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1 ted in leukemic progression in patients with severe congenital neutropenia.
2 e course in nearly half of all patients with severe congenital neutropenia.
3 ts with acute myeloid leukemia evolving from severe congenital neutropenia.
4 t of acute myeloid leukemia in patients with severe congenital neutropenia.
5 trophil numbers are cyclic hematopoiesis and severe congenital neutropenia.
6 ic neutropenia and most of the patients with severe congenital neutropenia.
7 myeloid progenitor cells in both cyclic and severe congenital neutropenia.
8 with acute myeloid leukemia associated with severe congenital neutropenia.
10 ell functions was confirmed in patients with severe congenital neutropenia and autoimmune neutropenia
11 are present in approximately 50% of cases of severe congenital neutropenia and nearly all cases of cy
12 otease neutrophil elastase, cause cyclic and severe congenital neutropenia, and recent evidence indic
14 stase are probably the most common cause for severe congenital neutropenia as well as the cause for s
15 se model of disease pathogenesis in cases of severe congenital neutropenia associated with ELA2 mutat
24 ts with acute myeloid leukemia evolving from severe congenital neutropenia, disrupted Gfi-1 up-regula
25 nia associated with ELA2 mutations and place severe congenital neutropenia in a growing list of human
26 ounts oscillate with a 21-day frequency, and severe congenital neutropenia, in which static neutropen
29 ases of cyclic neutropenia and most cases of severe congenital neutropenia result from heterozygous g
30 i-1 mutant, N382S, which was associated with severe congenital neutropenia, resulted in premature apo
31 own to be involved in apoptotic processes in severe congenital neutropenia (SCN) 3 (Kostmann disease
32 ase complex (chronic granulomatous disease), severe congenital neutropenia (SCN) and leukocyte adhesi
35 tor receptor (G-CSFR) in the pathogenesis of severe congenital neutropenia (SCN) and the subsequent d
37 the G-CSF receptor (G-CSFR) in patients with severe congenital neutropenia (SCN) are postulated to co
51 (G-CSFR) occur in a subset of patients with severe congenital neutropenia (SCN) who develop acute my
52 ion (HSCT) is the only curative treatment of severe congenital neutropenia (SCN), but data on outcome
53 Two hereditary human leukemia syndromes are severe congenital neutropenia (SCN), caused by mutations
63 in more than 15 genes are now known to cause severe congenital neutropenia (SCN); however, the pathol
64 and most cases of the pre-leukemic disorder severe congenital neutropenia (SCN; ref. 3) in humans.
66 ase-beta or G6PC3) deficiency, also known as severe congenital neutropenia syndrome 4, is characteriz
68 ounts for the different clinical phenotypes (severe congenital neutropenia versus cyclic neutropenia)
69 ent studies of the molecular pathogenesis of severe congenital neutropenia, with an emphasis on those
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