth will also be addressed. Finally the recently described …

MaleMAPK/ERK pathwayAgingMAP Kinase Signaling SystemCancer aging RAF MEK mTORApoptosisReviewBiologyPI3KModels BiologicalApoptosis; Cancer; Kinases; MEK; MTOR; PI3K; Protein phosphorylation; RAF; Signal transductionMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineCancer stem cellNeoplasmscancerAnimalsHumansPTENProtein kinase BCellular SenescencePI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biology0303 health sciencesKinaseTOR Serine-Threonine KinasesapoptosisPTEN PhosphohydrolaseRafCell BiologyMEKprotein phosphorylation3. Good healthCell biologyCrosstalk (biology)kinases030220 oncology & carcinogenesisMutationmTORCancer researchbiology.proteinFemaleraf KinasesProto-Oncogene Proteins c-aktCell agingsignal transduction
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Hormone replacement therapy enhances IGF-1 signaling in skeletal muscle by diminishing miR-182 and miR-223 expressions : a study on postmenopausal mo…

2014

MiRNAs are fine-tuning modifiers of skeletal muscle regulation, but knowledge of their hormonal control is lacking. We used a co-twin case-control study design, that is, monozygotic postmenopausal twin pairs discordant for estrogen-based hormone replacement therapy (HRT) to explore estrogen-dependent skeletal muscle regulation via miRNAs. MiRNA profiles were determined from vastus lateralis muscle of nine healthy 54-62-years-old monozygotic female twin pairs discordant for HRT (median 7 years). MCF-7 cells, human myoblast cultures and mouse muscle experiments were used to confirm estrogen's causal role on the expression of specific miRNAs, their target mRNAs and proteins and finally the act…

MaleMICRORNASMonozygotic twinmenopausePATHWAYMice0302 clinical medicineMyocyteInsulin-Like Growth Factor IIN-VIVO0303 health sciencesphosphorylationAge FactorsBREAST-CANCER CELLSWOMENMiddle Aged3142 Public health care science environmental and occupational healthPostmenopauseESTROGENmedicine.anatomical_structureMCF-7 CellsmTORGROWTHFemaleAUTOPHAGYMESSENGER-RNASignal TransductionIGF-1 receptormedicine.medical_specialtyHormone Replacement Therapymedicine.drug_classmiR-142-3pBiology03 medical and health sciencesInternal medicinemicroRNAmedicineAnimalsHumansMuscle SkeletalProtein kinase BPI3K/AKT/mTOR pathwayAged030304 developmental biologyAKTagingSkeletal muscleOriginal ArticlesTwins MonozygoticCell BiologyAKT; FOXO3A; IGF-1 signaling; IGF-1R; aging; mTOR; menopause; miR-142-3p; miR-182; miR-223; phosphorylationmiR-223EndocrinologyEstrogenCase-Control StudiesmiR-1823121 General medicine internal medicine and other clinical medicineFOXO3AIGF-1 signalingIGF-1R030217 neurology & neurosurgeryHUMAN LONGEVITYHormone
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Cytotoxic activity of the novel small molecule AKT inhibitor SC66 in hepatocellular carcinoma cells

2014

Hepatocellular carcinoma (HCC) is characterized by limited response to current drug therapies. Here, we report that SC66, a novel AKT inhibitor, reduced cell viability in a dose- and time-dependent manner, inhibited colony formation and induced apoptosis in HCC cells. SC66 treatment led to a reduction in total and phospho-AKT levels. This was associated with alterations in cytoskeleton organization, a reduction in expression levels of E-cadherin, β-catenin and phospho-FAK, together with up-regulation of Snail protein levels. All these alterations were coupled with anoikis cell death induction. In addition, SC66 induced the production of reactive oxygen species (ROS) and DNA damage. Pre-trea…

MaleProgrammed cell deathCarcinoma HepatocellularCytoskeleton organizationPyridinesMice NudeApoptosisBiologyMice03 medical and health sciences0302 clinical medicineanoikisCell Line TumorAnimalsHumansAnoikisViability assayHCCProtein Kinase InhibitorsProtein kinase BPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biologySC660303 health sciencesCyclohexanonesCell growthAKTLiver NeoplasmsXenograft Model Antitumor AssaysMolecular biology3. Good healthOncologyApoptosis030220 oncology & carcinogenesismTORCancer researchHCC AKT mTOR SC66 anoikisProto-Oncogene Proteins c-aktResearch Paper
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A prospective randomised, open-labeled, trial comparing sirolimus-containing versus mTOR-inhibitor-free immunosuppression in patients undergoing live…

2010

Abstract Background The potential anti-cancer effects of mammalian target of rapamycin (mTOR) inhibitors are being intensively studied. To date, however, few randomised clinical trials (RCT) have been performed to demonstrate anti-neoplastic effects in the pure oncology setting, and at present, no oncology endpoint-directed RCT has been reported in the high-malignancy risk population of immunosuppressed transplant recipients. Interestingly, since mTOR inhibitors have both immunosuppressive and anti-cancer effects, they have the potential to simultaneously protect against immunologic graft loss and tumour development. Therefore, we designed a prospective RCT to determine if the mTOR inhibito…

OncologyCancer ResearchTime Factorsmedicine.medical_treatmentMedizinIntracellular Signaling Peptides and Proteins - antagonists & inhibitors metabolismKaplan-Meier Estimate312 Clinical medicineProtein-Serine-Threonine KinaseLiver transplantationTHERAPYStudy ProtocolImmunosuppressive Agentendothelial growth-factor renal-cell carcinoma tumor progression rapamycin cancer cyclosporine efficacy therapy target model0302 clinical medicineRENAL-CELL CARCINOMARisk FactorsRecurrenceSurgical oncologyMedicine and Health SciencesLiver Neoplasms - drug therapy enzymology mortality surgerySirolimuProspective StudiesTUMOR PROGRESSIONTransplantation Homologoueducation.field_of_studyliver transplantationTOR Serine-Threonine KinasesLiver NeoplasmsIntracellular Signaling Peptides and ProteinsImmunosuppressionhepatocellular carcinomalcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensCANCER3. Good healthEuropeMulticenter StudyTreatment OutcomeTARGETsirolimusOncologyLiver Neoplasm030220 oncology & carcinogenesisHepatocellular carcinomaRandomized Controlled TrialmTORCarcinoma Hepatocellular - drug therapy enzymology mortality surgery030211 gastroenterology & hepatologyImmunosuppressive AgentsRCTHumanmedicine.drugCanadamedicine.medical_specialtyCarcinoma HepatocellularTime FactoreducationPopulationLiver Transplantation - adverse effects mortalityProtein Serine-Threonine Kinaseslcsh:RC254-282Disease-Free Survival03 medical and health sciencesInternal medicineGeneticsmedicineTransplantation HomologousHumansComparative StudyRapamycinddc:610educationProtein-Serine-Threonine Kinases - antagonists & inhibitors metabolismKaplan-Meiers Estimatebusiness.industryRisk FactorAustraliaImmunosuppressive Agents - therapeutic useSirolimus - therapeutic useEFFICACYHumans; Liver Transplantation; Hepatocellular Carcinoma; Randomized Controlled Trial; RCT; Multicenter Study; Comparative Study; Rapamycin; mTOR; Sirolimusmedicine.diseaseSurgeryMODELTransplantationClinical trialProspective StudieIntracellular Signaling Peptides and ProteinSirolimusENDOTHELIAL GROWTH-FACTORCYCLOSPORINERAPAMYCINbusiness
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Endocrine side-effects of new anticancer therapies: Overall monitoring and conclusions

2018

IF 0.795 (2017); International audience; The present final consensus statement of the French Society of Endocrinology lays out the assessments that are to be systematically performed before and during anticancer treatment by immunotherapy, tyrosine kinase inhibitors or mTOR inhibitors, even without onset of any endocrinopathy. It also discusses the CTCAE adverse event grading system in oncology and the difficulty of implementing it for endocrine side-effects of these anticancer treatments. Notably, this is why certain treatment steps applied in other side-effects (e.g., high-dose corticosteroids, contraindications to immunotherapy, etc.) need to be discussed before implementation for endocr…

Oncologymedicine.medical_specialtyConsensusEndocrinology Diabetes and Metabolismmedicine.medical_treatmentAntineoplastic Agents030209 endocrinology & metabolism[SDV.CAN]Life Sciences [q-bio]/CancerEndocrine System Diseases03 medical and health sciences0302 clinical medicineEndocrinologyDysthyroidismNeoplasmsInternal medicineAnimalsHumansMedicineEndocrine systemHypophysitisAdverse effectMTOR inhibitorsTyrosine kinase inhibitorsAdrenal failurebusiness.industryDiabetesGeneral MedicineImmunotherapy[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismDiscovery and development of mTOR inhibitors3. Good healthDyslipidemiaAnticancer treatment030220 oncology & carcinogenesisAdrenal failureImmunotherapybusiness
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Thromboprophylaxis after renal transplantation and patient risk stratification: The case of mTOR inhibitors.

2020

Oncologymedicine.medical_specialtymTORiPatient risk2720 HematologyMEDLINE610 Medicine & healthStratification (mathematics)Internal medicinemedicineHumansEverolimusSirolimusEverolimusHematologybusiness.industry10031 Clinic for AngiologyTOR Serine-Threonine KinasesAnticoagulantsHematologyVenous ThromboembolismDiscovery and development of mTOR inhibitorsKidney TransplantationTransplantationRenal transplantSirolimusbusinessImmunosuppressive AgentsVenous thromboembolismmedicine.drugThrombosis research
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