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1 se (the more severe case also presented with macrocytic anemia).
2 in SFXN4 as a cause of mitochondriopathy and macrocytic anemia.
3 of the MDS progenitors, which corrected the macrocytic anemia.
4 neutrophils and monocytes, associated with a macrocytic anemia.
5 ia, a disorder characterized by hypoplastic, macrocytic anemia.
6 are responsible for Pearsons syndrome with a macrocytic anemia.
7 ly with multiple female individuals who have macrocytic anemia.
8 Tc1 mice do not develop leukemia, they have macrocytic anemia and increased extramedullary hematopoi
9 ications of vitamin B-12 deficiency, such as macrocytic anemia and neurological complications affecti
10 duced serum vitamin B12 concentrations, mild macrocytic anemia, and fecal loss of Na+ and K+, the lat
11 ad to many clinical abnormalities, including macrocytic anemia, cardiovascular diseases, birth defect
12 mechanism is underscored in 5q- syndrome, a macrocytic anemia caused by a large monoallelic deletion
13 is characterized by red blood cell aplasia, macrocytic anemia, clinical heterogeneity, and increased
15 inal features of the 5q- syndrome, including macrocytic anemia, erythroid hypoplasia, and megakaryocy
16 cking the heme exporter FLVCR1 have a severe macrocytic anemia; however, the mechanisms that underlie
21 , encoding the ribosomal protein S14) caused macrocytic anemia, prominent erythroid dysplasia and mon
22 of the mtDNA polymerase, PolgA, and develop macrocytic anemia similar to that of patients with MDS.
24 hat mutant animals develop an age-dependent, macrocytic anemia with abnormal erythroid maturation and
26 defect observed in both individuals and the macrocytic anemia with megaloblastic features of the mor
27 pc (del/+)) accelerated the development of a macrocytic anemia with monocytosis, early features of t-
28 that is deleted neonatally develop a severe macrocytic anemia with proerythroblast maturation arrest
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