Fetal hemoglobin in sickle cell anemia: genetic determinants of response to hydroxyurea
about
Systematic documentation and analysis of human genetic variation in hemoglobinopathies using the microattribution approachHydroxyurea could be a good clinically relevant iron chelatorFetal hemoglobin in sickle cell anemia: genome-wide association studies suggest a regulatory region in the 5' olfactory receptor gene clusterSickle Cell Disease in the Post Genomic Era: A Monogenic Disease with a Polygenic Phenotype.How I use hydroxyurea to treat young patients with sickle cell anemia.Realities and expectations of pharmacogenomics and personalized medicine: impact of translating genetic knowledge into clinical practice.Hydroxyurea treatment in β-thalassemia patients: to respond or not to respond?Genetic modifiers of HbF and response to hydroxyurea in sickle cell disease.Candidate sequence variants and fetal hemoglobin in children with sickle cell disease treated with hydroxyureaHigh-density SNP genotyping to define beta-globin locus haplotypes.Population pharmacokinetics and pharmacodynamics of hydroxyurea in sickle cell anemia patients, a basis for optimizing the dosing regimen.Fetal hemoglobin in sickle cell anemiaPharmacotherapy in sickle cell disease--state of the art and future prospectsFetal hemoglobin levels in African American and Hispanic children with sickle cell disease at baseline and in response to hydroxyurea.Pharmacokinetics, pharmacodynamics, and pharmacogenetics of hydroxyurea treatment for children with sickle cell anemia.The proinflammatory cytokine GM-CSF downregulates fetal hemoglobin expression by attenuating the cAMP-dependent pathway in sickle cell disease.Genetic modifiers of sickle cell diseaseFetal haemoglobin response to hydroxycarbamide treatment and sar1a promoter polymorphisms in sickle cell anaemia.Pharmacogenomics and therapeutics of hemoglobinopathies.Hematologic, biochemical, and cardiopulmonary effects of L-arginine supplementation or phosphodiesterase 5 inhibition in patients with sickle cell disease who are on hydroxyurea therapyA phase 1/2 trial of HQK-1001, an oral fetal globin inducer, in sickle cell diseaseDifferences in the clinical and genotypic presentation of sickle cell disease around the world.Genomic polymorphisms in sickle cell disease: implications for clinical diversity and treatment.Role of stem cell factor in the reactivation of human fetal hemoglobin.Emerging science of hydroxyurea therapy for pediatric sickle cell disease.The case for and against initiating either hydroxyurea therapy, blood transfusion therapy or hematopoietic stem cell transplant in asymptomatic children with sickle cell disease.Evaluation of Novel Fetal Hemoglobin Inducer Drugs in Treatment of β-Hemoglobinopathy Disorders.Individualizing fetal hemoglobin augmenting therapy for β-type hemoglobinopathies patients.An Expert Review of Pharmacogenomics of Sickle Cell Disease Therapeutics: Not Yet Ready for Global Precision Medicine.Fetal hemoglobin response to hydroxyurea in Yemeni sickle cell disease patients.cAMP response element-binding protein 1 is required for hydroxyurea-mediated induction of γ-globin expression in K562 cells.Hydroxyurea responsiveness in β-thalassemic patients is determined by the stress response adaptation of erythroid progenitors and their differentiation propensity.Toward the prediction of FBPase inhibitory activity using chemoinformatic methods.Safety and efficacy of hydroxyurea in children and adolescents with sickle/beta-thalassemia: two-year experience.Whole transcriptome analysis of human erythropoietic cells during ontogenesis suggests a role of VEGFA gene as modulator of fetal hemoglobin and pharmacogenomic biomarker of treatment response to hydroxyurea in β-type hemoglobinopathy patientsPharmacogenomics of sickle cell disease: steps toward personalized medicine.Pharmacological and molecular approaches for the treatment of β-hemoglobin disorders.Clinical and hematological effects of hydroxyurea therapy in sickle cell patients: a single-center experience in Brazil.A single nucleotide polymorphism in the HBBP1 gene in the human β-globin locus is associated with a mild β-thalassemia disease phenotype.Genomic variation in the MAP3K5 gene is associated with β-thalassemia disease severity and hydroxyurea treatment efficacy.
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Fetal hemoglobin in sickle cell anemia: genetic determinants of response to hydroxyurea
description
article
@en
im Februar 2007 veröffentlichter wissenschaftlicher Artikel
@de
wetenschappelijk artikel
@nl
наукова стаття, опублікована в лютому 2007
@uk
name
Fetal hemoglobin in sickle cell anemia: genetic determinants of response to hydroxyurea
@en
Fetal hemoglobin in sickle cell anemia: genetic determinants of response to hydroxyurea
@nl
type
label
Fetal hemoglobin in sickle cell anemia: genetic determinants of response to hydroxyurea
@en
Fetal hemoglobin in sickle cell anemia: genetic determinants of response to hydroxyurea
@nl
prefLabel
Fetal hemoglobin in sickle cell anemia: genetic determinants of response to hydroxyurea
@en
Fetal hemoglobin in sickle cell anemia: genetic determinants of response to hydroxyurea
@nl
P2093
P2860
P356
P1476
Fetal hemoglobin in sickle cell anemia: genetic determinants of response to hydroxyurea
@en
P2093
P2860
P2888
P304
P356
10.1038/SJ.TPJ.6500433
P577
2007-02-13T00:00:00Z