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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 signature includes discrete changes in B and myelomonocytic cell composition, profoundly altered T ce
12 the myeloid compartment that evoked a clonal myelomonocytic cell expansion, splenomegaly, multi-organ
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 and highlight Ccr2 as the primary driver of myelomonocytic cell recruitment in acutely inflamed cont
22 eam to salivary glands and is dependent on a myelomonocytic cell type other than mature macrophages.
23 ) ASCs in the medullary cords migrated along myelomonocytic cells and arrested in contact with them.
25 mistry of lung autopsy samples revealed that myelomonocytic cells and endothelial cells express high
29 ne expression in monocytes, macrophages, and myelomonocytic cells as well as in epidermal keratinocyt
30 e and found EYFP gene expression not only in myelomonocytic cells but also in a fraction of HSCs as w
31 y described a mouse line that contains green myelomonocytic cells due to the knock-in of enhanced gre
32 dissect the branching between erythroid and myelomonocytic cells during in vitro differentiation of
33 grade Abeta(1-42), and ACE overexpression in myelomonocytic cells enhances their immune function.
34 Macrophages, THP-1 cells, and other human myelomonocytic cells expressed both PLD1 and PLD2 protei
35 o generate large numbers of patient-specific myelomonocytic cells for in vitro studies of human disea
36 porting this hypothesis, Siglec-9-expressing myelomonocytic cells found in human tumor samples were a
37 a similar protocol could be used to generate myelomonocytic cells from induced pluripotent stem cells
40 tions, spanning progenitor to mature myeloid/myelomonocytic cells in normal bone marrows with further
44 sults provide direct evidence that committed myelomonocytic cells such as macrophages can produce fun
46 iocytes (FLS) cell lines that were bereft of myelomonocytic cells to examine whether mesenchymal-deri
47 nctional analyses revealed that hESC-derived myelomonocytic cells were comparable to their correspond
49 to ILT4 leads to a tolerogenic phenotype of myelomonocytic cells with lower surface expression of de
50 cognition by innate MHC class I receptors on myelomonocytic cells, and functional impairment of DCs,
51 on maternal uterine natural killer (NK) and myelomonocytic cells, CD94/NKG2, leukocyte immunoglobuli
54 ifferentiation in certain cell types, namely myelomonocytic cells, osteoblasts, skeletal muscle cells
56 ermore, GATA-1 induced apoptosis of proB and myelomonocytic cells, which could not be prevented by en
68 and C/EBPalpha (Cebpa) have general roles in myelomonocytic development, but the transcriptional basi
72 lso been described, but a role for TIMP-1 in myelomonocytic differentiation has not been previously r
73 ology, and exhibited increased expression of myelomonocytic differentiation markers, including CD11b,
74 action of pro-T cells possess plasticity for myelomonocytic differentiation that can be activated by
75 ogenitors expressing activating Shp2 undergo myelomonocytic differentiation, despite being subjected
76 uration arrest at an identical late stage of myelomonocytic differentiation, putatively a monopotent
77 rylation, expression of RIG-E and RIG-G, and myelomonocytic differentiation-specific down-regulation
80 nced immune response, coupled with increased myelomonocytic expression of catalytically active ACE, p
81 ltipotential progenitor cell maintenance and myelomonocytic fate and suggests Glut1 as potential drug
82 ts EPO-stimulated HSCs to differentiate into myelomonocytic fates, altering in vivo HSC responses and
83 le attractors corresponding to erythroid and myelomonocytic fates, as well as an uncommitted metastab
85 ere mainly mediated by interactions with the myelomonocytic HLA class I receptor leukocyte immunoglob
86 -N-nitrosourea (ENU), MLL-CBP mice developed myelomonocytic hyperplasia and progressed to fatal myelo
87 MDS/MPN overlap syndromes including chronic myelomonocytic leukaemia (CMML), acute myeloid leukaemia
88 of developing leukaemia, especially juvenile myelomonocytic leukaemia (JMML), a childhood myeloprolif
89 ere applied to BALB/c mice with transplanted myelomonocytic leukaemia (WEHI-3) and Human promyelocyti
90 astic syndromes or non-proliferative chronic myelomonocytic leukaemia (white blood cell count <13 000
91 blasts (RAEB)-1, RAEB-2, RAEB-t, or chronic myelomonocytic leukaemia based on local site assessment,
92 ed after myelodysplastic syndrome or chronic myelomonocytic leukaemia); and relapsed or refractory AM
93 in 2 of 110 cases of non-syndromic juvenile myelomonocytic leukaemia, a childhood myeloproliferative
94 with blast-phase disease), one with chronic myelomonocytic leukaemia, and seven with myelofibrosis.
95 eukaemia, chronic myeloid leukaemia, chronic myelomonocytic leukaemia, myelodysplastic syndrome, or m
100 agnosed myelodysplastic syndromes or chronic myelomonocytic leukaemia; 43 of the enrolled patients we
101 ximately 75% incidence) and SRSF2 in chronic myelomonocytic leukemia ( approximately 28% incidence).
102 ed patients with higher-risk MDS and chronic myelomonocytic leukemia (CMML) 1:1:1 to azacitidine (75
104 s of myeloid malignancies resembling chronic myelomonocytic leukemia (CMML) and myelodysplastic syndr
105 B fusion oncogene is associated with chronic myelomonocytic leukemia (CMML) and results in the expres
106 ations in 5% and 9% of patients with chronic myelomonocytic leukemia (CMML) and sAML, and also in CML
110 mouse model resemble those of human chronic myelomonocytic leukemia (CMML) in its transformation to
117 myeloid leukemia (AML) patients, 32 chronic myelomonocytic leukemia (CMML) patients, and 96 healthy
120 Human ASXL1 is mutated frequently in chronic myelomonocytic leukemia (CMML) so an ASXL/BAP1 complex m
121 k myelodysplastic syndromes (MDS) or chronic myelomonocytic leukemia (CMML) were randomized 1:1 to re
123 omic DNA from 245 patients--119 with chronic myelomonocytic leukemia (CMML), 101 with MDS, 11 with hy
124 oring systems have been proposed for chronic myelomonocytic leukemia (CMML), a disease in which some
126 myeloproliferative neoplasms (MPNs), chronic myelomonocytic leukemia (CMML), and acute myeloid leukem
127 (CLL), acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML), colorectal cancer, endom
128 e myelomonocytic leukemia (JMML) and chronic myelomonocytic leukemia (CMML), including identical soma
129 tion, with a fully penetrant, lethal chronic myelomonocytic leukemia (CMML), which was serially trans
130 ras G12D/+ bone marrow cells develop chronic myelomonocytic leukemia (CMML), while approximately 8% o
131 ng the myeloproliferative variant of chronic myelomonocytic leukemia (CMML), with a prolonged latency
132 NRAS rapidly and efficiently induced chronic myelomonocytic leukemia (CMML)- or acute myeloid leukemi
141 ent in acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML)/atypical chronic myelogen
142 yeloid malignancies, particularly in chronic myelomonocytic leukemia (CMML; 48%) and MDS/MPD-unclassi
143 lts with MDS/MPN subtypes, including chronic myelomonocytic leukemia (CMML; n = 119), atypical chroni
144 y members are frequently mutated in juvenile myelomonocytic leukemia (JMML) and acute myeloid leukemi
145 features that overlap with those of juvenile myelomonocytic leukemia (JMML) and chronic myelomonocyti
146 acute lymphoblastic leukemia (ALL), juvenile myelomonocytic leukemia (JMML) and LEOPARD syndrome freq
147 hildren with NF1 are predisposed to juvenile myelomonocytic leukemia (JMML) and lethally irradiated m
148 matopoietic malignancies, including juvenile myelomonocytic leukemia (JMML) and T-cell lymphoblastic
149 ctive RAS signaling is prevalent in juvenile myelomonocytic leukemia (JMML) and the myeloproliferativ
150 myelomonocytic leukemia (CMML) and juvenile myelomonocytic leukemia (JMML) are myelodysplastic syndr
151 ) hypersensitivity is a hallmark of juvenile myelomonocytic leukemia (JMML) but has not been systemat
152 ndividuals with Noonan syndrome and juvenile myelomonocytic leukemia (JMML) have germline mutations i
169 myelodysplastic syndrome (MDS) and juvenile myelomonocytic leukemia (JMML) treated in a uniform fash
170 ting the molecular underpinnings of juvenile myelomonocytic leukemia (JMML) with the generation of in
171 own to underlie the pathogenesis of juvenile myelomonocytic leukemia (JMML), a fatal childhood diseas
172 s individuals to the development of juvenile myelomonocytic leukemia (JMML), a fatal myeloproliferati
173 PTPN11 (SHP-2) are associated with juvenile myelomonocytic leukemia (JMML), a myeloproliferative dis
174 sis type 1 (NF1) are predisposed to juvenile myelomonocytic leukemia (JMML), an aggressive myeloproli
175 al investigate the pathogenesis of juvenile myelomonocytic leukemia (JMML), demonstrating that mutan
176 ood acute leukemias, in addition to juvenile myelomonocytic leukemia (JMML), which is a myeloprolifer
184 nd the myeloproliferative variant of chronic myelomonocytic leukemia (MP-CMML) in humans, and both ar
185 ures and outcomes of therapy-related chronic myelomonocytic leukemia (t-CMML) and compare with those
186 ease: hematologic (MDS 84%, AML 14%, chronic myelomonocytic leukemia 8%), infectious (severe viral 70
188 tions are rare in pediatric MDS and juvenile myelomonocytic leukemia and are unlikely to operate as d
189 e-1 (FIP1L1)-PDGFRalpha, which cause chronic myelomonocytic leukemia and hypereosinophilic syndrome,
190 tantly, Bcl11a is expressed in human chronic myelomonocytic leukemia and juvenile myelomonocytic leuk
191 closely related neoplasms (including chronic myelomonocytic leukemia and MDS-myeloproliferative neopl
192 We found missense mutations in 2 juvenile myelomonocytic leukemia cases and in 1 child with system
193 uting to the pathogenesis of NS and juvenile myelomonocytic leukemia caused by PTPN11 gain-of-functio
194 MLL-AF6 leukemias as well as in ML2, a human myelomonocytic leukemia cell line bearing the t(6;11)(q2
197 detection of shared origin of LCH and acute myelomonocytic leukemia driven by TET2-mutant CD34(+) ce
203 n 161 of 1458 patients (11%); 26% of chronic myelomonocytic leukemia patients harbored 7q uniparental
205 Decitabine's mechanism of action in chronic myelomonocytic leukemia remains incompletely understood.
209 actory acute myelogenous leukemia or chronic myelomonocytic leukemia were treated with 10.36 to 37.0
210 mia [RA]/RA with ringed sideroblasts/chronic myelomonocytic leukemia with < 5% bone marrow blasts, 63
214 ferative neoplasm (SM-MPN), 36 (29%) chronic myelomonocytic leukemia, 28 (23%) myelodysplastic syndro
215 clinical and molecular features with chronic myelomonocytic leukemia, a similar disease in adults.
216 liferative neoplasm (MPN), including chronic myelomonocytic leukemia, according to the International
218 n specific human cancers, including juvenile myelomonocytic leukemia, an aggressive myeloproliferativ
219 tic AML, 7 (13%) of 52 patients with chronic myelomonocytic leukemia, and 1 (1%) of 68 patients with
220 h myelodysplastic syndrome, 118 with chronic myelomonocytic leukemia, and 126 with acute myeloid leuk
221 roblasts, TET2/SRSF2 comutation with chronic myelomonocytic leukemia, and activating CSF3R mutation w
222 All subtypes of myelodysplasia, chronic myelomonocytic leukemia, and acute myeloid leukemia with
223 re common in acute myeloid leukemia, chronic myelomonocytic leukemia, and myelodysplastic syndrome.
224 ted with marked thrombocytosis, and juvenile myelomonocytic leukemia, are clonal hematologic diseases
225 tive neoplasms (MDS/MPNs), including chronic myelomonocytic leukemia, atypical chronic myeloid leukem
226 ectively analyzed 110 patients with juvenile myelomonocytic leukemia, given single-unit, unrelated do
228 ons occur in children with sporadic juvenile myelomonocytic leukemia, myelodysplasic syndrome, B-cell
229 s SM-MPN, systemic mastocytosis with chronic myelomonocytic leukemia, SM-MDS, and systemic mastocytos
230 ed in human leukemias, particularly juvenile myelomonocytic leukemia, which is characterized by hyper
231 antation model efficiently induces a chronic myelomonocytic leukemia- or acute myeloid leukemia-like
254 sented the spectrum of therapy-induced acute myelomonocytic leukemia/chronic myelomonocytic leukemia/
255 nduced acute myelomonocytic leukemia/chronic myelomonocytic leukemia/myelodysplastic/myeloproliferati
256 true NK-cell tumors (n = 18), de novo acute myelomonocytic leukemias (1 of 14, 7%), or mature T-cell
257 uch as chronic myelogenous (CML) and chronic myelomonocytic leukemias (CMML) are frequently induced b
258 derived colonies in 28 patients with chronic myelomonocytic leukemias (CMML), the most frequent MPN/M
260 ptor (TEL-PDGFbetaR) is expressed in chronic myelomonocytic leukemias associated with t(5;12)(q33;p13
262 ave shown that MCK-2-enhanced recruitment of myelomonocytic leukocytes with an immature phenotype occ
263 rin CD11b is a differentiation marker of the myelomonocytic lineage and an important mediator of infl
264 is an autoinflammatory syndrome in which the myelomonocytic lineage appears to play a pivotal role.
265 Potential immunomodulatory receptors on myelomonocytic lineage cells that bind extracellular Hsp
267 lves with sialic acids, which can engage the myelomonocytic lineage inhibitory receptor Siglec-9, the
268 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).
279 sults confirmed that the infiltrate was of a myelomonocytic origin, and a diagnosis of acute myelomon
281 retrovirus-induced myeloid leukemias of the myelomonocytic phenotype were found to have hypermethyla
283 vitro, HOXB6 immortalized a factor-dependent myelomonocytic precursor capable of granulocytic and mon
284 riving PD-L1 overexpression in both immature myelomonocytic precursors and committed CD206(+) macroph
285 only fractions containing c-kit(+) immature myelomonocytic precursors are capable of contributing to
286 for PU.1 has been shown to cause a shift in myelomonocytic progenitor fate toward the myeloid lineag
287 hifts in the frequencies of erythroid versus myelomonocytic progenitors following Tet2 or Dnmt3a loss
291 ost response and causes a marked increase in myelomonocytic recruitment with an immature phenotype to
292 previously unidentified impact of inhibitory myelomonocytic Siglecs in cancer biology, with distinct
293 To investigate the function of inhibitory myelomonocytic Siglecs in vivo we studied mouse Siglec-E
294 DNAme changes with specific erythroid versus myelomonocytic skews, we provide evidence in support of
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