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1 ive depletion of all hematopoietic lineages (pancytopenia).
2 d by hypoplastic bone marrow and progressive pancytopenia.
3 e implicated in the development of anemia or pancytopenia.
4 tem cells prior to the development of severe pancytopenia.
5 e alterations of hematopoiesis, resulting in pancytopenia.
6 resented to the Cancer Clinic with fever and pancytopenia.
7 ne patient with grade 4 acute GVHD developed pancytopenia.
8 , the patient developed new skin lesions and pancytopenia.
9 n with Babesia may be associated with marked pancytopenia.
10 -1995) that presented data on MTX-associated pancytopenia.
11 rtality due to graft-versus-host disease and pancytopenia.
12 ypocellular bone marrow and peripheral blood pancytopenia.
13 up: one because of sepsis and one because of pancytopenia.
14 definitive therapies in patients with severe pancytopenia.
15 multiple tick bites presented with fever and pancytopenia.
16 occlusive disease, capillary hemorrhage, and pancytopenia.
17 erized by hypocellular marrow and peripheral pancytopenia.
18 ed severe macrocytic normochromic anemia and pancytopenia.
19 cell (HSC) division, rapid HSC depletion and pancytopenia.
20 cell transplant and relapse with refractory pancytopenia.
21 ell expansion and rescued animals from fatal pancytopenia.
22 irth, likely due to pulmonary hypoplasia and pancytopenia.
23 F-2alpha, encoded by the EPAS1 gene, exhibit pancytopenia.
24 veral stages that is characterized by severe pancytopenia.
25 hat the loss of EPAS1/HIF-2alpha resulted in pancytopenia.
26 One patient developed reversible pancytopenia.
27 ted with reduced doses because of persistent pancytopenia.
28 to produce immunosuppression had continuous pancytopenia.
29 Grade 3 events occurred in 3 patients-1 with pancytopenia, 1 with leukocytopenia, and 1 with pain fla
31 resented with fever, hepatosplenomegaly, and pancytopenia; 5 were previously healthy, but had a clini
34 que manifestation of bone marrow failure and pancytopenia among diseases caused by DNA damage respons
35 ilance data to investigate the occurrence of pancytopenia among patients with cancer treated with pol
37 two (2%) patients each in the benralizumab (pancytopenia and a suicide attempt, both considered unre
38 (one with acute myeloid leukaemia, one with pancytopenia and acute cardiac failure) and four patient
39 truction of hematopoietic stem cells causing pancytopenia and an empty bone marrow, which can be succ
40 nge of hematopoietic abnormalities including pancytopenia and BM hypoplasia similar to individuals wi
44 We investigated the mechanisms of profound pancytopenia and did not observe activation of CAR-37 T
47 conditions of anemia, thrombocytopenia, and pancytopenia and how the biochemical and biophysical pro
50 in addressing the immediate consequences of pancytopenia and in the long term because of the disease
51 mmon hematologic malignancy characterized by pancytopenia and marked susceptibility to infection.
52 xpression interferes with the development of pancytopenia and marrow hypoplasia, validating a major r
55 UCB, GVHD in 4 patients, and immune-mediated pancytopenia and nephrotic syndrome in the recipient of
58 specifically associated with neonatal-onset pancytopenia and severe autoinflammation/hemophagocytic
59 conferred in vivo resistance to BCNU-induced pancytopenia and significantly reduced BCNU-induced mort
61 estigated the mechanisms by which AML causes pancytopenia and suppresses patients' immune response.
62 ry disease in view of the longer duration of pancytopenia and susceptibility to life-threatening infe
65 topenias (thrombocytopenia, neutropenia, and pancytopenia) and HMs (acute myeloid leukemia, myelodysp
66 tis, 1 patient with an idiopathic autoimmune pancytopenia, and 1 patient with immune thrombocytopenia
68 d with congenital abnormalities, progressive pancytopenia, and a predisposition to leukemia and solid
69 with the principal diagnosis of hemorrhage/ pancytopenia, and a secondary diagnosis of metastatic he
70 d of mice die due to complications of severe pancytopenia, and about two thirds progress to a fatal a
72 icant lymphadenopathy, fever, liver failure, pancytopenia, and erythrophagocytosis indicative of a he
75 ee patients experienced prolonged and severe pancytopenia, and in 2 of these patients, efforts to abl
77 MDS, including multi-lineage myelodysplasia, pancytopenia, and occasional progression to overt leukem
78 , hepatotoxicity, interstitial lung disease, pancytopenia, and sepsis [n=1 each]), and two (1%) in th
80 absence of lymphodepletion died from severe pancytopenia, and this effect was recapitulated by regul
85 iglyceridemia associated with rapamycin, and pancytopenia associated with MTX), and 4 were SSc-relate
89 adult hematopoietic system results in severe pancytopenia but striking accumulation of HSCs and early
90 y immune-mediated bone marrow hypoplasia and pancytopenia, can be treated effectively with immunosupp
91 erations, the TIN2(+/DC) mice developed mild pancytopenia, consistent with hematopoietic dysfunction
93 We recently identified 3 patients in whom pancytopenia developed almost 50 years after high-level
94 rituximab, and 1 patient with an autoimmune pancytopenia developed PML after treatment with corticos
96 loblastic anemia, a disease characterized by pancytopenia due to the excessive apoptosis of hematopoi
97 munoconjugates are associated with transient pancytopenia during the first 3 months after treatment.
98 lastic syndrome (MDS) model characterized by pancytopenia, dysmegakaryopoiesis, dyserythropoiesis, an
101 HLS, including fever, multiple organomegaly, pancytopenia, hemophagocytosis, hyperfibrinogenemia with
102 a patient who experienced bleeding episodes, pancytopenia, hepatosplenomegaly, and recurrent pneumoni
103 -deficient mice develop fever, splenomegaly, pancytopenia, hypertriglyceridemia, hypofibrinogenemia,
106 e, BM hypocellularity, ablation of HSCs, and pancytopenia in control mice, whereas irradiated, EPC-tr
107 e moribund due to hematopoietic failure with pancytopenia in the blood and bone marrow 2 to 6 weeks a
108 irradiated Hoxa-9-/- mice develop persistent pancytopenia, indicating unusual sensitivity to ionizing
112 egenerative bone marrow failure resulting in pancytopenia is another common problem in advanced stage
115 contrast to individuals with LIG4 mutations, pancytopenia leading to bone marrow failure has not been
116 d histological lesions of TA-GVHD, including pancytopenia, marked splenomegaly, wasting, engraftment
117 d by associated physical anomalies and early pancytopenia, may be present in otherwise phenotypically
118 G-CSF) in patients with glycogenosis-related pancytopenia might ameliorate the IBD-like disease throu
119 a hematopoietic stem cell leading to severe pancytopenia, multilineage differentiation impairment, a
121 [(177)Lu]Lu-PSMA-617 plus standard of care (pancytopenia [n=2], bone marrow failure [n=1], subdural
122 3 and G4 events included anemia, leukopenia, pancytopenia, nausea, hyperbilirubinemia, hypophosphatem
126 IST produced significant improvement in the pancytopenia of a substantial proportion of patients wit
127 how that cerebral folate levels, anemia, and pancytopenia of DHFR deficiency can be corrected by trea
129 he most common grade 3-4 adverse events were pancytopenia (one patient at level 2, one at level 3, an
131 , and a reduction in almost all blood cells (pancytopenia), or as cutaneous leishmaniasis, characteri
132 icion of GvHD (skin rash, diarrhea, pyrexia, pancytopenia, or anemia, without an obvious alternative
135 rious types of sporadic tumors or idiopathic pancytopenia, peripheral-blood samples from 109 patients
137 row hypoplasia, ameliorated peripheral blood pancytopenia, preserved hematopoietic progenitors, and p
138 control group (anaemia, febrile neutropenia, pancytopenia, pulmonary sepsis, respiratory failure, and
142 od cell count is often incomplete, recurrent pancytopenia requires retreatment, and some patients dev
143 characterized by megaloblastic anemia and/or pancytopenia, severe cerebral folate deficiency, and cer
145 an inborn error of immunity characterized by pancytopenia, skin manifestations, and increased suscept
146 ociated with chromosomal breakage as well as pancytopenia, skin pigmentation, renal hypoplasia, cardi
147 auses a nonlethal phenotype characterized by pancytopenia, splenomegaly, and the accumulation of mono
148 and the genome of an individual with ataxia-pancytopenia syndrome and severe immune dysregulation.
149 nduce the severe marrow hypoplasia and fatal pancytopenia that is produced by injection of similar nu
150 eutropenia (seven [6%]), pyrexia (six [5%]), pancytopenia (three [3%]), and pneumonia (three [3%]).
151 rized by hematopoietic stem cell failure and pancytopenia, to improve platelet counts and stem cell f
153 minimal cumulative MTX dose leading to fatal pancytopenia was 10 mg, observed in one of our patients.
155 Mitomycin C (MMC) dosing, known to induce pancytopenia, was used to challenge the transplanted ani
161 l truncated AML1 mutant (S291fsX300) induced pancytopenia with erythroid dysplasia in transplanted mi
165 lly developed fever, skin rash, diarrhea, or pancytopenia within 2 to 6 weeks after their transplant.