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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 in previously untreated patients with severe aplastic anemia.
8 osomy 7 in severe congenital neutropenia and aplastic anemia.
9 other components of telomerase also occur in aplastic anemia.
10 e is an additional feature shared by PNH and aplastic anemia.
11 l-depleted inoculum and transplantations for aplastic anemia.
12 nfused with aplasia and can also evolve from aplastic anemia.
13 s durable treatment-free remission in severe aplastic anemia.
14 myelodysplasia and one of four patients with aplastic anemia.
15 h hematopoietic malignancy or progression to aplastic anemia.
16 atients, T-LDGL is reported as presenting as aplastic anemia.
17 cal characteristics were similar to acquired aplastic anemia.
18 ed in the differential diagnosis of acquired aplastic anemia.
19 n cases of leukopenia, thrombocytopenia, and aplastic anemia.
20 H was found in 25 of 115 (22%) patients with aplastic anemia.
21 , providing a unique insight into a cause of aplastic anemia.
22 degree of neutropenia or a prior history of aplastic anemia.
23 le, complete remission in most patients with aplastic anemia.
24 ay be relevant to the pathogenesis of MDS in aplastic anemia.
25 on are accepted treatments for patients with aplastic anemia.
26 red immunodeficiency syndrome, and 1 case of aplastic anemia.
27 al disorders, as do patients with idiopathic aplastic anemia.
28 sis is also seen in patients with idiopathic aplastic anemia.
29 -gamma (IFN-gamma) in the pathophysiology of aplastic anemia.
30 en with MDS secondary to therapy or acquired aplastic anemia.
31 G) plus cyclosporine in patients with severe aplastic anemia.
32 mia, immune thrombocytopenia, and idiopathic aplastic anemia.
33 atients with therapy-related MDS or acquired aplastic anemia.
34 in previously untreated patients with severe aplastic anemia.
35 city was seen except one patient with severe aplastic anemia.
36 cted in several hematologic malignancies and aplastic anemia.
37 e associated with dyskeratosis congenita and aplastic anemia.
38 thality due to acute bone marrow failure and aplastic anemia.
39 diseases, such as dyskeratosis congenita and aplastic anemia.
40 ival in patients who received HCT for severe aplastic anemia.
41 ytic leukemic, myelodysplastic syndrome, and aplastic anemia.
42 flicted with idiopathic, autosomal recessive aplastic anemia.
43 nomucor elegans in a patient with refractory aplastic anemia.
44 nses in some patients with refractory severe aplastic anemia.
45 an, phase 2 pilot study, in 35 patients with aplastic anemia.
46 telomere length (LTL) and increased risk for aplastic anemia.
47 transfusion, such as sickle cell disease and aplastic anemia.
48 amide is highly effective therapy for severe aplastic anemia.
49 and choice of graft source for patients with aplastic anemia.
50 n genes characterized originally in familial aplastic anemias.
51 coni's anemia, the commonest of the familial aplastic anemias.
53 py after transplantation or as treatment for aplastic anemia, 1 was receiving interferon for melanoma
55 ist, is clinically used for the treatment of aplastic anemia, a disease characterized by hematopoieti
59 nisms are involved in the pathophysiology of aplastic anemia (AA) and myelodysplastic syndrome (MDS).
60 cytopenias and can cooccur in the context of aplastic anemia (AA) and myelodysplastic syndromes (MDS)
62 nts with impaired platelet production due to aplastic anemia (AA) and with platelet destructive disor
63 patients with previously untreated nonsevere aplastic anemia (AA) as defined by a neutrophil count of
64 ain (VB) T-cell receptor (TCR) repertoire in aplastic anemia (AA) at initial presentation and after i
65 n, on the clonogenic potential of normal and aplastic anemia (AA) bone marrow mononuclear cells (BMMC
66 in 4 of 91 patients with apparently acquired aplastic anemia (AA) but not in 276 ethnically matched c
77 accumulating evidence strongly suggests that aplastic anemia (AA) is a T cell-mediated autoimmune dis
85 m cell compartment of patients with acquired aplastic anemia (AA) using the long-term culture-initiat
86 teristics and outcome of posttransplantation aplastic anemia (AA) were determined in 12 of 1,736 pati
88 in 55, 34, 43, and 5 patients with acquired aplastic anemia (AA), autoimmune uveitis, systemic lupus
90 in bone marrow failure syndromes, including aplastic anemia (AA), paroxysmal nocturnal hemoglobinuri
91 samples from a large number of patients with aplastic anemia (AA), paroxysmal nocturnal hemoglobinuri
98 failure syndromes dyskeratosis congenita and aplastic anemia, acute myeloid leukemia, liver cirrhosis
99 About one-third of patients with acquired aplastic anemia also have short telomeres, which in some
100 hemoglobinuria is frequently associated with aplastic anemia, although the basis of this relation is
102 s from 124 patients with apparently acquired aplastic anemia and 282 control subjects for sequence va
103 durable treatment-free remissions in severe aplastic anemia and a variety of other autoimmune disord
106 ies had shown that LCMV infection results in aplastic anemia and death in most of these mice and that
107 In FA-C, there was a later age of onset of aplastic anemia and fewer somatic abnormalities in patie
108 the diagnosis and treatment of patients with aplastic anemia and highlight a role for the THPO-MPL pa
109 cytopenia of undetermined significance, and aplastic anemia and how genetic approaches may help to b
111 omerase, cause short telomeres in congenital aplastic anemia and in some cases of apparently acquired
112 , remains controversial for the treatment of aplastic anemia and inherited bone marrow failure syndro
114 mphomas, Hodgkins disease, immunodeficiency, aplastic anemia and lymphohistiocytic disorders that cha
115 omere attrition in bone marrow cells rescues aplastic anemia and mouse survival compared with mice tr
116 lso are significantly lower in patients with aplastic anemia and NFAT1 protein levels are decreased o
120 kinase may prove useful in the treatment of aplastic anemia and other cytokine-mediated bone marrow
121 enita have shed light on the pathobiology of aplastic anemia and other forms of bone marrow dysfuncti
122 the skin in an 11-year-old child with severe aplastic anemia and prolonged neutropenia is reported.
123 he second featured a 31-year-old female with aplastic anemia and prolonged neutropenia who developed
124 d with telomere dysfunction, including AIDS, aplastic anemia and pulmonary fibrosis, has bolstered in
126 ights into the pathophysiology of idiopathic aplastic anemia and suggest new treatment options, becau
127 ave been described in patients with acquired aplastic anemia and the autosomal dominant form of dyske
128 athogenesis of hematologic disorders such as aplastic anemia and the development of neoplasia are bel
129 than leukemia (odds ratio=6.5 compared with aplastic anemia), and grade 4 graft-versus-host disease
130 5%) of 26 patients with hepatitis-associated aplastic anemia, and 0 of 17 patients with cryptogenic a
133 plain the association between B19 infection, aplastic anemia, and chronic neutropenia of childhood.
134 MECOM patients presented early-onset severe aplastic anemia, and ERCC6L2 patients, mild pancytopenia
135 ggesting mutations in patients with acquired aplastic anemia, and for selection of suitable hematopoi
136 ions associated with dyskeratosis congenita, aplastic anemia, and idiopathic pulmonary fibrosis disru
137 ow failure syndromes dyskeratosis congenita, aplastic anemia, and idiopathic pulmonary fibrosis.
138 ed for children and young adults with severe aplastic anemia, and immunosuppressive therapy is employ
144 r patients with hematologic malignancies and aplastic anemia are almost certain to follow up patients
146 tates, such as myelodysplastic syndromes and aplastic anemia, are used for the treatment of myelofibr
147 ated donor bone marrow transplant for severe aplastic anemia as a manifestation of Schwachman-Diamond
148 to horse ATG as a first treatment for severe aplastic anemia, as indicated by hematologic response an
149 factors for immunocompromise included AIDS, aplastic anemia, asplenia, hematological cancer, chemoth
150 coexpression of wild-type TERT and TERT with aplastic anemia-associated mutations in a telomerase-def
151 emoglobinuria (PNH) is intimately related to aplastic anemia because many patients with bone marrow f
152 ssays in 18 consecutive patients with severe aplastic anemia before and after treatment with high-dos
153 nts of HLA-identical sibling transplants for aplastic anemia between 1976 and 1992, reported to the I
156 bone marrow suppression to chronic or fatal aplastic anemia; bone marrow suppression was thought to
157 ailure, dyskeratosis congenita, and acquired aplastic anemia, both diseases that predispose to acute
158 n associated with dyskeratosis congenita and aplastic anemia, both typified by impaired haemopoietic
159 telomere length have been reported in severe aplastic anemia but their clinical significance is unkno
163 ce polymorphisms found in some patients with aplastic anemia can inhibit telomerase activity by disru
164 st universally fatal just a few decades ago, aplastic anemia can now be cured or ameliorated by stem-
165 ty syndrome characterized by childhood-onset aplastic anemia, cancer or leukemia susceptibility, and
166 utosomal recessive disorder characterized by aplastic anemia, cancer susceptibility, and cellular sen
167 utosomal recessive disorder characterized by aplastic anemia, cancer susceptibility, and cellular sen
168 sted telomere length of patients with severe aplastic anemia consecutively enrolled in immunosuppress
169 ic anemia in general; some of the idiopathic aplastic anemias could prove to be due to mutations in g
170 tability disorder characterized by childhood aplastic anemia, developmental abnormalities and cancer
171 The hepatitis of the hepatitis-associated aplastic anemia does not appear to be caused by any of t
172 e Tert gene in 2 independent mouse models of aplastic anemia due to short telomeres (Trf1- and Tert-d
173 ns associated with dyskeratosis congenita or aplastic anemia either impair the specific activity of t
174 ion, marrow transplantation in patients with aplastic anemia established long-term normal hematopoies
175 mia is a variant of aplastic anemia in which aplastic anemia follows an acute attack of hepatitis.
177 at presentation in almost all patients with aplastic anemia; FOXP3 protein and mRNA levels also are
178 the patients with the CFH variant had severe aplastic anemia from eculizumab initiation until 6 month
179 40 patients received transplants for severe aplastic anemia from related donors other than HLA genot
183 ant dyskeratosis congenita (DKC), as well as aplastic anemia, has been linked to mutations in the RNA
184 eratosis congenita, another familial form of aplastic anemia, have a high incidence of hematopoietic
186 those obtained in a series of patients with aplastic anemia, healthy donors, and patients with a his
189 in chronic inflammatory conditions, such as aplastic anemia, HIV, and graft-versus-host disease, is
192 lose relationship between PNH and idiopathic aplastic anemia (IAA), it has been suggested that the 2
194 anemias are good in vivo models for studying aplastic anemia in general; some of the idiopathic aplas
197 C partial loss-of-function allele results in aplastic anemia in the homozygous state and mild thrombo
198 tinct cell surface receptor and cause severe aplastic anemia in vivo and erythroblast destruction in
199 s-associated aplastic anemia is a variant of aplastic anemia in which aplastic anemia follows an acut
207 d tumor may become even higher as death from aplastic anemia is reduced and as patients survive longe
209 Our understanding of the pathophysiology of aplastic anemia is undergoing significant revision, with
210 keratosis congenita, pulmonary fibrosis, and aplastic anemia, is characterized by severely short telo
213 netically identical twins into patients with aplastic anemia may help define how frequently these fac
214 ening is also described in cases of acquired aplastic anemia, most likely secondary to increased turn
215 uced in patients' peripheral blood and in an aplastic anemia murine model, infusion of regulatory T c
217 t-refractory, thrombocytopenic patients with aplastic anemia, myelodysplastic syndrome, or acute myel
218 rast, bone marrow from karyotypically normal aplastic anemia, myelodysplastic syndrome, or healthy in
219 dels of marrow failure, and to patients with aplastic anemia, myeloid, and lymphoid cell malignancies
220 uch as sickle cell disease, thalassemia, and aplastic anemia--necessitate chronic transfusion before
221 e more common in developing countries, where aplastic anemia occurs more frequently than it does in t
223 rformed on a limited number of patients with aplastic anemia or acute leukemia, but only transient en
225 tent stem cells (iPSCs) from 4 patients with aplastic anemia or hypocellular bone marrow carrying het
226 rvival after bone marrow transplantation for aplastic anemia or leukemia was poor in both cohorts.
227 cted by high-sensitivity flow cytometry have aplastic anemia or low-risk myelodysplastic syndrome.
228 ldren initially labeled as having idiopathic aplastic anemia or myelodysplasia represent cryptic case
229 a may be warranted in selected patients with aplastic anemia or myelodysplastic syndrome, as this may
231 utations and the effects of THPO agonists in aplastic anemia, our results have clinical implications
233 that gammac cytokines contribute to GVHD and aplastic anemia pathology by promoting these characteris
234 t the increased IFN-gamma levels observed in aplastic anemia patients are the result of active transc
235 Bone marrow (BM) and lymphocyte samples from aplastic anemia patients show up-regulated Fas and Fas-l
237 oing autologous stem cell transplant or with aplastic anemia, prophylactic platelet transfusion is no
238 esents a novel therapeutic strategy to treat aplastic anemia provoked or associated with short telome
243 is efficacious in a subset of patients with aplastic anemia refractory to immunosuppressive therapy,
244 patibility in 16 alloimmunized patients with aplastic anemia refractory to random donor platelet tran
246 About a quarter of patients with severe aplastic anemia remain pancytopenic despite immunosuppre
250 mbilical cord blood transplantation and with aplastic anemia, results from insufficient numbers of ea
251 ation for the treatment of refractory severe aplastic anemia (rSAA) based on treatment of 43 patients
256 bone marrow (BM) transplantation for severe aplastic anemia (SAA) has improved, with survival rates
268 d in patients with dyskeratosis congenita or aplastic anemia show loss of function without any indica
269 were noted in analyses stratified on severe aplastic anemia subtype, recipient age, HLA matching, ca
270 play a critical role in the pathogenesis of aplastic anemia, suggesting that selective pharmacologic
275 cted a phase 2 study involving patients with aplastic anemia that was refractory to immunosuppression
277 great majority of young patients with severe aplastic anemia; the major challenges are extending the
279 mance score, graft type, HLA matching, prior aplastic anemia therapy, race/ethnicity, and calendar ye
280 he records and reevaluated 212 patients with aplastic anemia transplanted at the Fred Hutchinson Canc
281 analyzed results in 700 patients with severe aplastic anemia treated with allogeneic marrow transplan
282 Approximately half of patients with severe aplastic anemia treated with antithymocyte globulin and
284 ween 1970 and 1996, 333 patients with severe aplastic anemia underwent HLA-matched related marrow tra
287 even patients with hematologic malignancy or aplastic anemia were prepared to receive a transplant wi
289 argest group, was mostly immune or inherited aplastic anemia, whereas cluster B comprised underrepres
291 viduals is highlighted by an individual with aplastic anemia who appears to lack six contiguous IGHD
292 ested that survivors of childhood cancer and aplastic anemia who are infected with the hepatitis C vi
293 serves further study in patients with severe aplastic anemia who are not suitable candidates for allo
295 me of unrelated transplants in patients with aplastic anemia who had received multiple transfusions.
297 itution analysis of 183 patients with severe aplastic anemia who were treated in sequential prospecti
298 cer Research Center for patients with severe aplastic anemia whose donors were HLA-nonidentical relat
299 s of patients with dyskeratosis congenita or aplastic anemia with mutations in telomerase genes can i