Search results for "Threonine"

showing 10 items of 294 documents

Phase I Pharmacokinetic/Pharmacodynamic Study of MLN8237, an Investigational, Oral, Selective Aurora A Kinase Inhibitor, in Patients with Advanced So…

2012

Abstract Purpose: Aurora A kinase (AAK) is a key regulator of mitosis and a target for anticancer drug development. This phase I study investigated the safety, pharmacokinetics, and pharmacodynamics of MLN8237 (alisertib), an investigational, oral, selective AAK inhibitor, in 59 adults with advanced solid tumors. Experimental Design: Patients received MLN8237 once daily or twice daily for 7, 14, or 21 consecutive days, followed by 14 days recovery, in 21-, 28-, or 35-day cycles. Dose-limiting toxicities (DLT) and the maximum-tolerated dose (MTD) for the 7- and 21-day schedules were determined. Pharmacokinetic parameters were derived from plasma concentration–time profiles. AAK inhibition in…

AdultMaleCancer ResearchNeutropeniaMaximum Tolerated DoseBiopsyAurora A kinaseAntineoplastic AgentsProtein Serine-Threonine KinasesPharmacologyNeutropeniachemistry.chemical_compoundPharmacokineticsAurora KinasesNeoplasmsBiopsyHumansMedicineStomatitisAgedNeoplasm StagingStomatitismedicine.diagnostic_testbusiness.industryCancerAzepinesMiddle Agedmedicine.diseasePyrimidinesOncologychemistryPharmacodynamicsAlisertibFemalebusinessClinical Cancer Research
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BRCA1/BRCA2 rearrangements and CHEK2 common mutations are infrequent in Italian male breast cancer cases

2008

Male breast cancer (MBC) is a rare and poorly known disease. Germ-line mutations of BRCA2 and, to lesser extent, BRCA1 genes are the highest risk factors associated with MBC. Interestingly, BRCA2 germ-line rearrangements have been described in high-risk breast/ovarian cancer families which included at least one MBC case. Germ-line mutations of CHEK2 gene have been also implicated in inherited MBC predisposition. The CHEK2 1100delC mutation has been shown to increase the risk of breast cancer in men lacking BRCA1/BRCA2 mutations. Intriguingly, two other CHEK2 mutations (IVS2+1G>A and I157T) and a CHEK2 large genomic deletion (del9-10) have been associated with an elevated risk for prostate c…

AdultMaleCancer Researchendocrine system diseasesGenes BRCA2Genes BRCA1male breast cancerProtein Serine-Threonine KinasesBiologychek2medicine.disease_causeBreast Neoplasms Malebrca1Breast cancerbrca2medicineHumansBRCA1/BRCA2germ-line mutationsMultiplex ligation-dependent probe amplificationmlpaskin and connective tissue diseasesneoplasmsCHEK2Germ-Line MutationGene RearrangementMutationCancerGene rearrangementmedicine.diseaseCheckpoint Kinase 2Oncologylarge genomic rearrangementsMale breast cancerCancer researchbrca1; brca2; chek2; germ-line mutations; large genomic rearrangements; male breast cancer; mlpaBreast diseaseBreast Cancer Research and Treatment
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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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Ten new cases further delineate the syndromic intellectual disability phenotype caused by mutations in DYRK1A.

2015

The dual-specificity tyrosine-phosphorylation-regulated kinase 1A (DYRK1A) gene, located on chromosome 21q22.13 within the Down syndrome critical region, has been implicated in syndromic intellectual disability associated with Down syndrome and autism. DYRK1A has a critical role in brain growth and development primarily by regulating cell proliferation, neurogenesis, neuronal plasticity and survival. Several patients have been reported with chromosome 21 aberrations such as partial monosomy, involving multiple genes including DYRK1A. In addition, seven other individuals have been described with chromosomal rearrangements, intragenic deletions or truncating mutations that disrupt specificall…

AdultMaleMicrocephalyMonosomyDown syndromeAdolescentChromosomes Human Pair 21BiologyProtein Serine-Threonine KinasesArticleIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansAutistic DisorderChildGenetics (clinical)Chromosomal DeletionGeneticsProtein-Tyrosine Kinasesmedicine.diseasePhenotypeChild PreschoolSpeech delayMutationMicrocephalyAutismFemalemedicine.symptomChromosome DeletionDown SyndromeChromosome 21European journal of human genetics : EJHG
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Phase III Study to Evaluate Temsirolimus Compared With Investigator's Choice Therapy for the Treatment of Relapsed or Refractory Mantle Cell Lymphoma

2009

Purpose Temsirolimus, a specific inhibitor of the mammalian target of rapamycin kinase, has shown clinical activity in mantle cell lymphoma (MCL). We evaluated two dose regimens of temsirolimus in comparison with investigator's choice single-agent therapy in relapsed or refractory disease. Patients and Methods In this multicenter, open-label, phase III study, 162 patients with relapsed or refractory MCL were randomly assigned (1:1:1) to receive one of two temsirolimus regimens: 175 mg weekly for 3 weeks followed by either 75 mg (175/75-mg) or 25 mg (175/25-mg) weekly, or investigator's choice therapy from prospectively approved options. The primary end point was progression-free survival (P…

AdultMaleOncologyCancer Researchmedicine.medical_specialtyAntineoplastic AgentsKaplan-Meier EstimateLymphoma Mantle-CellDisease-Free SurvivalDrug Administration ScheduleRidaforolimuschemistry.chemical_compoundRefractoryRecurrenceInternal medicinemedicineHumansProspective StudiesProtein Kinase InhibitorsAgedNeoplasm StagingAged 80 and overSirolimusbusiness.industryLymphoma Non-HodgkinTOR Serine-Threonine KinasesMiddle Agedmedicine.diseaseTemsirolimusSurgeryFludarabineOncologychemistryDrug Resistance NeoplasmSirolimusRefractory Mantle Cell LymphomaFemaleRituximabMantle cell lymphomabusinessProtein Kinasesmedicine.drugJournal of Clinical Oncology
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Analysis of genetic variations of protein tyrosine kinase fyn and their association with alcohol dependence in two independent cohorts.

2003

Abstract Background Decreased sensitivity to and increased tolerance for the effects of alcohol is a phenotype, which was shown to be associated with an increased risk for alcoholism in humans and was observed in protein tyrosine kinase (PTK) fyn knockout mice. Methods We performed an association study of genetic variations of PTK fyn in 430 alcohol-dependent patients and 365 unrelated control subjects from two independent samples. Results In a combined analysis, we found an association of alcohol dependence with the single nucleotide polymorphism (SNP) T137346C in the 5′ untranslated region (UTR) of the gene. A relevant association could be excluded for the remaining two informative SNPs. …

AdultMaleThreonineLinkage disequilibriumGenotypeGlycineSingle-nucleotide polymorphismBiologyProto-Oncogene Proteins c-fynPolymorphism Single NucleotideCohort StudiesFYNGene FrequencyProto-Oncogene ProteinsGenotypeSNPHumansCysteineAlleleBiological PsychiatryGeneticsAlanineChi-Square DistributionAlcohol dependenceGenetic VariationMiddle AgedAlcoholismCase-Control StudiesFemale5' Untranslated RegionsTyrosine kinaseBiological psychiatry
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Myocardial 123metaiodobenzylguanidine uptake in genetic Parkinson's disease.

2008

Myocardial (123)Metaiodobenzylguanidine (MIBG) enables the assessment of postganglionic sympathetic cardiac innervation. MIBG uptake is decreased in nearly all patients with Parkinson's disease (PD). Our objective was to evaluate MIBG uptake in patients with genetic PD. We investigated MIBG uptake in 14 patients with PD associated with mutations in different genes (Parkin, DJ-1, PINK], and leucine-rich repeat kinase 2 -LRRK2), in 15 patients with idiopathic PD, and 10 control subjects. The myocardial MIGB uptake was preserved in 3 of the 4 Parkin-associated Parkinsonisms, in I of the 2 patients with DJ-1 mutations, in 1 of the 2 brothers with PINK] mutations, in 3 of the 6 unrelated patient…

AdultMalemedicine.medical_specialtyParkinson's diseaseGenotypeUbiquitin-Protein LigasesDNA Mutational AnalysisProtein Deglycase DJ-1PINK1Gene mutationProtein Serine-Threonine Kinasesmedicine.disease_causeLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Severity of Illness IndexParkinCentral nervous system diseaseDiagnosis DifferentialDegenerative diseaseParkinsonian DisordersInternal medicineSurveys and QuestionnairesmedicineHumansPoint MutationPromoter Regions GeneticGenetic PD Myocardial scintigraphyOncogene ProteinsTomography Emission-Computed Single-PhotonMutationMovement Disordersbusiness.industryMyocardiumIntracellular Signaling Peptides and ProteinsParkinson DiseaseGalvanic Skin ResponseMiddle Agedmedicine.diseaseLRRK2nervous system diseases3-IodobenzylguanidineEndocrinologyNeurologySettore MED/26 - NeurologiaFemaleNeurology (clinical)RadiopharmaceuticalsbusinessProtein KinasesMovement disorders : official journal of the Movement Disorder Society
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Aurora-A overexpression as an early marker of reflux-related columnar mucosa and Barrett's oesophagus.

2007

Abstract BACKGROUND: The development of oesophageal adenocarcinoma is generally closely associated with the presence of a specialised intestinal-type epithelium such as that found in Barrett's oesophagus (BO). A particular histological condition is when the distal oesophagus showing cardiac and/or fundic mucosa without intestinal metaplasia cannot be defined as 'Barrett's mucosa' [condition that we call 'columnar-lined oesophagus' (CLO)] and up till now, there has been no agreement in literature about the management of this condition. Aurora-A overexpression leads to centrosome amplification, chromosomal instability and aneuploidy in mammalian cells. PATIENTS AND METHODS: A prospective stud…

AdultMalemedicine.medical_specialtyPathologyEsophageal NeoplasmsSettore MED/06 - Oncologia MedicaAneuploidySettore BIO/11 - Biologia MolecolareAdenocarcinomaProtein Serine-Threonine KinasesSettore MED/08 - Anatomia PatologicaGastroenterologyBarrett EsophagusAurora KinasesInternal medicineBiopsymedicineHumansAurora-A overexpression Barrett’s oesophagus cell cycle columnar-lined oesophagus p53 proteinProspective StudiesEsophagusMucous Membranemedicine.diagnostic_testEsophageal diseasebusiness.industryIntestinal metaplasiaHematologyMiddle Agedmedicine.diseasemedicine.anatomical_structureOncologyDysplasiaBarrett's esophagusGastroesophageal RefluxFemalebusinessImmunostainingBiomarkers
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A Novel Loss-of-Function Mutation (N48K) in the PTEN Gene in a Spanish Patient with Cowden Disease

2003

Cowden disease, also known as multiple hamartoma syndrome, is a rare disease inherited in an autosomal dominant pattern, which confers a high risk of developing breast and thyroid carcinomas. Mutations in PTEN, a tumor suppressor gene located on chromosome 10q23, have been identified in patients with Cowden disease. In this work, the direct sequencing of all coding regions of the PTEN gene led us to the identification of N48K, a new germline PTEN missense mutation, in a patient suffering from Cowden disease. The genetic analysis of 200 chromosomes from healthy individuals revealed that the variant was not common in our population. Moreover, by functional analysis we found that the ability o…

AdultPTENcongenital hereditary and neonatal diseases and abnormalitiesTumor suppressor geneDNA Mutational AnalysisMolecular Sequence DataLoss of Heterozygositygenetic analysisDermatologyProtein Serine-Threonine Kinasesmedicine.disease_causeProto-Oncogene MasBiochemistryGenètica molecularfunctional analysisLoss of heterozygosityStructure-Activity RelationshipProto-Oncogene ProteinsmedicineLeukocytesMissense mutationPTENHumansPoint MutationCowden diseaseAmino Acid SequenceMolecular BiologyTumorsGeneticsMutationbiologySequence Homology Amino AcidPoint mutationTumor Suppressor ProteinsPTEN PhosphohydrolaseMultiple hamartoma syndromeCowden syndromeCell Biologymedicine.diseasePhosphoric Monoester HydrolasesN48KSpainbiology.proteinCancer researchFemaleHamartoma Syndrome MultipleProto-Oncogene Proteins c-akt
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