Search results for "HAp"

showing 10 items of 2767 documents

Functional characterisation of alpha-galactosidase a mutations as a basis for a new classification system in fabry disease.

2013

Fabry disease (FD) is an X-linked hereditary defect of glycosphingolipid storage caused by mutations in the gene encoding the lysosomal hydrolase α-galactosidase A (GLA, α-gal A). To date, over 400 mutations causing amino acid substitutions have been described. Most of these mutations are related to the classical Fabry phenotype. Generally in lysosomal storage disorders a reliable genotype/phenotype correlation is difficult to achieve, especially in FD with its X-linked mode of inheritance. In order to predict the metabolic consequence of a given mutation, we combined in vitro enzyme activity with in vivo biomarker data. Furthermore, we used the pharmacological chaperone (PC) 1-deoxygalacto…

Cancer Research1-Deoxynojirimycinlcsh:QH426-470Nonsense mutationMutantBiologymedicine.disease_causeGeneticsmedicineHumansBiologyMolecular BiologyGenetics (clinical)Ecology Evolution Behavior and SystematicsGeneticsSphingolipidsMutationAlpha-galactosidasePoint mutationmedicine.diseasePhenotypeFabry diseasePharmacological chaperoneProtein Transportlcsh:GeneticsPhenotypeAmino Acid Substitutionalpha-GalactosidaseMutationComputer Sciencebiology.proteinFabry DiseaseMedicineGlycolipidsResearch Articlemedicine.drugPLoS Genetics
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Advances in haploidentical stem cell transplantation for hematologic malignancies

2016

One of the most important advances in allogeneic hematopoietic stem cell transplantation (allo-HSCT) is the use of alternative donors and cell sources, such as haploidentical transplants (haplo-HSCT) from family donors. Several approaches have been developed to overcome the challenging bidirectional alloreactivity. We discuss these approaches, including ex vivo T-cell-depleted grafts with megadose of CD34(+) cells, not requiring immunosuppression after allogeneic transplantation for graft-versus-host disease (GVHD) prophylaxis, and other strategies using unmanipulated T-cell-replete grafts with intensive immunosuppression or post-transplantation cyclophosphamide to minimize the GVHD. We als…

Cancer ResearchAllogeneic transplantationmedicine.medical_treatmentGraft vs Host DiseaseContext (language use)Hematopoietic stem cell transplantationT-Lymphocytes RegulatoryLymphocyte DepletionDonor Selection03 medical and health sciences0302 clinical medicineReceptors KIRHLA AntigensmedicineHumansCyclophosphamideDonor selectionbusiness.industryHistocompatibility TestingHematopoietic Stem Cell TransplantationImmunosuppressionHematologyAllograftsTransplantationTreatment Outcomesurgical procedures operativeClinical Trials Phase III as TopicOncologyHematologic Neoplasms030220 oncology & carcinogenesisTransplantation HaploidenticalImmunologyStem cellUnrelated DonorsbusinessImmunosuppressive AgentsEx vivo030215 immunologyLeukemia & Lymphoma
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Inhibition of HSP70: a challenging anti-cancer strategy.

2012

HSP70 is a chaperone that accumulates in the cells after many different stresses promoting cell survival in response to the adverse conditions. In contrast to normal cells, most cancer cells abundantly express HSP70 at the basal level to resist to various insults at different stages of tumorigenesis and during anti-cancer treatment. This cancer cells addiction for HSP70 is the rational for its targeting in cancer therapy. Much effort has been dedicated in the last years for the active search of HSP70 inhibitors. Additionally, the recent clinical trials on highly promising inhibitors of another stress protein, HSP90, showed compensatory increase in HSP70 levels and raised the question of nec…

Cancer ResearchAntineoplastic AgentsApoptosismedicine.disease_cause03 medical and health sciences0302 clinical medicineImmune systemStress PhysiologicalHeat shock proteinNeoplasmsmedicineAutophagyAnimalsHumansHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsMolecular Targeted Therapy030304 developmental biology0303 health sciencesbiologyHsp903. Good healthNeoplasm ProteinsProtein Structure TertiaryClinical trialOncologyApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisChaperone (protein)Drug DesignCancer cellImmunologybiology.proteinCancer researchDrug Screening Assays AntitumorCarcinogenesisMolecular ChaperonesCancer letters
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In human retinoblastoma Y79 cells okadaic acid-parthenolide co-treatment induces synergistic apoptotic effects, with PTEN as a key player.

2013

Retinoblastoma is the most common intraocular malignancy of childhood. In developing countries, treatment is limited, long-term survival rates are low and current chemotherapy causes significant morbidity to pediatric patients and significantly limits dosing. Therefore there is an urgent need to identify new therapeutic strategies to improve the clinical outcome of patients with retinoblastoma. here, we investigated the effects of two natural compounds okadaic acid (OKa) and parthenolide (PN) on human retinoblastoma Y79 cells. For the first time we showed that OKa/PN combination at subtoxic doses induces potent synergistic apoptotic effects accompanied by lowering in p-akt levels, increasin…

Cancer ResearchCell SurvivalGene ExpressionAntineoplastic AgentsApoptosisBiologychemistry.chemical_compoundSettore BIO/10 - BiochimicaCell Line TumorOkadaic AcidmedicinePTENCytotoxic T cellHumansParthenolideViability assayProtein kinase BCell ShapePharmacologyRetinoblastomaPTEN PhosphohydrolaseRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2Okadaic acidmedicine.diseaseGlutathioneOxidative StressOncologychemistryApoptosisCancer researchbiology.proteinMolecular Medicineretinoblastoma Y79 cells synergistic apoptotic effects oxidative stress natural drugs PTEN/Akt/Mdm2/p53 pathway parthenolide okadaic acid.Drug Screening Assays AntitumorTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktSesquiterpenesResearch PaperCancer biologytherapy
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Mitochondrial chaperones in cancer: From molecular biology to clinical diagnostics

2006

Mitochondria are cell organelles involved in processes of cell life and death, and therefore also in tumoral transformation. Indeed, mitochondria dysfunction is a prominent feature of cancer cells. Mitochondrial proteins and DNA have also been previously studied as markers of tumorigenesis. Heat shock proteins (HSPs) are ubiquitous evolutionary conserved proteins. HSPs enhance their expression in stressed cells and they are involved in gene expression regulation, DNA replication, signal transduction, differentiation, apoptosis, cellular senescence or immortalization. This review reflects recent views on the role of some mitochondrial molecular chaperones as prohibitin, mortalin and HSP60/HS…

Cancer ResearchCellBiologyMitochondrionmedicine.disease_causeMitochondrial ProteinsNeoplasmsHeat shock proteinmedicineHumanscancerProhibitinHeat-Shock ProteinsPharmacologyMolecular biologyMitochondriaCell biologyCell Transformation Neoplasticmedicine.anatomical_structureOncologyCancer cellMolecular MedicineHSP60Signal transductionCarcinogenesisMolecular ChaperonesCancer Biology & Therapy
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Functional impact and evolution of a novel human polymorphic inversion that disrupts a gene and creates a fusion transcript

2015

Despite many years of study into inversions, very little is known about their functional consequences, especially in humans. A common hypothesis is that the selective value of inversions stems in part from their effects on nearby genes, although evidence of this in natural populations is almost nonexistent. Here we present a global analysis of a new 415-kb polymorphic inversion that is among the longest ones found in humans and is the first with clear position effects. This inversion is located in chromosome 19 and has been generated by non-homologous end joining between blocks of transposable elements with low identity. PCR genotyping in 541 individuals from eight different human populatio…

Cancer ResearchDNA End-Joining Repairlcsh:QH426-470GenotypeChromosome inversionPopulationChromosome BreakpointsBiologyChromosome breakpointsGenoma humàPolymorphism Single NucleotideEvolution MolecularChromosome Breakpoints03 medical and health sciences0302 clinical medicinePolymorphism Single nucleotideChromosome 19DNA end-joining repairGeneticsTranscription factorsHumansAlleleeducationMolecular BiologyGeneGenetics (clinical)Ecology Evolution Behavior and Systematics030304 developmental biologyChromosomal inversionGeneticsGene expression regulation0303 health scienceseducation.field_of_studyGenètica de poblacionsHaplotypelcsh:GeneticsDNA transposable elementsGenetics PopulationGene Expression RegulationFusion transcriptChromosome InversionDNA Transposable ElementsChromosomes Human Pair 19030217 neurology & neurosurgeryResearch ArticleTranscription Factors
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Cancer Prevention with Resistant Starch in Lynch Syndrome Patients in the CAPP2-Randomized Placebo Controlled Trial : Planned 10-Year Follow-up

2022

Abstract The CAPP2 trial investigated the long-term effects of aspirin and resistant starch on cancer incidence in patients with Lynch syndrome (LS). Participants with LS were randomized double-blind to 30 g resistant starch (RS) daily or placebo for up to 4 years. We present long-term cancer outcomes based on the planned 10-year follow-up from recruitment, supplemented by National Cancer Registry data to 20 years in England, Wales, and Finland. Overall, 463 participants received RS and 455 participants received placebo. After up to 20 years follow-up, there was no difference in colorectal cancer incidence (n = 52 diagnosed with colorectal cancer among those randomized to RS against n = 53…

Cancer ResearchLIVER3122 CancerstärkkelysCOLORECTAL-CANCERBUTYRATESDG 3 - Good Health and Well-beingasetyylisalisyylihappoHumansLynchin oireyhtymäpaksusuolisyöpäRISKIncidenceCOLON-CANCERResistant StarchColorectal Neoplasms/drug therapyCONSUMPTIONColorectal Neoplasms Hereditary NonpolyposisASPIRINMICROBIOMEOncologyAspirin/therapeutic useCELLSDIETARY FIBER INTAKE/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingsyöpätauditennaltaehkäisyseurantatutkimusColorectal Neoplasms Hereditary Nonpolyposis/complicationsColorectal NeoplasmsilmaantuvuusFollow-Up Studies
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Late steps of parvoviral infection induce changes in cell morphology.

2008

Previously, virus-induced non-filopodial extensions have not been encountered in connection with viral infections. Here, we report emergence of long extensions protruding from Norden laboratory feline kidney (NLFK) and A72 (canine fibroma) cells infected with canine parvovirus for 72 h. These extensions significantly differ in length and number from those appearing in control cells. The most striking feature in the extensions is the length, reaching up to 130 microm, almost twice the average length of a healthy NLFK cell. In A72 cells, the extensions were even longer, up to 200 microm. The results presented here also suggest that the events leading to the growth of these extensions start ea…

Cancer ResearchMorphology (linguistics)biologyParvovirus CanineCellCanine parvovirusmedicine.diseasebiology.organism_classificationVirologyVirusCell LineParvoviridae InfectionsInfectious Diseasesmedicine.anatomical_structureDogsVirologymedicineCatsAnimalsAbnormal extensionCell Surface ExtensionsDog DiseasesFibromaCell ShapeVirus research
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Low frequency of HLA haplotype loss associated with loss of heterozygocity in chromosome region 6p21 in clear renal cell carcinomas.

2004

HLA class I loss or downregulation is a widespread mechanism used by tumor cells to avoid tumor recognition by cytotoxic T lymphocytes favoring tumor immune escape. Multiple molecular mechanisms are responsible for these altered HLA class I tumor phenotypes. It has been described in different epithelial tumors that loss of heterozygosity (LOH) at chromosome region 6p21.3 is a frequent mechanism that leads to HLA haplotype loss, ranging between 40 and 50%, depending on the tumor entity analyzed. Here we have tested the frequency of LOH at 6p21 chromosome region in Renal Cell Carcinomas (RCC) of the clear cell and chromophobe subtype. A low frequency of HLA haplotype loss (6.6%) was found in …

Cancer ResearchPathologymedicine.medical_specialtyLoss of HeterozygosityChromophobe cellHuman leukocyte antigenBiologyurologic and male genital diseasesLoss of heterozygosityAntigens NeoplasmHLA AntigensmedicineCytotoxic T cellHumansneoplasmsCarcinoma Renal CellHaplotypeCytogeneticsKidney NeoplasmsGene Expression Regulation NeoplasticOncologyHaplotypesClear cell carcinomaChromosomes Human Pair 6Clear cellAdenocarcinoma Clear CellMicrosatellite RepeatsInternational journal of cancer
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Hsp60 and Hsp10 down-regulation predicts bronchial epithelial carcinogenesis in smokers with chronic obstructive pulmonary disease.

2006

BACKGROUND. The relation between smoking, chronic obstructive pulmonary disease (COPD), and lung cancer (LC) is an open field of investigation. A higher frequency of adenocarcinoma has been reported in patients with COPD. Heat shock proteins (Hsps) are implicated in tumoral cell growth and differentiation. The aim of the present study was to investigate the expression of Hsp60 and Hsp10 in bronchial biopsies from smokers with COPD and in 10 lung cancer patients and to evaluate the association between Hsps expression and carcinogenetic steps of LC. METHODS. An immunohistochemical study was performed for Hsp60 and Hsp10 in bronchial biopsies from 35 COPD (postbronchodilator forced expiratory …

Cancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsAdenosquamous carcinomaBlotting WesternDown-Regulationchemical and pharmacologic phenomenaRespiratory MucosaAdenocarcinomaCarcinoma AdenosquamousPulmonary Disease Chronic ObstructivemedicineChaperonin 10HumansLung cancerAgedsmoking chaperone expression lung obstruction lung tumorsCOPDSettore BIO/16 - Anatomia Umanabusiness.industryRespiratory diseaseSmokingCancerChaperonin 60Middle Agedmedicine.diseasePrognosisSquamous metaplasiarespiratory tract diseasesCarcinoma BronchogenicOncologyDysplasiaDisease ProgressionAdenocarcinomabusinessCancer
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