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1 of sickle cell anemia (SCA), a prototypical hemoglobinopathy.
2 , and sickle cell anemia is a common type of hemoglobinopathy.
3 ll chemicals may provide a novel therapy for hemoglobinopathy.
4 py is to increase fetal hemoglobin and treat hemoglobinopathy.
5 rythropoiesis to the pathophysiology of this hemoglobinopathy.
6 O processing may characterize a new class of hemoglobinopathy.
7 for therapeutic benefit in treating the beta-hemoglobinopathies.
8 on complication in patients with sickle cell hemoglobinopathies.
9 or therapeutic targeting in the treatment of hemoglobinopathies.
10 ng epigenetic approach for treatment of beta-hemoglobinopathies.
11 lkylator regimens for MHC-mismatched BMT for hemoglobinopathies.
12 in variants and all types of thalassemia and hemoglobinopathies.
13 n understanding of phenotypic variability in hemoglobinopathies.
14 KLF1 mutations can play a modulatory role in hemoglobinopathies.
15 therapeutic genome engineering for the beta-hemoglobinopathies.
16 for therapeutic targeting of BCL11A in beta-hemoglobinopathies.
17 nology holds vast promises for a cure to the hemoglobinopathies.
18 re higher levels of corrected cells, such as hemoglobinopathies.
19 ential as a treatment for patients with beta-hemoglobinopathies.
20 for several hematopoietic diseases including hemoglobinopathies.
21 s for fetal hemoglobin induction in the beta-hemoglobinopathies.
22 promise for improved treatment of the major hemoglobinopathies.
23 successful clinical outcome in patients with hemoglobinopathies.
24 goal of translational research aimed toward hemoglobinopathies.
25 domide as an innovative new therapy for beta-hemoglobinopathies.
26 ifier of fetal hemoglobin levels in the beta hemoglobinopathies.
27 f stem cell-based gene therapy in the severe hemoglobinopathies.
28 otential clinical trials of gene therapy for hemoglobinopathies.
29 lopment of new treatment rationales for beta hemoglobinopathies.
30 c goal for patients with beta-thalassemia or hemoglobinopathies.
31 t the efficacy of gene therapy in the severe hemoglobinopathies.
32 for genome-editing-mediated therapy of beta-hemoglobinopathies.
33 are needed for optimal treatment of the beta-hemoglobinopathies.
34 e ongoing evaluation and treatment of sickle hemoglobinopathies.
35 tal clinical importance for the treatment of hemoglobinopathies.
36 in patients with end-stage organ disease or hemoglobinopathies.
37 lowing therapeutic application for some beta-hemoglobinopathies.
38 express globin at sufficient levels to treat hemoglobinopathies.
39 c (epsilon) genes in individuals with severe hemoglobinopathies.
40 els have proven benefit for people with beta-hemoglobinopathies, all current HbF-inducing agents have
41 It is estimated that 10% of patients with hemoglobinopathies and 0.5% of patients with HIV infecti
42 d may have direct implications to alpha/beta hemoglobinopathies and design of oxidatively stable Hb-b
43 al target for therapeutic genome editing for hemoglobinopathies and highlight the power of chromosome
44 nancies, marrow failure, immunodeficiencies, hemoglobinopathies and inherited metabolic diseases.
46 and unpublished genetic variation related to hemoglobinopathies and thalassemia and implemented micro
47 d epsilon globin in individuals with defined hemoglobinopathies and thalassemias, would serve as a ph
49 tically beneficial for treatment of the beta hemoglobinopathies and useful for the oral treatment of
50 encompass the clear interaction between this hemoglobinopathy and both malarial and nonmalarial infec
51 Plt12 mouse is a model of high O(2)-affinity hemoglobinopathy and provides insights into hematopoiesi
52 potential for the treatment of malignancies, hemoglobinopathies, and autoimmune diseases, as well as
53 zed that sickle cell disease (SCD) and other hemoglobinopathies are associated with a state of chroni
58 ely to benefit from new advances include the hemoglobinopathies (beta-thalassemia and sickle cell dis
59 s effectively used in the management of beta-hemoglobinopathies by augmenting the production of fetal
60 ing EBR/GZR and placebo; among patients with hemoglobinopathies, change in mean hemoglobin levels was
61 PNG), numerous blood group polymorphisms and hemoglobinopathies characterize the human population.
62 T) offers curative therapy for patients with hemoglobinopathies, congenital immunodeficiencies, and o
63 population raises the possibility that these hemoglobinopathies contribute to a decline in kidney fun
64 dult animal model for the most severe of the hemoglobinopathies, Cooley anemia, which should prove us
66 te understanding of the genetics of the beta-hemoglobinopathies for several decades, definitive treat
67 f oncoretroviral vectors in gene therapy for hemoglobinopathies has been impeded by low titer vectors
68 Progress toward gene therapy of beta-chain hemoglobinopathies has been limited in part by poor expr
69 based vector system in gene therapy of human hemoglobinopathies in general and sickle-cell anemia and
70 ove useful in nonmalignant disorders such as hemoglobinopathies in which moderate levels of donor chi
71 hways are used in beta-thalassemia, a common hemoglobinopathy in which beta-globin gene mutations cau
72 d to antagonize EKLF function in adults with hemoglobinopathy, in an attempt to reactivate gamma-glob
73 in targeting BCL11A as a treatment for beta-hemoglobinopathies, including sickle cell disease (SCD)
74 his consensus statement does not cover other hemoglobinopathies, including thalassemia intermedia and
75 sociated with splenectomy, and patients with hemoglobinopathies is a possible consequence of increase
77 ) globin gene expression for therapy of beta-hemoglobinopathies likely requires local chromatin modif
79 moglobin-based blood substitute therapy, the hemoglobinopathies, malaria, and other acquired and gene
80 viduals with beta-thalassemia intermedia and hemoglobinopathies of equivalent severity who are infreq
81 Mutations in the adult form cause inherited hemoglobinopathies or globin disorders, including sickle
82 of age, without evidence of iron deficiency, hemoglobinopathy, or chronic inflammation, found an aver
85 in (HbF) synthesis for the treatment of beta-hemoglobinopathies probably involve protein modification
86 of Plasmodium falciparum suggests that this hemoglobinopathy provides a selective advantage against
87 ell polymorphism, ABO blood group, and other hemoglobinopathies remain the few major determinants in
91 globin SS = 184; and 116 with other sickling hemoglobinopathies: SC, SD, and S-beta thalassemia); alb
95 n (HbF) ameliorates the clinical severity of hemoglobinopathies such as beta-thalassemia and sickle c
96 lls (ECs) may be pathologically important in hemoglobinopathies such as sickle cell disease and thala
98 pedigree is the absence of any cosegregating hemoglobinopathy, thus allowing observation of the segre
99 United States to determine the prevalence of hemoglobinopathy traits and quantify their influence on
101 the influence of sickle cell trait and other hemoglobinopathy traits on anemia in dialysis patients h
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