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1 IFP expression was sufficient to induce a myelomonocytic AML even when expressed in wild type bone
2 giogenesis involves both bone marrow-derived myelomonocytic and endothelial progenitor cells as well
4 rminal kinase signaling pathways, leading to myelomonocytic and monocytic AML cell differentiation.
7 ith impaired mobilization of endothelial and myelomonocytic angiogenic progenitors from the bone marr
11 the myeloid compartment that evoked a clonal myelomonocytic cell expansion, splenomegaly, multi-organ
13 7 constructs were introduced into the murine myelomonocytic cell line, 32D, and assayed for their eff
19 onocytic leukemia (JMML) is characterized by myelomonocytic cell overproduction and commonly bears ac
20 results in a hyperproliferative response of myelomonocytic cell populations to growth factor stimula
21 eam to salivary glands and is dependent on a myelomonocytic cell type other than mature macrophages.
22 ) ASCs in the medullary cords migrated along myelomonocytic cells and arrested in contact with them.
26 ne expression in monocytes, macrophages, and myelomonocytic cells as well as in epidermal keratinocyt
27 e and found EYFP gene expression not only in myelomonocytic cells but also in a fraction of HSCs as w
28 y described a mouse line that contains green myelomonocytic cells due to the knock-in of enhanced gre
29 dissect the branching between erythroid and myelomonocytic cells during in vitro differentiation of
30 grade Abeta(1-42), and ACE overexpression in myelomonocytic cells enhances their immune function.
31 Macrophages, THP-1 cells, and other human myelomonocytic cells expressed both PLD1 and PLD2 protei
32 o generate large numbers of patient-specific myelomonocytic cells for in vitro studies of human disea
33 porting this hypothesis, Siglec-9-expressing myelomonocytic cells found in human tumor samples were a
34 a similar protocol could be used to generate myelomonocytic cells from induced pluripotent stem cells
37 tions, spanning progenitor to mature myeloid/myelomonocytic cells in normal bone marrows with further
41 sults provide direct evidence that committed myelomonocytic cells such as macrophages can produce fun
43 iocytes (FLS) cell lines that were bereft of myelomonocytic cells to examine whether mesenchymal-deri
44 nctional analyses revealed that hESC-derived myelomonocytic cells were comparable to their correspond
46 to ILT4 leads to a tolerogenic phenotype of myelomonocytic cells with lower surface expression of de
47 cognition by innate MHC class I receptors on myelomonocytic cells, and functional impairment of DCs,
48 on maternal uterine natural killer (NK) and myelomonocytic cells, CD94/NKG2, leukocyte immunoglobuli
50 rrow of the lys-EGFP mice revealed that most myelomonocytic cells, especially mature neutrophil granu
51 ifferentiation in certain cell types, namely myelomonocytic cells, osteoblasts, skeletal muscle cells
53 ermore, GATA-1 induced apoptosis of proB and myelomonocytic cells, which could not be prevented by en
65 and C/EBPalpha (Cebpa) have general roles in myelomonocytic development, but the transcriptional basi
69 lso been described, but a role for TIMP-1 in myelomonocytic differentiation has not been previously r
70 ology, and exhibited increased expression of myelomonocytic differentiation markers, including CD11b,
71 action of pro-T cells possess plasticity for myelomonocytic differentiation that can be activated by
72 ogenitors expressing activating Shp2 undergo myelomonocytic differentiation, despite being subjected
73 uration arrest at an identical late stage of myelomonocytic differentiation, putatively a monopotent
74 rylation, expression of RIG-E and RIG-G, and myelomonocytic differentiation-specific down-regulation
78 nced immune response, coupled with increased myelomonocytic expression of catalytically active ACE, p
79 ltipotential progenitor cell maintenance and myelomonocytic fate and suggests Glut1 as potential drug
80 ts EPO-stimulated HSCs to differentiate into myelomonocytic fates, altering in vivo HSC responses and
81 le attractors corresponding to erythroid and myelomonocytic fates, as well as an uncommitted metastab
83 ere mainly mediated by interactions with the myelomonocytic HLA class I receptor leukocyte immunoglob
84 -N-nitrosourea (ENU), MLL-CBP mice developed myelomonocytic hyperplasia and progressed to fatal myelo
85 MDS/MPN overlap syndromes including chronic myelomonocytic leukaemia (CMML), acute myeloid leukaemia
86 of developing leukaemia, especially juvenile myelomonocytic leukaemia (JMML), a childhood myeloprolif
87 ere applied to BALB/c mice with transplanted myelomonocytic leukaemia (WEHI-3) and Human promyelocyti
88 astic syndromes or non-proliferative chronic myelomonocytic leukaemia (white blood cell count <13 000
89 blasts (RAEB)-1, RAEB-2, RAEB-t, or chronic myelomonocytic leukaemia based on local site assessment,
90 in 2 of 110 cases of non-syndromic juvenile myelomonocytic leukaemia, a childhood myeloproliferative
91 with blast-phase disease), one with chronic myelomonocytic leukaemia, and seven with myelofibrosis.
92 eukaemia, chronic myeloid leukaemia, chronic myelomonocytic leukaemia, myelodysplastic syndrome, or m
95 ximately 75% incidence) and SRSF2 in chronic myelomonocytic leukemia ( approximately 28% incidence).
96 ed patients with higher-risk MDS and chronic myelomonocytic leukemia (CMML) 1:1:1 to azacitidine (75
98 s of myeloid malignancies resembling chronic myelomonocytic leukemia (CMML) and myelodysplastic syndr
99 B fusion oncogene is associated with chronic myelomonocytic leukemia (CMML) and results in the expres
100 ations in 5% and 9% of patients with chronic myelomonocytic leukemia (CMML) and sAML, and also in CML
103 However, monocytoid precursors in chronic myelomonocytic leukemia (CMML) expressed VEGF in an inte
104 3;p13) translocation associated with chronic myelomonocytic leukemia (CMML) generates a TEL/PDGFbetaR
106 mouse model resemble those of human chronic myelomonocytic leukemia (CMML) in its transformation to
113 myeloid leukemia (AML) patients, 32 chronic myelomonocytic leukemia (CMML) patients, and 96 healthy
115 Human ASXL1 is mutated frequently in chronic myelomonocytic leukemia (CMML) so an ASXL/BAP1 complex m
117 omic DNA from 245 patients--119 with chronic myelomonocytic leukemia (CMML), 101 with MDS, 11 with hy
118 oring systems have been proposed for chronic myelomonocytic leukemia (CMML), a disease in which some
120 myeloproliferative neoplasms (MPNs), chronic myelomonocytic leukemia (CMML), and acute myeloid leukem
121 (CLL), acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML), colorectal cancer, endom
122 e myelomonocytic leukemia (JMML) and chronic myelomonocytic leukemia (CMML), including identical soma
123 tion, with a fully penetrant, lethal chronic myelomonocytic leukemia (CMML), which was serially trans
124 ras G12D/+ bone marrow cells develop chronic myelomonocytic leukemia (CMML), while approximately 8% o
125 ng the myeloproliferative variant of chronic myelomonocytic leukemia (CMML), with a prolonged latency
126 NRAS rapidly and efficiently induced chronic myelomonocytic leukemia (CMML)- or acute myeloid leukemi
136 ent in acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML)/atypical chronic myelogen
137 yeloid malignancies, particularly in chronic myelomonocytic leukemia (CMML; 48%) and MDS/MPD-unclassi
139 y members are frequently mutated in juvenile myelomonocytic leukemia (JMML) and acute myeloid leukemi
140 features that overlap with those of juvenile myelomonocytic leukemia (JMML) and chronic myelomonocyti
141 acute lymphoblastic leukemia (ALL), juvenile myelomonocytic leukemia (JMML) and LEOPARD syndrome freq
142 hildren with NF1 are predisposed to juvenile myelomonocytic leukemia (JMML) and lethally irradiated m
143 matopoietic malignancies, including juvenile myelomonocytic leukemia (JMML) and T-cell lymphoblastic
144 ctive RAS signaling is prevalent in juvenile myelomonocytic leukemia (JMML) and the myeloproliferativ
145 myelomonocytic leukemia (CMML) and juvenile myelomonocytic leukemia (JMML) are myelodysplastic syndr
146 ) hypersensitivity is a hallmark of juvenile myelomonocytic leukemia (JMML) but has not been systemat
147 ndividuals with Noonan syndrome and juvenile myelomonocytic leukemia (JMML) have germline mutations i
163 myelodysplastic syndrome (MDS) and juvenile myelomonocytic leukemia (JMML) treated in a uniform fash
164 ting the molecular underpinnings of juvenile myelomonocytic leukemia (JMML) with the generation of in
165 own to underlie the pathogenesis of juvenile myelomonocytic leukemia (JMML), a fatal childhood diseas
166 s individuals to the development of juvenile myelomonocytic leukemia (JMML), a fatal myeloproliferati
167 PTPN11 (SHP-2) are associated with juvenile myelomonocytic leukemia (JMML), a myeloproliferative dis
168 sis type 1 (NF1) are predisposed to juvenile myelomonocytic leukemia (JMML), an aggressive myeloproli
169 al investigate the pathogenesis of juvenile myelomonocytic leukemia (JMML), demonstrating that mutan
170 ood acute leukemias, in addition to juvenile myelomonocytic leukemia (JMML), which is a myeloprolifer
179 nd the myeloproliferative variant of chronic myelomonocytic leukemia (MP-CMML) in humans, and both ar
180 ures and outcomes of therapy-related chronic myelomonocytic leukemia (t-CMML) and compare with those
181 ease: hematologic (MDS 84%, AML 14%, chronic myelomonocytic leukemia 8%), infectious (severe viral 70
183 tions are rare in pediatric MDS and juvenile myelomonocytic leukemia and are unlikely to operate as d
184 e-1 (FIP1L1)-PDGFRalpha, which cause chronic myelomonocytic leukemia and hypereosinophilic syndrome,
185 tantly, Bcl11a is expressed in human chronic myelomonocytic leukemia and juvenile myelomonocytic leuk
186 closely related neoplasms (including chronic myelomonocytic leukemia and MDS-myeloproliferative neopl
187 We found missense mutations in 2 juvenile myelomonocytic leukemia cases and in 1 child with system
188 uting to the pathogenesis of NS and juvenile myelomonocytic leukemia caused by PTPN11 gain-of-functio
189 MLL-AF6 leukemias as well as in ML2, a human myelomonocytic leukemia cell line bearing the t(6;11)(q2
192 detection of shared origin of LCH and acute myelomonocytic leukemia driven by TET2-mutant CD34(+) ce
197 n 161 of 1458 patients (11%); 26% of chronic myelomonocytic leukemia patients harbored 7q uniparental
199 Decitabine's mechanism of action in chronic myelomonocytic leukemia remains incompletely understood.
203 actory acute myelogenous leukemia or chronic myelomonocytic leukemia were treated with 10.36 to 37.0
204 mia [RA]/RA with ringed sideroblasts/chronic myelomonocytic leukemia with < 5% bone marrow blasts, 63
208 ferative neoplasm (SM-MPN), 36 (29%) chronic myelomonocytic leukemia, 28 (23%) myelodysplastic syndro
209 clinical and molecular features with chronic myelomonocytic leukemia, a similar disease in adults.
210 liferative neoplasm (MPN), including chronic myelomonocytic leukemia, according to the International
212 n specific human cancers, including juvenile myelomonocytic leukemia, an aggressive myeloproliferativ
213 tic AML, 7 (13%) of 52 patients with chronic myelomonocytic leukemia, and 1 (1%) of 68 patients with
214 h myelodysplastic syndrome, 118 with chronic myelomonocytic leukemia, and 126 with acute myeloid leuk
215 roblasts, TET2/SRSF2 comutation with chronic myelomonocytic leukemia, and activating CSF3R mutation w
216 All subtypes of myelodysplasia, chronic myelomonocytic leukemia, and acute myeloid leukemia with
217 re common in acute myeloid leukemia, chronic myelomonocytic leukemia, and myelodysplastic syndrome.
218 r gene is frequently inactivated in juvenile myelomonocytic leukemia, and Nf1 mutant mice model this
219 ted with marked thrombocytosis, and juvenile myelomonocytic leukemia, are clonal hematologic diseases
220 tive neoplasms (MDS/MPNs), including chronic myelomonocytic leukemia, atypical chronic myeloid leukem
221 ectively analyzed 110 patients with juvenile myelomonocytic leukemia, given single-unit, unrelated do
223 ons occur in children with sporadic juvenile myelomonocytic leukemia, myelodysplasic syndrome, B-cell
224 s SM-MPN, systemic mastocytosis with chronic myelomonocytic leukemia, SM-MDS, and systemic mastocytos
225 ed in human leukemias, particularly juvenile myelomonocytic leukemia, which is characterized by hyper
226 antation model efficiently induces a chronic myelomonocytic leukemia- or acute myeloid leukemia-like
252 sented the spectrum of therapy-induced acute myelomonocytic leukemia/chronic myelomonocytic leukemia/
253 nduced acute myelomonocytic leukemia/chronic myelomonocytic leukemia/myelodysplastic/myeloproliferati
254 true NK-cell tumors (n = 18), de novo acute myelomonocytic leukemias (1 of 14, 7%), or mature T-cell
255 uch as chronic myelogenous (CML) and chronic myelomonocytic leukemias (CMML) are frequently induced b
256 derived colonies in 28 patients with chronic myelomonocytic leukemias (CMML), the most frequent MPN/M
258 ptor (TEL-PDGFbetaR) is expressed in chronic myelomonocytic leukemias associated with t(5;12)(q33;p13
260 ave shown that MCK-2-enhanced recruitment of myelomonocytic leukocytes with an immature phenotype occ
261 rin CD11b is a differentiation marker of the myelomonocytic lineage and an important mediator of infl
262 ominantly expressed in immature cells of the myelomonocytic lineage and in a subset of CD11b (Mac-1)-
263 is an autoinflammatory syndrome in which the myelomonocytic lineage appears to play a pivotal role.
264 Potential immunomodulatory receptors on myelomonocytic lineage cells that bind extracellular Hsp
266 lves with sialic acids, which can engage the myelomonocytic lineage inhibitory receptor Siglec-9, the
267 HPCs impaired their differentiation into the myelomonocytic lineage, it potently promoted hemoglobin
272 identified the presence of B cells, several myelomonocytic lineages, fibroblast and epithelial cell
274 uce macrophage morphology or upregulation of myelomonocytic markers in U937 cells, suggesting that th
278 c-KIT and provide the first animal model of myelomonocytic neoplasia initiated by human KIT(D816V).
280 sults confirmed that the infiltrate was of a myelomonocytic origin, and a diagnosis of acute myelomon
282 retrovirus-induced myeloid leukemias of the myelomonocytic phenotype were found to have hypermethyla
284 vitro, HOXB6 immortalized a factor-dependent myelomonocytic precursor capable of granulocytic and mon
286 only fractions containing c-kit(+) immature myelomonocytic precursors are capable of contributing to
287 for PU.1 has been shown to cause a shift in myelomonocytic progenitor fate toward the myeloid lineag
288 in primary murine marrow immortalizes a late myelomonocytic progenitor, preventing it from executing
292 ost response and causes a marked increase in myelomonocytic recruitment with an immature phenotype to
293 previously unidentified impact of inhibitory myelomonocytic Siglecs in cancer biology, with distinct
294 To investigate the function of inhibitory myelomonocytic Siglecs in vivo we studied mouse Siglec-E
296 lete TFPI-K1 in endothelial (TFPI(Tie2)) and myelomonocytic (TFPI(LysM)) cells resulted in viable and
297 ray of cytokines in stably transfected human myelomonocytic U937 cells in response to other TLR agoni
298 tigated by examining the localization of pro-myelomonocytic U937 cells into synovial tissue transplan
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