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1 MDS/MPN overlap syndrome (including chronic myelomonocytic leukemia).
2 n found in a subset of patients with chronic myelomonocytic leukemia.
3 ice that closely models juvenile and chronic myelomonocytic leukemia.
4 eloproliferative disorder resembling chronic myelomonocytic leukemia.
5 loid metaplasia, and, less commonly, chronic myelomonocytic leukemia.
6 es, including an increased risk for juvenile myelomonocytic leukemia.
7 viously described BTs with transformation to myelomonocytic leukemia.
8 ws efficacy in a nude mouse model of chronic myelomonocytic leukemia.
9 duct of the t(5;12) translocation in chronic myelomonocytic leukemia.
10 ight loss as initial manifestations of acute myelomonocytic leukemia.
11 d growth factor beta receptor causes chronic myelomonocytic leukemia.
12 in leukemic cells of a patient with chronic myelomonocytic leukemia.
13 ents with acute myeloid leukemia and chronic myelomonocytic leukemia.
14 ice had a disease similar to the human acute myelomonocytic leukemia.
15 ents with acute myeloid leukemia and chronic myelomonocytic leukemia.
16 r (PDGFbetaR) gene in a patient with chronic myelomonocytic leukemia.
17 5;12) translocation in patients with chronic myelomonocytic leukemia.
18 tosis, including but not limited to, chronic myelomonocytic leukemia.
19 No patient with JXG developed chronic myelomonocytic leukemia.
20 ren with CBL syndrome and transient juvenile myelomonocytic leukemia.
21 elevant proportion of children with juvenile myelomonocytic leukemia.
22 yelodysplastic syndromes (MDSs), and chronic myelomonocytic leukemia.
23 d SRSF2 in 371 children with MDS or juvenile myelomonocytic leukemia.
24 A 3-year-old boy was treated for juvenile myelomonocytic leukemia.
25 econdary acute myeloid leukemia, and chronic myelomonocytic leukemia.
26 , genomic instability, and aggressive, fatal myelomonocytic leukemia.
27 s, myeloproliferative neoplasms, and chronic myelomonocytic leukemia.
28 bling the myeloproliferative form of chronic myelomonocytic leukemia.
29 true NK-cell tumors (n = 18), de novo acute myelomonocytic leukemias (1 of 14, 7%), or mature T-cell
31 ferative neoplasm (SM-MPN), 36 (29%) chronic myelomonocytic leukemia, 28 (23%) myelodysplastic syndro
32 ease: hematologic (MDS 84%, AML 14%, chronic myelomonocytic leukemia 8%), infectious (severe viral 70
33 clinical and molecular features with chronic myelomonocytic leukemia, a similar disease in adults.
34 liferative neoplasm (MPN), including chronic myelomonocytic leukemia, according to the International
36 ner gene in the t(8;16) that occurs in acute myelomonocytic leukemia (AML-M4) de novo and rarely in t
37 n specific human cancers, including juvenile myelomonocytic leukemia, an aggressive myeloproliferativ
39 tions are rare in pediatric MDS and juvenile myelomonocytic leukemia and are unlikely to operate as d
40 e-1 (FIP1L1)-PDGFRalpha, which cause chronic myelomonocytic leukemia and hypereosinophilic syndrome,
41 tantly, Bcl11a is expressed in human chronic myelomonocytic leukemia and juvenile myelomonocytic leuk
42 closely related neoplasms (including chronic myelomonocytic leukemia and MDS-myeloproliferative neopl
44 tic AML, 7 (13%) of 52 patients with chronic myelomonocytic leukemia, and 1 (1%) of 68 patients with
45 h myelodysplastic syndrome, 118 with chronic myelomonocytic leukemia, and 126 with acute myeloid leuk
46 roblasts, TET2/SRSF2 comutation with chronic myelomonocytic leukemia, and activating CSF3R mutation w
48 re common in acute myeloid leukemia, chronic myelomonocytic leukemia, and myelodysplastic syndrome.
49 r gene is frequently inactivated in juvenile myelomonocytic leukemia, and Nf1 mutant mice model this
50 ximately 75% incidence) and SRSF2 in chronic myelomonocytic leukemia ( approximately 28% incidence).
51 ted with marked thrombocytosis, and juvenile myelomonocytic leukemia, are clonal hematologic diseases
52 ptor (TEL-PDGFbetaR) is expressed in chronic myelomonocytic leukemias associated with t(5;12)(q33;p13
53 tive neoplasms (MDS/MPNs), including chronic myelomonocytic leukemia, atypical chronic myeloid leukem
54 We found missense mutations in 2 juvenile myelomonocytic leukemia cases and in 1 child with system
55 uting to the pathogenesis of NS and juvenile myelomonocytic leukemia caused by PTPN11 gain-of-functio
56 MLL-AF6 leukemias as well as in ML2, a human myelomonocytic leukemia cell line bearing the t(6;11)(q2
58 rminants of differentiation and apoptosis in myelomonocytic leukemia cells (U937) exposed to the nove
61 at 50% of the cellular topo I in HL-60 human myelomonocytic leukemia cells became covalently bound to
63 2 cells and apoptosis-proficient HL-60 acute myelomonocytic leukemia cells to etoposide were compared
65 sented the spectrum of therapy-induced acute myelomonocytic leukemia/chronic myelomonocytic leukemia/
66 ed patients with higher-risk MDS and chronic myelomonocytic leukemia (CMML) 1:1:1 to azacitidine (75
68 s of myeloid malignancies resembling chronic myelomonocytic leukemia (CMML) and myelodysplastic syndr
69 B fusion oncogene is associated with chronic myelomonocytic leukemia (CMML) and results in the expres
70 ations in 5% and 9% of patients with chronic myelomonocytic leukemia (CMML) and sAML, and also in CML
73 However, monocytoid precursors in chronic myelomonocytic leukemia (CMML) expressed VEGF in an inte
74 3;p13) translocation associated with chronic myelomonocytic leukemia (CMML) generates a TEL/PDGFbetaR
76 mouse model resemble those of human chronic myelomonocytic leukemia (CMML) in its transformation to
82 tients and from 12 of 20 (60%) adult chronic myelomonocytic leukemia (CMML) patients to 10(-9) mol/L
84 myeloid leukemia (AML) patients, 32 chronic myelomonocytic leukemia (CMML) patients, and 96 healthy
86 Human ASXL1 is mutated frequently in chronic myelomonocytic leukemia (CMML) so an ASXL/BAP1 complex m
88 r (PDGFbetaR) gene in a patient with chronic myelomonocytic leukemia (CMML) with a t(5;7)(q33;q11.2)
89 omic DNA from 245 patients--119 with chronic myelomonocytic leukemia (CMML), 101 with MDS, 11 with hy
90 oring systems have been proposed for chronic myelomonocytic leukemia (CMML), a disease in which some
92 myeloproliferative neoplasms (MPNs), chronic myelomonocytic leukemia (CMML), and acute myeloid leukem
94 (CLL), acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML), colorectal cancer, endom
95 e myelomonocytic leukemia (JMML) and chronic myelomonocytic leukemia (CMML), including identical soma
96 tion, with a fully penetrant, lethal chronic myelomonocytic leukemia (CMML), which was serially trans
97 ras G12D/+ bone marrow cells develop chronic myelomonocytic leukemia (CMML), while approximately 8% o
98 ng the myeloproliferative variant of chronic myelomonocytic leukemia (CMML), with a prolonged latency
99 NRAS rapidly and efficiently induced chronic myelomonocytic leukemia (CMML)- or acute myeloid leukemi
112 ent in acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML)/atypical chronic myelogen
113 yeloid malignancies, particularly in chronic myelomonocytic leukemia (CMML; 48%) and MDS/MPD-unclassi
114 uch as chronic myelogenous (CML) and chronic myelomonocytic leukemias (CMML) are frequently induced b
115 derived colonies in 28 patients with chronic myelomonocytic leukemias (CMML), the most frequent MPN/M
116 astic syndrome (MDS) most similar to chronic myelomonocytic leukemia (CMMoL) and one other had dysery
119 detection of shared origin of LCH and acute myelomonocytic leukemia driven by TET2-mutant CD34(+) ce
120 ectively analyzed 110 patients with juvenile myelomonocytic leukemia, given single-unit, unrelated do
125 y members are frequently mutated in juvenile myelomonocytic leukemia (JMML) and acute myeloid leukemi
126 features that overlap with those of juvenile myelomonocytic leukemia (JMML) and chronic myelomonocyti
127 acute lymphoblastic leukemia (ALL), juvenile myelomonocytic leukemia (JMML) and LEOPARD syndrome freq
128 hildren with NF1 are predisposed to juvenile myelomonocytic leukemia (JMML) and lethally irradiated m
129 matopoietic malignancies, including juvenile myelomonocytic leukemia (JMML) and T-cell lymphoblastic
130 ctive RAS signaling is prevalent in juvenile myelomonocytic leukemia (JMML) and the myeloproliferativ
131 myelomonocytic leukemia (CMML) and juvenile myelomonocytic leukemia (JMML) are myelodysplastic syndr
132 ) hypersensitivity is a hallmark of juvenile myelomonocytic leukemia (JMML) but has not been systemat
133 ndividuals with Noonan syndrome and juvenile myelomonocytic leukemia (JMML) have germline mutations i
151 lear cells from five of seven (71%) juvenile myelomonocytic leukemia (JMML) patients and from 12 of 2
152 myelodysplastic syndrome (MDS) and juvenile myelomonocytic leukemia (JMML) treated in a uniform fash
153 ting the molecular underpinnings of juvenile myelomonocytic leukemia (JMML) with the generation of in
154 own to underlie the pathogenesis of juvenile myelomonocytic leukemia (JMML), a fatal childhood diseas
155 s individuals to the development of juvenile myelomonocytic leukemia (JMML), a fatal myeloproliferati
156 PTPN11 (SHP-2) are associated with juvenile myelomonocytic leukemia (JMML), a myeloproliferative dis
157 sis type 1 (NF1) are predisposed to juvenile myelomonocytic leukemia (JMML), an aggressive myeloproli
158 dysplastic syndrome (A-MDS), 60 had juvenile myelomonocytic leukemia (JMML), and 6 infants with Down
159 al investigate the pathogenesis of juvenile myelomonocytic leukemia (JMML), demonstrating that mutan
160 te promyelocytic leukemia (APL) and juvenile myelomonocytic leukemia (JMML), we evaluated UAB8 isomer
161 ood acute leukemias, in addition to juvenile myelomonocytic leukemia (JMML), which is a myeloprolifer
172 nd the myeloproliferative variant of chronic myelomonocytic leukemia (MP-CMML) in humans, and both ar
173 ons occur in children with sporadic juvenile myelomonocytic leukemia, myelodysplasic syndrome, B-cell
174 nduced acute myelomonocytic leukemia/chronic myelomonocytic leukemia/myelodysplastic/myeloproliferati
175 th chronic myeloid leukemia (n = 6), chronic myelomonocytic leukemia (n = 6), acute myeloid leukemia
176 antation model efficiently induces a chronic myelomonocytic leukemia- or acute myeloid leukemia-like
179 n 161 of 1458 patients (11%); 26% of chronic myelomonocytic leukemia patients harbored 7q uniparental
180 s and for treatment of the subset of chronic myelomonocytic leukemia patients with a TEL-PDGFR fusion
182 Decitabine's mechanism of action in chronic myelomonocytic leukemia remains incompletely understood.
185 s SM-MPN, systemic mastocytosis with chronic myelomonocytic leukemia, SM-MDS, and systemic mastocytos
186 ures and outcomes of therapy-related chronic myelomonocytic leukemia (t-CMML) and compare with those
189 actory acute myelogenous leukemia or chronic myelomonocytic leukemia were treated with 10.36 to 37.0
190 ed in human leukemias, particularly juvenile myelomonocytic leukemia, which is characterized by hyper
191 mia [RA]/RA with ringed sideroblasts/chronic myelomonocytic leukemia with < 5% bone marrow blasts, 63
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