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1 a rate similar to that seen in patients with aplastic anemia).
2 expression and diminished Treg frequency in aplastic anemia.
3 ng the immunodominant Ag H60, produced fatal aplastic anemia.
4 ns in the perforin gene occurred in acquired aplastic anemia.
5 ) is increased in T cells from patients with aplastic anemia.
6 (total of 99 immunosuppressive courses) with aplastic anemia.
7 osomy 7 in severe congenital neutropenia and aplastic anemia.
8 other components of telomerase also occur in aplastic anemia.
9 e is an additional feature shared by PNH and aplastic anemia.
10 l-depleted inoculum and transplantations for aplastic anemia.
11 nfused with aplasia and can also evolve from aplastic anemia.
12 en with MDS secondary to therapy or acquired aplastic anemia.
13 s durable treatment-free remission in severe aplastic anemia.
14 atients with therapy-related MDS or acquired aplastic anemia.
15 myelodysplasia and one of four patients with aplastic anemia.
16 h hematopoietic malignancy or progression to aplastic anemia.
17 atients, T-LDGL is reported as presenting as aplastic anemia.
18 cal characteristics were similar to acquired aplastic anemia.
19 ed in the differential diagnosis of acquired aplastic anemia.
20 n cases of leukopenia, thrombocytopenia, and aplastic anemia.
21 H was found in 25 of 115 (22%) patients with aplastic anemia.
22 , providing a unique insight into a cause of aplastic anemia.
23 e associated with dyskeratosis congenita and aplastic anemia.
24 degree of neutropenia or a prior history of aplastic anemia.
25 le, complete remission in most patients with aplastic anemia.
26 ay be relevant to the pathogenesis of MDS in aplastic anemia.
27 on are accepted treatments for patients with aplastic anemia.
28 thality due to acute bone marrow failure and aplastic anemia.
29 diseases, such as dyskeratosis congenita and aplastic anemia.
30 red immunodeficiency syndrome, and 1 case of aplastic anemia.
31 al disorders, as do patients with idiopathic aplastic anemia.
32 sis is also seen in patients with idiopathic aplastic anemia.
33 -gamma (IFN-gamma) in the pathophysiology of aplastic anemia.
34 ival in patients who received HCT for severe aplastic anemia.
35 ytic leukemic, myelodysplastic syndrome, and aplastic anemia.
36 in previously untreated patients with severe aplastic anemia.
37 flicted with idiopathic, autosomal recessive aplastic anemia.
38 nomucor elegans in a patient with refractory aplastic anemia.
39 nses in some patients with refractory severe aplastic anemia.
40 an, phase 2 pilot study, in 35 patients with aplastic anemia.
41 telomere length (LTL) and increased risk for aplastic anemia.
42 transfusion, such as sickle cell disease and aplastic anemia.
43 amide is highly effective therapy for severe aplastic anemia.
44 and choice of graft source for patients with aplastic anemia.
45 n genes characterized originally in familial aplastic anemias.
46 coni's anemia, the commonest of the familial aplastic anemias.
48 py after transplantation or as treatment for aplastic anemia, 1 was receiving interferon for melanoma
53 nisms are involved in the pathophysiology of aplastic anemia (AA) and myelodysplastic syndrome (MDS).
54 cytopenias and can cooccur in the context of aplastic anemia (AA) and myelodysplastic syndromes (MDS)
55 nts with impaired platelet production due to aplastic anemia (AA) and with platelet destructive disor
56 patients with previously untreated nonsevere aplastic anemia (AA) as defined by a neutrophil count of
57 ain (VB) T-cell receptor (TCR) repertoire in aplastic anemia (AA) at initial presentation and after i
58 n, on the clonogenic potential of normal and aplastic anemia (AA) bone marrow mononuclear cells (BMMC
59 in 4 of 91 patients with apparently acquired aplastic anemia (AA) but not in 276 ethnically matched c
66 accumulating evidence strongly suggests that aplastic anemia (AA) is a T cell-mediated autoimmune dis
74 m cell compartment of patients with acquired aplastic anemia (AA) using the long-term culture-initiat
75 teristics and outcome of posttransplantation aplastic anemia (AA) were determined in 12 of 1,736 pati
77 in 55, 34, 43, and 5 patients with acquired aplastic anemia (AA), autoimmune uveitis, systemic lupus
79 in bone marrow failure syndromes, including aplastic anemia (AA), paroxysmal nocturnal hemoglobinuri
80 samples from a large number of patients with aplastic anemia (AA), paroxysmal nocturnal hemoglobinuri
87 failure syndromes dyskeratosis congenita and aplastic anemia, acute myeloid leukemia, liver cirrhosis
88 About one-third of patients with acquired aplastic anemia also have short telomeres, which in some
89 hemoglobinuria is frequently associated with aplastic anemia, although the basis of this relation is
91 s from 124 patients with apparently acquired aplastic anemia and 282 control subjects for sequence va
92 durable treatment-free remissions in severe aplastic anemia and a variety of other autoimmune disord
95 ies had shown that LCMV infection results in aplastic anemia and death in most of these mice and that
96 In FA-C, there was a later age of onset of aplastic anemia and fewer somatic abnormalities in patie
97 the diagnosis and treatment of patients with aplastic anemia and highlight a role for the THPO-MPL pa
98 omerase, cause short telomeres in congenital aplastic anemia and in some cases of apparently acquired
99 , remains controversial for the treatment of aplastic anemia and inherited bone marrow failure syndro
101 mphomas, Hodgkins disease, immunodeficiency, aplastic anemia and lymphohistiocytic disorders that cha
102 omere attrition in bone marrow cells rescues aplastic anemia and mouse survival compared with mice tr
103 lso are significantly lower in patients with aplastic anemia and NFAT1 protein levels are decreased o
107 kinase may prove useful in the treatment of aplastic anemia and other cytokine-mediated bone marrow
108 enita have shed light on the pathobiology of aplastic anemia and other forms of bone marrow dysfuncti
109 the skin in an 11-year-old child with severe aplastic anemia and prolonged neutropenia is reported.
110 he second featured a 31-year-old female with aplastic anemia and prolonged neutropenia who developed
111 d with telomere dysfunction, including AIDS, aplastic anemia and pulmonary fibrosis, has bolstered in
113 ights into the pathophysiology of idiopathic aplastic anemia and suggest new treatment options, becau
114 ave been described in patients with acquired aplastic anemia and the autosomal dominant form of dyske
115 athogenesis of hematologic disorders such as aplastic anemia and the development of neoplasia are bel
116 than leukemia (odds ratio=6.5 compared with aplastic anemia), and grade 4 graft-versus-host disease
117 5%) of 26 patients with hepatitis-associated aplastic anemia, and 0 of 17 patients with cryptogenic a
120 plain the association between B19 infection, aplastic anemia, and chronic neutropenia of childhood.
121 MECOM patients presented early-onset severe aplastic anemia, and ERCC6L2 patients, mild pancytopenia
122 ggesting mutations in patients with acquired aplastic anemia, and for selection of suitable hematopoi
123 ions associated with dyskeratosis congenita, aplastic anemia, and idiopathic pulmonary fibrosis disru
124 ow failure syndromes dyskeratosis congenita, aplastic anemia, and idiopathic pulmonary fibrosis.
125 ed for children and young adults with severe aplastic anemia, and immunosuppressive therapy is employ
131 r patients with hematologic malignancies and aplastic anemia are almost certain to follow up patients
133 ated donor bone marrow transplant for severe aplastic anemia as a manifestation of Schwachman-Diamond
134 to horse ATG as a first treatment for severe aplastic anemia, as indicated by hematologic response an
135 coexpression of wild-type TERT and TERT with aplastic anemia-associated mutations in a telomerase-def
136 emoglobinuria (PNH) is intimately related to aplastic anemia because many patients with bone marrow f
137 ssays in 18 consecutive patients with severe aplastic anemia before and after treatment with high-dos
138 nts of HLA-identical sibling transplants for aplastic anemia between 1976 and 1992, reported to the I
141 bone marrow suppression to chronic or fatal aplastic anemia; bone marrow suppression was thought to
142 ailure, dyskeratosis congenita, and acquired aplastic anemia, both diseases that predispose to acute
143 n associated with dyskeratosis congenita and aplastic anemia, both typified by impaired haemopoietic
144 telomere length have been reported in severe aplastic anemia but their clinical significance is unkno
148 ce polymorphisms found in some patients with aplastic anemia can inhibit telomerase activity by disru
149 st universally fatal just a few decades ago, aplastic anemia can now be cured or ameliorated by stem-
150 ty syndrome characterized by childhood-onset aplastic anemia, cancer or leukemia susceptibility, and
151 utosomal recessive disorder characterized by aplastic anemia, cancer susceptibility, and cellular sen
152 utosomal recessive disorder characterized by aplastic anemia, cancer susceptibility, and cellular sen
153 sted telomere length of patients with severe aplastic anemia consecutively enrolled in immunosuppress
154 ic anemia in general; some of the idiopathic aplastic anemias could prove to be due to mutations in g
155 tability disorder characterized by childhood aplastic anemia, developmental abnormalities and cancer
156 The hepatitis of the hepatitis-associated aplastic anemia does not appear to be caused by any of t
157 e Tert gene in 2 independent mouse models of aplastic anemia due to short telomeres (Trf1- and Tert-d
158 ns associated with dyskeratosis congenita or aplastic anemia either impair the specific activity of t
159 ion, marrow transplantation in patients with aplastic anemia established long-term normal hematopoies
160 mia is a variant of aplastic anemia in which aplastic anemia follows an acute attack of hepatitis.
161 at presentation in almost all patients with aplastic anemia; FOXP3 protein and mRNA levels also are
162 40 patients received transplants for severe aplastic anemia from related donors other than HLA genot
166 ant dyskeratosis congenita (DKC), as well as aplastic anemia, has been linked to mutations in the RNA
167 eratosis congenita, another familial form of aplastic anemia, have a high incidence of hematopoietic
169 those obtained in a series of patients with aplastic anemia, healthy donors, and patients with a his
172 in chronic inflammatory conditions, such as aplastic anemia, HIV, and graft-versus-host disease, is
174 lose relationship between PNH and idiopathic aplastic anemia (IAA), it has been suggested that the 2
176 anemias are good in vivo models for studying aplastic anemia in general; some of the idiopathic aplas
179 C partial loss-of-function allele results in aplastic anemia in the homozygous state and mild thrombo
180 tinct cell surface receptor and cause severe aplastic anemia in vivo and erythroblast destruction in
181 s-associated aplastic anemia is a variant of aplastic anemia in which aplastic anemia follows an acut
188 d tumor may become even higher as death from aplastic anemia is reduced and as patients survive longe
190 Our understanding of the pathophysiology of aplastic anemia is undergoing significant revision, with
193 netically identical twins into patients with aplastic anemia may help define how frequently these fac
194 ening is also described in cases of acquired aplastic anemia, most likely secondary to increased turn
195 uced in patients' peripheral blood and in an aplastic anemia murine model, infusion of regulatory T c
197 rast, bone marrow from karyotypically normal aplastic anemia, myelodysplastic syndrome, or healthy in
198 dels of marrow failure, and to patients with aplastic anemia, myeloid, and lymphoid cell malignancies
199 uch as sickle cell disease, thalassemia, and aplastic anemia--necessitate chronic transfusion before
200 e more common in developing countries, where aplastic anemia occurs more frequently than it does in t
202 rformed on a limited number of patients with aplastic anemia or acute leukemia, but only transient en
204 tent stem cells (iPSCs) from 4 patients with aplastic anemia or hypocellular bone marrow carrying het
205 rvival after bone marrow transplantation for aplastic anemia or leukemia was poor in both cohorts.
206 cted by high-sensitivity flow cytometry have aplastic anemia or low-risk myelodysplastic syndrome.
207 a may be warranted in selected patients with aplastic anemia or myelodysplastic syndrome, as this may
209 utations and the effects of THPO agonists in aplastic anemia, our results have clinical implications
211 t the increased IFN-gamma levels observed in aplastic anemia patients are the result of active transc
212 Bone marrow (BM) and lymphocyte samples from aplastic anemia patients show up-regulated Fas and Fas-l
213 esents a novel therapeutic strategy to treat aplastic anemia provoked or associated with short telome
218 is efficacious in a subset of patients with aplastic anemia refractory to immunosuppressive therapy,
219 patibility in 16 alloimmunized patients with aplastic anemia refractory to random donor platelet tran
221 About a quarter of patients with severe aplastic anemia remain pancytopenic despite immunosuppre
225 mbilical cord blood transplantation and with aplastic anemia, results from insufficient numbers of ea
228 bone marrow (BM) transplantation for severe aplastic anemia (SAA) has improved, with survival rates
239 d in patients with dyskeratosis congenita or aplastic anemia show loss of function without any indica
240 were noted in analyses stratified on severe aplastic anemia subtype, recipient age, HLA matching, ca
241 play a critical role in the pathogenesis of aplastic anemia, suggesting that selective pharmacologic
246 cted a phase 2 study involving patients with aplastic anemia that was refractory to immunosuppression
248 great majority of young patients with severe aplastic anemia; the major challenges are extending the
250 mance score, graft type, HLA matching, prior aplastic anemia therapy, race/ethnicity, and calendar ye
251 he records and reevaluated 212 patients with aplastic anemia transplanted at the Fred Hutchinson Canc
252 analyzed results in 700 patients with severe aplastic anemia treated with allogeneic marrow transplan
253 Approximately half of patients with severe aplastic anemia treated with antithymocyte globulin and
255 ween 1970 and 1996, 333 patients with severe aplastic anemia underwent HLA-matched related marrow tra
258 even patients with hematologic malignancy or aplastic anemia were prepared to receive a transplant wi
261 viduals is highlighted by an individual with aplastic anemia who appears to lack six contiguous IGHD
262 ested that survivors of childhood cancer and aplastic anemia who are infected with the hepatitis C vi
263 serves further study in patients with severe aplastic anemia who are not suitable candidates for allo
265 me of unrelated transplants in patients with aplastic anemia who had received multiple transfusions.
267 itution analysis of 183 patients with severe aplastic anemia who were treated in sequential prospecti
268 cer Research Center for patients with severe aplastic anemia whose donors were HLA-nonidentical relat
269 s of patients with dyskeratosis congenita or aplastic anemia with mutations in telomerase genes can i
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