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2 tional T cells and sustained gene marking in myeloid and B-cell lineages up to 20 months of observati
3 he NOD-like receptor family, is expressed in myeloid and bone marrow cells and was implicated as a ch
7 sive molecular disease detection in selected myeloid and lymphoid neoplasms, with a focus on the curr
8 f commitment, resolving how innate lymphoid, myeloid, and dendritic, and B-cell fate alternatives are
9 alysis of these cultures indicates lymphoid, myeloid, and erythroid differentiation, indicating that
10 ating that Myd88 and FcRgamma, presumably on myeloid APCs, were required to downregulate T cell help
11 eactivation and downstream production of the myeloid attractant CCL2 in BRAFi-resistant melanoma cell
14 loid bone marrow cells restore quiescence of myeloid-biased HSCs, with implications for blood disorde
16 e-dependent feedback mechanism through which myeloid bone marrow cells restore quiescence of myeloid-
17 icities of the human and murine forms of the myeloid C-type lectin receptor langerin for simple and c
18 tions tend to occur in the founding clone of myeloid cancers, and these mutations have recently been
19 we identified changes in tumor-infiltrating myeloid cell (TIM) subsets that likely compromise anti-t
20 llel with depression of serum markers of the myeloid cell activation, such as CCL5, CCL11, and C-X-C
21 umor gene expression signatures specific for myeloid cell chemotaxis and homeostasis reappeared in BR
24 molecular transcriptome switch that controls myeloid cell differentiation and maturation and that mal
25 iR-155 collaborates with FLT3-ITD to promote myeloid cell expansion in vivo and that this involves a
28 with expression of the BCL-2 family members myeloid cell leukemia 1 (MCL-1) and BCL-XL in lymphoma c
29 cellular signal-regulated kinase+/BCL-XL(+) /myeloid cell leukemia 1+ signature, deregulated in Alb-R
30 -PTP1B(-/-) mice lacking PTP1B in the innate myeloid cell lineage displayed a dysregulation of bone m
31 erized by excess accumulation of one or more myeloid cell lineages and a tendency to transform to acu
32 om NFI-A myeloid cell-deficient mice impeded myeloid cell maturation and promoted immune repressor fu
34 rowth factor receptor 1 positive (VEGFR1(+)) myeloid cell recruitment and pro-metastatic protein expr
35 ce of GMP and MDP differentiation shapes the myeloid cell repertoire during homeostasis and following
37 r results identify RXR as a regulator in the myeloid cell-assisted metastatic process and establish l
38 n of NFI-A in myeloid progenitors from NFI-A myeloid cell-deficient mice impeded myeloid cell maturat
39 noclonal antibodies, KWAR23 greatly augments myeloid cell-dependent killing of a collection of hemato
43 /f) and Villin-CreER(T2); Egfr(f/f) mice) or myeloid cells (LysM-Cre; Egfr(f/f) mice) on a mixed back
46 gene TREM2 (triggering receptor expressed on myeloid cells 2) confer greatly elevated risk for develo
49 FR1-dependent accumulation of CD11b-positive myeloid cells and higher expression of the VEGFR1 ligand
50 ed human colorectal tumors for EGFR-positive myeloid cells and investigated their association with pa
52 S100A9 inhibits B lymphopoiesis by acting on myeloid cells and promoting the release of inflammatory
53 that Aid loss in mice leads to expansion of myeloid cells and reduced erythroid progenitors resultin
54 alendronate in PLN reversed these effects on myeloid cells and shifted the profile of multi-cytokine
56 on of PD-L1 expression in tumor-infiltrating myeloid cells and, therefore, reprogramming of PGE2 meta
57 oliferation and function by immunoregulatory myeloid cells are an essential means of preventing self-
59 port that bone marrow (BM) Gr-1(lo) immature myeloid cells are responsible for the elevated, patholog
63 enewal ability and leukemogenesis of MLL-Af4 myeloid cells could contribute to the strong B-cell ALL
69 n and functions of infiltrating and resident myeloid cells in GBM, establishing a rationale to target
73 on of canonical NF-kappaB signaling (p65) in myeloid cells inhibited syngeneic glioblastoma (GBM) thr
74 Human cytomegalovirus (HCMV) infection of myeloid cells is closely linked with the differentiation
75 show that translation of VEGFA mRNA in human myeloid cells is dictated by a bi-directional interactio
79 varian adenocarcinoma, Gadd45b inhibition in myeloid cells restored activation of proinflammatory tum
81 nthase (iNOS) generates nitric oxide (NO) in myeloid cells that acts as a defense mechanism to suppre
82 belong to a lineage of adult tissue-resident myeloid cells that develop during organogenesis from yol
83 cted keratinocytes attracts virus-permissive myeloid cells that inadvertently spread DENV infection.
84 on of HIV-1 was rescued in IFN-alpha-treated myeloid cells via upregulation of CD169 and a subsequent
86 e pattern of involvement of peripheral blood myeloid cells was indistinguishable between LCH and ECD,
88 activation in NF-kappaB sensor cells, THP-1 myeloid cells, and primary human B cells as well as in m
89 ration and permeability of tumor-stimulatory myeloid cells, and suppressed EC-mediated stimulation of
90 dramatic increase in fat, increased CD11b(+) myeloid cells, and upregulated expression of the inflamm
91 s study, we find that activation of NLRP3 in myeloid cells, but not mesenchymal cells triggers chroni
92 progenitor populations produce lymphoid and myeloid cells, but they remain incompletely characterize
95 -regulation of fatty acid oxidation (FAO) in myeloid cells, including macrophages and granulocytic an
96 by accumulation of CD11b(+)Gr-1(+) immature myeloid cells, indicating a potential antitumorigenic ef
97 inflammatory monocytes, but not DCs or other myeloid cells, resulted in lower levels of IL-18 and a c
98 del in which FlnA is selectively depleted in myeloid cells, such as neutrophils, we show that FlnA ne
99 and thereby enhanced migration of VEGFR1(+) myeloid cells, which were reversed by siRNA or pharmacol
110 f these patients experienced declining donor myeloid chimerism (DMC) levels with eventual return of d
111 itioning recipients have better B-lymphocyte/myeloid chimerism and are free from immunoglobulin repla
112 leads to transcriptomic changes in the lung myeloid compartment characterized by increased expressio
113 ts meningeal coverings accommodate a diverse myeloid compartment that includes parenchymal microglia
117 nt mutation, JAK2V617F, activates the 3 main myeloid cytokine receptors (erythropoietin receptor, gra
119 etween the main DC subsets, plasmacytoid and myeloid DCs (mDCs) was necessary for increased chemokine
120 that developed spontaneous stroke because of myeloid deficiency of TGF-beta (transforming growth fact
122 erferon (IFN-gamma), TNF-alpha, and IL-12 in myeloid dendritic cells are of importance in generating
124 llowing for constitutive Nlrp3 activation in myeloid derived cells in mice deficient in IL-17 or TNF.
125 e activation, have an increased frequency of myeloid derived suppressor cells (MDSC) and are at incre
129 d with tumor-associated macrophage (TAM) and myeloid-derived suppressor cell (MDSC) infiltration in t
130 hepatic stellate cells allowed generation of myeloid-derived suppressor cells (MDSC) from precursors
132 arrier to efficacy may be the recruitment of myeloid-derived suppressor cells (MDSC) into the tumor m
134 KDR expression increased in myeloid cells as myeloid-derived suppressor cells (MDSCs) accumulated, wh
137 decreased the frequency of immunosuppressive myeloid-derived suppressor cells in a syngeneic TNBC mou
138 he expansion of neutrophils and granulocytic myeloid-derived suppressor cells in the tumor microenvir
139 (mMDSC) and granulocytic (gMDSC) subsets of myeloid-derived suppressor cells infiltrate in the prima
140 n of reactive oxygen species in granulocytic myeloid-derived suppressor cells, whereas the antioxidan
143 , we reevaluated the role of RelB in cDC and myeloid development using a series of radiation chimeras
146 ts from mice with genetic deletion of MyD88 (myeloid differentiation factor 88) or TLRs (Toll-like re
147 hat upregulation of GFI1 expression leads to myeloid differentiation morphologically and immunophenot
148 iver genes while also confirming the role of myeloid differentiation primary response gene 88 in the
149 f it lacks the innate defense protein MyD88 (myeloid differentiation primary response gene 88), or af
150 LR2 polymorphism alters the functions of the myeloid differentiation primary response protein 88 (MyD
155 atenin in hematopoietic cells yielded lethal myeloid disease in a NUP98-HOXD13 mouse model of MDS, co
159 cant elevation of the soluble form of MerTK (myeloid-epithelial-reproductive tyrosine kinase; ie, sol
160 dysregulated expression of Cebpa and Gata1, myeloid/erythroid lineage-specific transcription factors
167 ardiac inflammation as a result of increased myeloid invading injured myocardium in response to MI.
168 marrow cancer cells from patients with acute myeloid leukaemia (AML) and induce the differentiation o
169 sponse of leukocytes in bone marrow of acute myeloid leukaemia (AML) patients, and the complex immune
170 cation mutations in FLT3 are common in acute myeloid leukaemia and are associated with rapid relapse
172 5 years) patients with treatment-naive acute myeloid leukaemia who were not candidates for intensive
174 icacy in myelodysplastic syndromes and acute myeloid leukaemia, but complete tumour responses are inf
181 o xenobiotic nucleosides used to treat acute myeloid leukemia (AML) and other cancers remains a major
182 in of and a key therapeutic target for acute myeloid leukemia (AML) and other forms of cancer.(1-4) T
183 engraftment of primary patient-derived acute myeloid leukemia (AML) and other hematologic malignancie
184 etic stem/progenitor cells (HSPCs) and acute myeloid leukemia (AML) cells carrying t(11q23), t(15;17)
194 tor (CAR) T cells in preclinical human acute myeloid leukemia (AML) models at the cost of severe hema
196 ession profiling analysis of 542 human acute myeloid leukemia (AML) samples and identified 55% with u
197 echanisms offer therapeutic targets in acute myeloid leukemia (AML) that are of great current interes
198 ished a mouse xenograft model of human acute myeloid leukemia (AML) that enabled chemotherapy-induced
199 EG20) in relapsed/refractory/poor-risk acute myeloid leukemia (AML) was evaluated in 43 patients in a
200 e patients with relapsed or refractory acute myeloid leukemia (AML) were enrolled between January 201
202 Patients with SCN are predisposed to acute myeloid leukemia (AML), and progression from SCN to AML
204 -ALL and T-ALL, respectively), but not acute myeloid leukemia (AML), in mouse models of these tumors.
205 -075 efficiently triggers apoptosis in acute myeloid leukemia (AML), non-Hodgkin lymphoma, and multip
214 l hematologic malignancies including chronic myeloid leukemia (CML) and myelodysplastic syndromes (MD
215 the LSC population in chronic phase chronic myeloid leukemia (CML) patients at diagnosis and followi
216 ibitors (TKI) changed the outcome of chronic myeloid leukemia (CML), turning a life-threatening disea
217 ve clonal hematopoiesis resembling a chronic myeloid leukemia (CML)-like disease manifesting in "lymp
219 merge as patients with chronic phase chronic myeloid leukemia (CP-CML) are treated with tyrosine kina
220 bitors in a model of Kras(G12D) mutant acute myeloid leukemia and propose its use as a predictive bio
221 the role of clonal evolution in lymphoid and myeloid leukemia as a driver of tumor initiation, diseas
222 ATS-DVR to RNA-seq data of the human chronic myeloid leukemia cell line K562 in response to shRNA kno
223 nticancer activity was demonstrated in acute myeloid leukemia cell lines, where significant impairmen
225 7f inhibited the growth of acute and chronic myeloid leukemia cells and the phosphorylation and trans
228 on of the BCR-ABL1 fusion delineates chronic myeloid leukemia from classic BCR-ABL1(-) MPNs, which ar
231 ailed picture of the BM vasculature in acute myeloid leukemia using intravital two-photon microscopy.
233 gene is associated typically with aggressive myeloid leukemia, but is also detectable in breast carci
234 ers, including secondary glioblastoma, acute myeloid leukemia, intrahepatic cholangiocarcinoma, and c
235 odgkin lymphoma, non-Hodgkin lymphoma, acute myeloid leukemia, soft-tissue sarcoma, and central nervo
243 ivation in mice is sufficient to drive acute myeloid leukemia.Significance: This study defines a tumo
244 al trials investigating primary murine acute myeloid leukemias (AMLs) generated by retroviral inserti
250 ischemic muscles at day 2 revealed increased myeloid lineage cells in ECFC + MPC-injected muscles com
251 ish a tumor suppressor role for PTP1B in the myeloid lineage cells, with evidence that its genetic in
252 or the protein tyrosine phosphatase PTP1B in myeloid lineage cells, with evidence that its genetic in
254 e CD39-overexpressing mice (transgenic, n=9; myeloid lineage, n=6) demonstrated significantly smaller
255 across all progenitors was required for the myeloid lineage, whereas the other leukemia-induced lncR
258 function and structure, including skewing to myeloid lineages, lower reconstitution potential and los
259 ed with adjuvant RAI should be monitored for myeloid malignancies as part of cancer surveillance.
260 at CNL has much in common with other chronic myeloid malignancies at the genetic level, such as the c
261 iers and signaling factors often co-occur in myeloid malignancies, including TET2 and NRAS mutations.
266 elevance in the context of chronic and acute myeloid malignancies; (3) age-related niche changes and
267 udy niche-leukemic cell interaction in human myeloid malignancies; and finally, (5) how the knowledge
268 CD45(+) Ly6C(hi) CD11b(+) CCR2(+) activated myeloid mononuclear cells (MMCs) and the levels of proin
269 brain and that a subset of peripheral blood myeloid mononuclear cells represent a key effector cell
271 cantly increased the risk of therapy-related myeloid neoplasm development (hazard ratio 13.7, 95% CI
272 ween clonal haemopoiesis and therapy-related myeloid neoplasm development, we also analysed the preva
274 therapy, and did not develop therapy-related myeloid neoplasms after at least 5 years of follow-up.
276 the cumulative incidence of therapy-related myeloid neoplasms at 10 years was significantly higher i
279 G-CSFRs associated with SCN/AML may protect myeloid precursor cells from apoptosis induced by the NE
280 ved common lymphoid progenitor (CLP), common myeloid progenitor (CMP), megakaryocyte-erythroid progen
281 air of our bones are formed from bone marrow myeloid progenitor cells by a complex differentiation pr
282 p during organogenesis from yolk-sac erythro-myeloid progenitors (EMPs) distinct from haematopoietic
284 In contrast, ectopic expression of NFI-A in myeloid progenitors from NFI-A myeloid cell-deficient mi
288 ther manipulations, Dnmt3a+/- mice developed myeloid skewing over time, and their hematopoietic stem/
290 In this study, we report that global or myeloid-specific deficiency of PTP1B in mice decreases l
291 d LDL receptor-deficient (Ldlr-/-) mice with myeloid-specific deletion of CaMKII had smaller necrotic
293 gradation, because neither MMB treatment nor myeloid-specific deletion of JAK2 affected FPN1 expressi
294 c M2 macrophage activation was diminished in myeloid-specific Egfr-deficient mice, as marked by decre
295 al regulatory protein-alpha (SIRPalpha) is a myeloid-specific immune checkpoint that engages the "don
298 D) expression in hematopoietic cells induced myeloid transformation, with a fully penetrant, lethal c
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