Search results for "Bone marrow failure"

showing 10 items of 14 documents

Paroxysmal nocturnal haemoglobinuria: When delay in diagnosis and long therapy occurs

2017

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare clonal disorder characterized by hemolytic anemia, bone marrow failure and thrombosis, caused by a somaticmutation in PIG-A gene that results in theabsence of CD55 and CD59, two important complement regulatory proteins. In thispaper, a case of PNH is retrospectively examined looking for clinical and laboratory features, and the entire course of the disease from the onset of the symptoms isdescribed, together with an adequate follow-up over a 7-years treatment period. Inthis case, the not specificity and the limited clinical relevance of the symptoms led to adelay in diagnosis. After thrombosis, Eculizumab therapy has been shown to be effec…

0301 basic medicineHemolytic anemiaPediatricsmedicine.medical_specialtyrenal failureParoxysmal nocturnal haemoglobinuriaparoxysmal nocturnal hemoglobinuriaCase ReportDiseaseCD5903 medical and health sciencesthrombotic eventshemic and lymphatic diseasesMedicineClinical significancebusiness.industrylcsh:RC633-647.5Bone marrow failureHematologylcsh:Diseases of the blood and blood-forming organsEculizumabEculizumabmedicine.diseaseThrombosisparoxysmal nocturnal hemoglo-binuria thrombotic events renal failure Eculizumab030104 developmental biologyParoxysmal nocturnal hemoglobinuriabusinessmedicine.drug
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The severe phenotype of Diamond-Blackfan anemia is modulated by heat shock protein 70.

2017

International audience; Diamond-Blackfan anemia (DBA) is a rare congenital bone marrow failure syndrome that exhibits an erythroid-specific phenotype. In at least 70% of cases, DBA is related to a haploinsufficient germ line mutation in a ribosomal protein (RP) gene. Additional cases have been associated with mutations in GATA1. We have previously established that the RPL11+/Mut phenotype is more severe than RPS19+/Mut phenotype because of delayed erythroid differentiation and increased apoptosis of RPL11+/Mut erythroid progenitors. The HSP70 protein is known to protect GATA1, the major erythroid transcription factor, from caspase-3 mediated cleavage during normal erythroid differentiation.…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesIdentificationApoptosis-Inducing FactorGata1 MutationsInhibits ApoptosisBiologyHsp7003 medical and health sciencesGermline mutationRed Cells Iron and Erythropoiesishemic and lymphatic diseasesmedicine[ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/HematologyNuclear ImportErythropoiesisDiamond–Blackfan anemiaHuman ErythroblastsBone marrow failure[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyGATA1Hematologymedicine.diseasePhenotypeMolecular biology3. Good healthHsp70030104 developmental biologyRibosomal-ProteinsProtein Gene DeletionsErythropoiesisHaploinsufficiencyBlood advances
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Congenital neutropenia with retinopathy, a new phenotype without intellectual deficiency or obesity secondary toVPS13Bmutations

2013

Over one hundred VPS13B mutations are reported in Cohen syndrome (CS). Most cases exhibit a homogeneous phenotype that includes intellectual deficiency (ID), microcephaly, facial dysmorphism, slender extremities, truncal obesity, progressive chorioretinal dystrophy, and neutropenia. We report on a patient carrying two VPS13B splicing mutations with an atypical phenotype that included microcephaly, retinopathy, and congenital neutropenia, but neither obesity nor ID. RNA analysis of the IVS34+2T_+3AinsT mutation did not reveal any abnormal splice fragments but mRNA quantification showed a significant decrease in VPS13B expression. RNA sequencing analysis up- and downstream from the IVS57+2T>C…

AdultPathologymedicine.medical_specialtyMicrocephalyNeutropeniaDNA Mutational AnalysisVesicular Transport ProteinsNeutropeniamedicine.disease_causeRetinal DiseasesIntellectual DisabilityGene OrderGeneticsmedicineCongenital Bone Marrow Failure SyndromesHumansObesityCongenital NeutropeniaGenetics (clinical)GeneticsMutationCohen syndromebusiness.industryFaciesSyndromemedicine.diseasePhenotypePedigreeVPS13BPhenotypeMutationFemalebusinessRetinopathyAmerican Journal of Medical Genetics Part A
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Eltrombopag in chronic hepatitis C

2014

Chronic hepatitis C is a public health problem worldwide. Unfortunately, not all patients may benefit from antiviral therapy due to thrombocytopenia. Its causes are represented by portal hypertension and platelet sequestration in the spleen, decreased serum levels or activity of thrombopoietin, the bone marrow suppression induced by hepatitis C virus and a possible adverse effect of interferon. Thrombopoietin receptor analogs may contribute to increase platelet counts in these patients. Eltrombopag binds to another region of the thrombopoietin receptor compared to endogenous thrombopoietin and stimulates the proliferation and maturation of megakaryocytes and the platelet production in a dos…

Blood PlateletsCirrhosisHepatitis C virusEltrombopagmedicine.disease_causeAntiviral AgentsBenzoatesThrombopoiesischemistry.chemical_compoundRisk FactorsHematologic AgentsmedicineHumansThrombopoiesisThrombopoietinThrombopoietin receptorbusiness.industryGastroenterologyBone marrow failureMinireviewsGeneral MedicineHepatitis C Chronicmedicine.diseaseThrombocytopeniaHydrazinesTreatment OutcomeBone marrow suppressionchemistryImmunologyPyrazolesbusinessReceptors ThrombopoietinSignal TransductionWorld Journal of Gastroenterology
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Interleukins

1994

With interleukins (IL), a new class of potential drugs has been introduced into clinical research. These signal peptides are involved in the regulation of many physiological and pathophysiological processes. IL-1, -2, -3, -4, -6 and -11 have been tested in clinical trials. The growth promoting, growth inhibiting or immunomodulatory activities of interleukins represent the theoretical basis for large scale clinical testing, predominantly in malignant disease. Dose-dependent effects on numbers of peripheral blood cells and recovery from bone marrow failure have been demonstrated for IL-1, -3, -6 and -11. Phase III trials are in progress to determine their value for clinical practice. However,…

Clinical Trials as TopicClinical pharmacologybusiness.industryInterleukinsMelanomamedicine.medical_treatmentBone marrow failuremedicine.diseaseBioinformaticslaw.inventionClinical trialHaematopoiesisClinical researchCytokineAdjuvants ImmunologiclawRenal cell carcinomaNeoplasmsImmunologyAnimalsHumansMedicinePharmacology (medical)businessDrugs
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Lentiviral-Mediated Gene Therapy in Fanconi Anemia-A Mice Reveals Long-Term Engraftment and Continuous Turnover of Corrected HSCs

2015

International audience; Fanconi anemia is a DNA repair-deficiency syndrome mainly characterized by cancer predisposition and bone marrow failure. Trying to restore the hematopoietic function in these patients, lentiviral vector-mediated gene therapy trials have recently been proposed. However, because no insertional oncogenesis studies have been conducted so far in DNA repair-deficiency syndromes such as Fanconi anemia, we have carried out a genome-wide screening of lentiviral insertion sites after the gene correction of Fanca-/- hematopoietic stem cells (HSCs), using LAM-PCR and 454-pyrosequencing. Our studies first demonstrated that transduction of Fanca-/- HSCs with a lentiviral vector d…

DNA RepairDNA repair[SDV]Life Sciences [q-bio]Genetic enhancementGenetic VectorsBiologymedicine.disease_causePolymerase Chain ReactionViral vectorCell LineMiceFanconi anemiaTransduction Genetichemic and lymphatic diseasesDrug DiscoveryGeneticsmedicineAnimalsMolecular BiologyGenetics (clinical)Mice KnockoutFanconi Anemia Complementation Group A ProteinLentivirusBone marrow failureGenetic Therapymedicine.diseaseHematopoietic Stem CellsFANCA3. Good health[SDV] Life Sciences [q-bio]Fanconi AnemiaCancer researchMolecular MedicineStem cellCarcinogenesis
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CD8 T-Cell Immunotherapy of Cytomegalovirus Disease in the Murine Model

2010

Publisher Summary Cytomegaloviruses (CMVs) are conditional pathogens that are strictly species specific and are usually well controlled in their respective mammalian hosts by the effector mechanisms of both innate and adaptive immunity. Human CMV (hCMV) is mostly acquired perinatally as well as in early childhood and is transmitted, for instance, through breast milk and saliva. Whilst the immune response in an immunocompetent host prevents an overt CMV disease and rapidly terminates the productive acute infection, viral genome is maintained in most tissues for the life span of the infected host in a state known as viral latency. Latency implies that infectious virions are no longer produced…

HepatitisAdrenalitisEffectormedicine.medical_treatmentBone marrow failureImmunotherapyBiologymedicine.diseaseAcquired immune systemVirologyImmune systemImmunologymedicineCytotoxic T cell
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Application of whole-exome sequencing to unravel the molecular basis of undiagnosed syndromic congenital neutropenia with intellectual disability

2016

International audience; Neutropenia can be qualified as congenital when of neonatal onset or when associated with extra-hematopoietic manifestations. Overall, 30% of patients with congenital neutropenia (CN) remain without a molecular diagnosis after a multidisciplinary consultation and tedious diagnostic strategy. In the rare situations when neutropenia is identified and associated with intellectual disability (ID), there are few diagnostic hypotheses to test. This retrospective multicenter study reports on a clinically heterogeneous cohort of 10 unrelated patients with CN associated with ID and no molecular diagnosis prior to whole-exome sequencing (WES). WES provided a diagnostic yield o…

Male0301 basic medicinePediatricsmedicine.medical_specialtyNeutropeniaAdolescentNeonatal onsetNeutropenia03 medical and health sciences0302 clinical medicinecongenital neutropenia[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyIntellectual DisabilityIntellectual disabilityGeneticsmedicineCongenital Bone Marrow Failure SyndromesHumansExomeChildCongenital NeutropeniaGenetic Association StudiesGenetics (clinical)Exome sequencingRetrospective Studiesbusiness.industryHigh-Throughput Nucleotide SequencingInfantSyndromemedicine.disease3. Good healthPhenotype030104 developmental biologyCHD2Child Preschool030220 oncology & carcinogenesisCohortEtiologyFemalebusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyBiomarkersAmerican Journal of Medical Genetics Part A
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HLA association is different in children and adults with severe acquired aplastic anemia

2007

Background Severe aplastic anemia (SAA) is defined as pancytopenia caused by bone marrow failure. The pathogenesis of SAA is thought to involve autoimmune processes. Increased susceptibility to autoimmunity has been shown to be associated with several different HLA alleles. In SAA, few large studies based on data mainly from adults describe a positive HLA correlation with HLA-DR2 (DRB1*15) and HLA-B14. Procedure This study explored the HLA constitution of 181 children with SAA who were enrolled in the prospective multi-center study SAA94 between January 1994 and January 2002. The control group consisted of 303 healthy individuals of comparable demographic background. Allelic frequencies bet…

MaleAdolescentHuman leukocyte antigenmedicine.disease_causeAutoimmunityPathogenesisHLA-B14 AntigenHLA Antigenshemic and lymphatic diseasesmedicineHumansHLA-DR2 AntigenProspective StudiesChildAllelesbusiness.industryBone marrow failureAnemia AplasticInfantHematologymedicine.diseasePancytopeniaPathophysiologyExact testOncologyHLA-B AntigensChild PreschoolPediatrics Perinatology and Child HealthImmunologyCohortFemalebusinessPediatric Blood & Cancer
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Clinical manifestations and management of four children with Pearson syndrome.

2011

Pearson marrow-pancreas syndrome is a fatal disorder mostly diagnosed during infancy and caused by mutations of mitochondrial DNA. We hereby report on four children affected by Pearson syndrome with hematological disorders at onset. The disease was fatal to three of them and the fourth one, who received hematopoietic stem cell transplantation, died of secondary malignancy. In this latter patient transplantation corrected hematological and non-hematological issues like metabolic acidosis, and we therefore argue that it could be considered as a useful option in an early stage of the disease.

MalePediatricsmedicine.medical_specialtyMitochondrial DiseasesAnemiaMitochondrial diseasemedicine.medical_treatmenttrapianto cellule staminali emopoieticheHematopoietic stem cell transplantationDiseaseDNA MitochondrialLipid Metabolism Inborn Errorsmitochondrial disordersFatal OutcomeMuscular DiseasesCause of Deathhematopoietic stem cell transplantation; mitochondrial disorders; Pearson marrow-pancreas syndrome; trapianto cellule staminali emopoietiche; malattie mitocondriali; sindrome di PearsonGeneticsmedicineCongenital Bone Marrow Failure SyndromesHumansChildGenetics (clinical)Pearson marrow-pancreas syndromeCause of deathPearson syndromebusiness.industryAcyl-CoA Dehydrogenase Long-ChainHematopoietic Stem Cell TransplantationInfantMetabolic acidosissindrome di Pearsonmedicine.diseaseAnemia SideroblasticTransplantationChild PreschoolImmunologymalattie mitocondrialiFemalebusinessGene DeletionAmerican journal of medical genetics. Part A
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