Search results for "raf Kinases"

showing 8 items of 8 documents

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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Sorafenib in advanced hepatocellular carcinoma

2008

none 25 BACKGROUND: No effective systemic therapy exists for patients with advanced hepatocellular carcinoma. A preliminary study suggested that sorafenib, an oral multikinase inhibitor of the vascular endothelial growth factor receptor, the platelet-derived growth factor receptor, and Raf may be effective in hepatocellular carcinoma. METHODS: In this multicenter, phase 3, double-blind, placebo-controlled trial, we randomly assigned 602 patients with advanced hepatocellular carcinoma who had not received previous systemic treatment to receive either sorafenib (at a dose of 400 mg twice daily) or placebo. Primary outcomes were overall survival and the time to symptomatic progression. Seconda…

SorafenibMaleNiacinamidemedicine.medical_specialtyCarcinoma HepatocellularPyridinesPlaceboGastroenterologyDouble-Blind MethodInternal medicinemedicineCarcinomaHumansHEPATOCELLULAR CARCINOMAProtein Kinase InhibitorsAgedNeoplasm StagingProportional Hazards Modelsbusiness.industryPhenylurea CompoundsHazard ratioBenzenesulfonatesLiver NeoplasmsGeneral MedicineTREATMENTMiddle AgedSorafenibmedicine.diseaseInterim analysisSurvival AnalysisRecurrent Hepatocellular Carcinomadigestive system diseasesSurgeryHEPATOCELLULAR CARCINOMA; SORAFENIB; TREATMENTChemotherapy AdjuvantHepatocellular carcinomaDisease ProgressionFemaleraf KinasesbusinessLiver cancermedicine.drug
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Therapeutic resistance resulting from mutations in Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR signaling pathways.

2011

Chemotherapy remains a commonly used therapeutic approach for many cancers. Indeed chemotherapy is relatively effective for treatment of certain cancers and it may be the only therapy (besides radiotherapy) that is appropriate for certain cancers. However, a common problem with chemotherapy is the development of drug resistance. Many studies on the mechanisms of drug resistance concentrated on the expression of membrane transporters and how they could be aberrantly regulated in drug resistant cells. Attempts were made to isolate specific inhibitors which could be used to treat drug resistant patients. Unfortunately most of these drug transporter inhibitors have not proven effective for ther…

MAPK/ERK pathwayPTENTumor suppressor genekinase inhibitorPhysiologymedicine.medical_treatmentClinical Biochemistrygrowth factor receptorAntineoplastic AgentsDrug resistancePharmacologyBiologyTargeted therapy03 medical and health sciencesMicePhosphatidylinositol 3-Kinases0302 clinical medicineGrowth factor receptormedicinePTENAnimalsHumansExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesTOR Serine-Threonine KinasesPTEN PhosphohydrolaseCell BiologyMAP Kinase Kinase Kinases3. Good healthErbB ReceptorsDrug Resistance Neoplasm030220 oncology & carcinogenesisMutationCancer researchbiology.proteinraf KinasesProto-Oncogene Proteins c-aktDrug resistance therapeutic sensitivity targeted therapy RAF ERKACUTE MYELOID LEUKAEMIASignal TransductionJournal of cellular physiology
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The Ras/Raf-1/MEK1/ERK Signaling Pathway Coupled to Integrin Expression Mediates Cholinergic Regulation of Keratinocyte Directional Migration

2005

The physiologic mechanisms that determine directionality of lateral migration are a subject of intense research. Galvanotropism in a direct current (DC) electric field represents a natural model of cell re-orientation toward the direction of future migration. Keratinocyte migration is regulated through both the nicotinic and muscarinic classes of acetylcholine (ACh) receptors. We sought to identify the signaling pathway mediating the cholinergic regulation of chemotaxis and galvanotropism. The pharmacologic and molecular modifiers of the Ras/Raf-1/MEK1/ERK signaling pathway altered both chemotaxis toward choline and galvanotropism toward the cathode in a similar way, indicating that the sam…

KeratinocytesMAPK/ERK pathwayIntegrinsalpha7 Nicotinic Acetylcholine ReceptorMAP Kinase Signaling SystemIntegrinMAP Kinase Kinase 1Receptors NicotinicBiologyTransfectionBiochemistryMuscarinic acetylcholine receptormedicineHumansRNA Small InterferingKeratinocyte migrationExtracellular Signal-Regulated MAP KinasesMolecular BiologyCells CulturedChemotaxisReceptor Muscarinic M1ChemotaxisCell BiologyAcetylcholineUp-RegulationCell biologyElectrophysiologyras Proteinsbiology.proteinraf KinasesLamellipodiumSignal transductionAcetylcholineSignal Transductionmedicine.drugJournal of Biological Chemistry
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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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Targeting prohibitins with chemical ligands inhibits KRAS-mediated lung tumours.

2017

KRAS is one of the most frequently mutated oncogenes in human non-small cell lung cancers (NSCLCs). RAS proteins trigger multiple effector signalling pathways including the highly conserved RAF-MAPK pathway. CRAF, a direct RAS effector protein, is required for KRAS-mediated tumourigenesis. Thus, the molecular mechanisms driving the activation of CRAF are intensively studied. Prohibitin 1 (PHB1) is an evolutionarily conserved adaptor protein and interaction of CRAF with PHB1 at the plasma membrane is essential for CRAF activation. Here, we demonstrate that PHB1 is highly expressed in NSCLC patients and correlates with poor survival. Targeting of PHB1 with two chemical ligands (rocaglamide an…

0301 basic medicineCancer ResearchEGF Family of ProteinsLung NeoplasmsBiologyLigandsProto-Oncogene Proteins p21(ras)03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineGrowth factor receptorRocaglamideEpidermal growth factorCarcinoma Non-Small-Cell LungCell Line TumorProhibitinsGeneticsAnimalsHumansMolecular Targeted TherapyProhibitinMolecular BiologyBenzofuransCell ProliferationRas InhibitorMice KnockoutTNF Receptor-Associated Factor 3EffectorXenograft Model Antitumor Assaysrespiratory tract diseasesCell biologyProto-Oncogene Proteins p21(ras)Gene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologychemistry030220 oncology & carcinogenesisras Proteinsraf KinasesSignal transductionSignal TransductionOncogene
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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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Influences of TP53 and the anti-aging DDR1 receptor in controlling Raf/MEK/ERK and PI3K/Akt expression and chemotherapeutic drug sensitivity in prost…

2020

Background TP53 plays critical roles in sensitivity to chemotherapy, and aging. Collagen is very important in aging. The molecular structure and biochemical properties of collagen changes during aging. The discoidin domain receptor (DDR1) is regulated in part by collagen. Elucidating the links between TP53 and DDR1 in chemosensitivity and aging could improve therapies against cancer and aging. Results Restoration of WT-TP53 activity resulted in increased sensitivity to chemotherapeutic drugs and elevated expression of key components of the Raf/MEK/ERK, PI3K/Akt and DDR1 pathways. DDR1 could modulate the levels of Raf/MEK/ERK and PI3K/Akt pathways as well as sensitize the cells to chemothera…

MAPK/ERK pathwayMalecollagenAgingRAF/MEK/ERKMAP Kinase Signaling SystemAntineoplastic Agentsdiscoidin domain receptor (DDR1)DDRCollagen receptorPhosphatidylinositol 3-KinasesDiscoidin Domain Receptor 1Cell Line TumorHumansRapamycinTP53ReceptorProtein kinase BPI3K/AKT/mTOR pathwayDDR1ChemistryWild typeProstateProstatic NeoplasmschemoresistanceCell Biologyprostate cancerDrug Resistance NeoplasmMutationCancer researchraf KinasesTumor Suppressor Protein p53Discoidin domainResearch Paper
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