Search results for "Kinase"

showing 10 items of 2635 documents

Molecular-Biology-Driven Frontline Treatment for Chronic Lymphocytic Leukemia: A Network Meta-Analysis of Randomized Clinical Trials

2023

The treatment of chronic lymphocytic leukemia (CLL) currently relies on the use of chemo-immunotherapy, Bruton’s tyrosine kinase inhibitors, or BCL2 inhibitors alone or combined with an anti-CD20 monoclonal antibody. However, the availability of multiple choices for the first-line setting and a lack of direct head-to-head comparisons pose a challenge for treatment selection. To overcome these limitations, we performed a systematic review and a network meta-analysis on published randomized clinical trials performed in the first-line treatment setting of CLL. For each study, we retrieved data on progression-free survival (according to del17/P53 and IGHV status), overall response rate, complet…

network metanalysiBruton’s tyrosine kinase inhibitorschronic lymphocitic leukemiaCLL
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Structural Manipulations of Marine Natural Products Inspire a New Library of 3-Amino-1,2,4-Triazine PDK Inhibitors Endowed with Antitumor Activity in…

2023

Pancreatic ductal adenocarcinoma (PDAC) is one of the main aggressive types of cancer, characterized by late prognosis and drug resistance. Among the main factors sustaining PDAC progression, the alteration of cell metabolism has emerged to have a key role in PDAC cell proliferation, invasion, and resistance to standard chemotherapeutic agents. Taking into account all these factors and the urgency in evaluating novel options to treat PDAC, in the present work we reported the synthesis of a new series of indolyl-7-azaindolyl triazine compounds inspired by marine bis-indolyl alkaloids. We first assessed the ability of the new triazine compounds to inhibit the enzymatic activity of pyruvate de…

nortopsentin analoguespancreatic ductal adenocarcinoma (PDAC); nortopsentin analogues; antitumor activity; pyruvate dehydrogenase kinases (PDKs); cytotoxic activity; metabolic alterations; ligand-based homology modeling; KRASDrug Discoveryligand-based homology modelingKRASPharmaceutical Scienceantitumor activitymetabolic alterationspancreatic ductal adenocarcinoma (PDAC)Pharmacology Toxicology and Pharmaceutics (miscellaneous)cytotoxic activitypyruvate dehydrogenase kinases (PDKs)
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Increased dosage of Ink4/Arf protects against glucose intolerance and insulin resistance associated with aging

2013

Recent genome-wide association studies have linked type-2 diabetes mellitus to a genomic region in chromosome 9p21 near the Ink4/Arf locus, which encodes tumor suppressors that are up-regulated in a variety of mammalian organs during aging. However, it is unclear whether the susceptibility to type-2 diabetes is associated with altered expression of the Ink4/Arf locus. In the present study, we investigated the role of Ink4/Arf in age-dependent alterations of insulin and glucose homeostasis using Super-Ink4/Arf mice which bear an extra copy of the entire Ink4/Arf locus. We find that, in contrast to age-matched wild-type controls, Super-Ink4/Arf mice do not develop glucose intolerance with agi…

p16ink4amedicine.medical_specialtyAgingGlucose uptakemedicine.medical_treatmentMice TransgenicCarbohydrate metabolismCDKN2BMiceCDKN2AInsulin resistanceInsulin receptor substrateInternal medicineDiabetes mellitusinsulin resistanceGlucose IntolerancemedicineGlucose homeostasisAnimalsInsulininsulin signalingCyclin-Dependent Kinase Inhibitor p16biologydiabetesADP-Ribosylation FactorsInsulin18F-fluorodeoxyglucose-PETARFCell Biologypancreatic isletmedicine.diseaseMice Inbred C57BLInsulin receptorEndocrinologyGlucosebiology.proteinInsulin Resistancep15ink4bGenome-Wide Association Study
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Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS.

2005

Phosphorylated p38 mitogen-activated protein kinase (p38MAPK), but not activated c-jun-N-terminal kinase (JNK), increases in the motor neurons of transgenic mice overexpressing ALS-linked SOD1 mutants at different stages of the disease. This effect is associated with a selective increase of phosphorylated MKK3-6, MKK4 and ASK1 and a concomitant upregulation of the TNFalpha receptors (TNFR1 and TNFR2), but not IL1beta and Fas receptors. Activation of both p38 MAPK and JNK occurs in the activated microglial cells of SOD1 mutant mice at the advanced stage of the disease; however, this effect is not accompanied by the concomitant activation of the upstream kinases ASK1 and MKK3,4,6, while both …

p38 mitogen-activated protein kinasesMAP Kinase Kinase 3Mice TransgenicMAP Kinase Kinase 6BiologyMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein KinasesReceptors Tumor Necrosis FactorCellular and Molecular NeuroscienceMiceSuperoxide Dismutase-1Downregulation and upregulationAnimalsHumansASK1RNA Messengerfas ReceptorPhosphorylationReceptorProtein kinase AMolecular BiologyP38MAPK cascadeMotor NeuronsKinaseSuperoxide DismutaseTumor Necrosis Factor-alphaAmyotrophic Lateral SclerosisJNK Mitogen-Activated Protein KinasesReceptors Interleukin-1Cell BiologyCell biologyEnzyme ActivationMice Inbred C57BLDisease Models AnimalTumor Necrosis Factor Decoy ReceptorsSpinal CordReceptors Tumor Necrosis Factor Type IDisease ProgressionTumor necrosis factor alphaSignal TransductionMolecular and cellular neurosciences
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Protein Phosphorylation by Peroxisome Proliferators: Species-specific Stimulation of Protein Kinases and Its Role in PP-induced Transcriptional Activ…

1996

p38 mitogen-activated protein kinasesMicrobodiesGene Expression Regulation EnzymologicGeneral Biochemistry Genetics and Molecular BiologyMAP2K7Retinoblastoma-like protein 1History and Philosophy of ScienceAnimalsHumansProtein phosphorylationClofibrateRNA MessengerAcetyl-CoA C-AcetyltransferaseProtein kinase ACells CulturedProtein Kinase CHypolipidemic AgentsbiologyChemistryKinaseGeneral NeuroscienceGRB10Autophagy-related protein 13PhosphoproteinsStaurosporineRats Inbred F344RatsCell biologybiology.proteinProtein KinasesAnnals of the New York Academy of Sciences
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Genetic profile and immunohistochemical study of clear cell renal carcinoma: Pathological-anatomical correlation and prognosis.

2021

Abstract Introduction Renal cell carcinoma (RCC) accounts for 2–3% of all tumors being the most frequent solid lesion in the kidney. Objective To determine what genetic alterations and immunohistochemical (IHC) of clear cell renal carcinoma (ccRCC) are associated with prognosis and tumor aggressiveness. Patients and Methods Experimental analytical study with 57 patients who underwent radical and partial nephrectomy between 2005 and 2011, all with diagnosis of ccRCC and minimum post-operative follow-up of 36 months. The pathological study included IHC determination of biomarkers associated (CAIX, CAM 5.2, CD10, c-erbB-2, EGFR, HIF-1a, Ki67, MDM2, PAX-2 y 8, p53, survivin and VEGFR 1 and 2). …

p530301 basic medicineMaleCancer Researchmedicine.medical_treatmentGastroenterologyNephrectomy0302 clinical medicineFHITRenal cell carcinomaCDKN2ANeoplasm MetastasisClear cell renal carcinomaRC254-282KidneyBRCA1 y 2Neoplasms. Tumors. Oncology. Including cancer and carcinogensCDKN2A: cyclin-dependent kinase Inhibitor 2AMiddle AgedPrognosisImmunohistochemistryNephrectomyKidney NeoplasmsMLPATumor BurdenSurvival Ratemedicine.anatomical_structureOncology030220 oncology & carcinogenesisImmunohistochemistryFemalemedicine.medical_specialty03 medical and health sciencesInternal medicinemedicineHumansMultiplex ligation-dependent probe amplificationCarbonic Anhydrase IXSurvival rateCarcinoma Renal CellAgedNeoplasm Stagingbusiness.industryCAIXmedicine.disease030104 developmental biologyNeoplasm GradingNeoplasm Recurrence LocalbusinessTranscriptomeFollow-Up StudiesCancer treatment and research communications
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Cell-cycle control in cell-biomaterial interactions

2000

Current biocompatibility testing involves the demonstration of cell proliferation, which is usually interpreted as a sign of positive biocompatibility when the materials sustain cell proliferation. As the field of biomaterials research is rapidly moving toward tissue-engineered devices and hybrid organs, control of cell function has become a main topic. Cell function, which involves specific differentiation pathways, cannot be separated from cell-cycle control. The study of cell-cycle control is an important extension of routine proliferation assays and has extensive roots in developmental and tumor biology. We studied the expression of the tumour suppressor gene p53 and the proliferation-a…

p53BiocompatibilityBiomedical EngineeringFOCAL ADHESION KINASEHUMAN BONEPROTEINBiologyFlow cytometryBiomaterialsFocal adhesionbiomaterials testing methodsmedicineKI-67BREAST-CANCERmedicine.diagnostic_testCell growthINDUCTIONPROLIFERATIONBiomaterialCell cycleCell biologyAPOPTOSISEndothelial stem cellFibronectinDNA-DAMAGEImmunologybiology.proteinendothelial cellcell cycleGROWTH ARRESTJournal of Biomedical Materials Research
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Endoderm development requires centrioles to restrain p53-mediated apoptosis in the absence of ERK activity

2021

Centrioles comprise the heart of centrosomes, microtubule-organizing centers. To study the function of centrioles in lung and gut development, we genetically disrupted centrioles throughout the mouse endoderm. Surprisingly, removing centrioles from the endoderm did not disrupt intestinal growth or development but blocked lung branching. In the lung, acentriolar SOX2-expressing airway epithelial cells apoptosed. Loss of centrioles activated p53, and removing p53 restored survival of SOX2-expressing cells, lung branching, and mouse viability. To investigate how endodermal p53 activation specifically killed acentriolar SOX2-expressing cells, we assessed ERK, a prosurvival cue. ERK was active t…

p53Cell SurvivalApoptosisInbred C57BLMedical and Health SciencesArticleGeneral Biochemistry Genetics and Molecular BiologyMiceMorphogenesis2.1 Biological and endogenous factorsAnimalscentrioleintestine developmentAetiologyExtracellular Signal-Regulated MAP KinasesendodermLungMolecular BiologyCentriolesSOXB1 Transcription FactorsStem CellsEndodermapoptosisEpithelial CellsCell BiologyBiological SciencesIntestinesMice Inbred C57BLlung branchingERKembryonic structuresTumor Suppressor Protein p53Microtubule-Associated ProteinsDevelopmental BiologyDevelopmental Cell
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Molecular mechanisms of MYCN-dependent apoptosis and the MDM2-p53 pathway: an Achille’s heel to be exploited for the therapy of MYCN amplified neurob…

2012

The p53 oncosuppressor is very seldom mutated in neuroblastoma, but several mecha- nisms cooperate to its functional inactivation in this tumor. Increased MDM2 levels, due to genetic amplification or constitutive inhibition of p14ARF, significantly contribute to this event highlighting p53 reactivation as an attractive perspective for neuroblastoma treat- ment. In addition to its role in tumorigenesis, MYCN sensitizes untransformed and cancer cells to apoptosis. This is associated to a fine modulation of the MDM2-p53 pathway Indeed MYCN induces p53 and MDM2 transcription, and, by evoking a DNA damage response (DDR), it stabilizes p53 and its proapoptotic kinase Homeodomain Interacting Prote…

p53Programmed cell deathCancer ResearchHMGA1HIPK2Biologymedicine.disease_causelcsh:RC254-28203 medical and health sciencesNeuroblastoma0302 clinical medicineMDM2NeuroblastomaMYCNmedicineProtein kinase Aneoplasms030304 developmental biology0303 health sciencesKinaseHMGA1amedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensHMGA13. Good healthOncology030220 oncology & carcinogenesisCancer cellPerspective ArticleMDM2-antagonistsbiology.proteinCancer researchMdm2CarcinogenesisMDM2-antagonistFrontiers in Oncology
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New indole and 7-azaindole derivatives as protein kinase inhibitors

2023

protein kinase inhibitorantiproliferativebis-indoleindole derivative7-azaindole derivativeanticancerSettore CHIM/08 - Chimica Farmaceutica
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