ライフサイエンスコーパス: myeloid

1 Furthermore, the loss of myeloid AC protects from tumor incidence in colitis-asso

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

4 patients and were also present in downstream myeloid and erythroid progenitor cells.

5 with diverse potencies and can give rise to myeloid and lymphoid lineage progenitors.

6 on of hematopoietic stem cells (HSCs) to the myeloid and lymphoid lineages.

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

12 ng a unique molecular pathway that regulates myeloid bias in an extramedullary niche.

13 pulating activity of young HSCs and impart a myeloid bias.

14 loid bone marrow cells restore quiescence of myeloid-biased HSCs, with implications for blood disorde

15 We studied whether myeloid Bmal1 deletion promotes atherosclerosis by enhan

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

22 rotection allows for the identification of a myeloid cell contribution to tissue repair.

23 es PU.1, a transcription factor critical for myeloid cell development and function.

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

26 ce lacking IRF3 also developed lung disease, myeloid cell expansion, and T cell cytopenia.

27 red as a result of reduced demyelination and myeloid cell infiltration into the CNS tissue.

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

33 SMA, implying a differential role of SMN in myeloid cell ontogeny.

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

36 e responses and differential infiltration of myeloid cell subsets.

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

40 data to foster our understanding of lymphoid/myeloid cell-fate decisions.

41 Here, we reported that myeloid cell-specific Nrp1-deficient mice exhibited enha

42 To address this problem, we generated myeloid cell-specific Nrp1-knockout (Nrp1(myel-KO)) mice

43 /f) and Villin-CreER(T2); Egfr(f/f) mice) or myeloid cells (LysM-Cre; Egfr(f/f) mice) on a mixed back

44 Triggering receptor expressed on myeloid cells 2 (TREM2) is a single transmembrane molecu

45 Triggering receptor expressed on myeloid cells 2 (TREM2) is a transmembrane protein expre

46 gene TREM2 (triggering receptor expressed on myeloid cells 2) confer greatly elevated risk for develo

47 gene TREM2 (triggering receptor expressed on myeloid cells 2).

48 s acquire pathogenicity and communicate with myeloid cells and cells of the CNS remain unclear.

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

51 try and flow cytometry were used to identify myeloid cells and neuronal loss.

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

55 In vivo, myeloid cells and their progenitors are an important sit

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-

58 Furthermore, HD myeloid cells are hyper-reactive compared to control.

59 port that bone marrow (BM) Gr-1(lo) immature myeloid cells are responsible for the elevated, patholog

60 KDR expression increased in myeloid cells as myeloid-derived suppressor cells (MDSCs

61 In the absence of IL-27R myeloid cells become hyperactivated, produce pro-inflamm

62 ing IL-4Ralpha and IL-13Ralpha1 give rise to myeloid cells but not T cells.

63 enewal ability and leukemogenesis of MLL-Af4 myeloid cells could contribute to the strong B-cell ALL

64 The roles of these receptors in myeloid cells during B cell autoimmune activation remain

65 Both peripheral and intestinal myeloid cells expressed INAVA.

66 transient increase in a population of CD11b+ myeloid cells expressing HLA-DR, CD11c, and CX3CR1.

67 Increased expression of EGFR in myeloid cells from the colorectal tumor stroma associate

68 e for keratinocytes and their interplay with myeloid cells in dengue.

69 n and functions of infiltrating and resident myeloid cells in GBM, establishing a rationale to target

70 ressive inflammation in tumors by recruiting myeloid cells in part via the CCR2 pathway.

71 arity and a restored balance of lymphoid and myeloid cells in peripheral blood.

72 EGFR-deficient myeloid cells in the colon of DSS-treated LysM-Cre; Egfr

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

76 ne viral gene expressed by latently infected myeloid cells is US28.

77 Committed Hdc(+) myeloid cells lie in close anatomical proximity to MB-HS

78 oth together, had no impact on the number of myeloid cells migrating into the eye.

79 varian adenocarcinoma, Gadd45b inhibition in myeloid cells restored activation of proinflammatory tum

80 Ablation of Tet2 in myeloid cells suppressed melanoma growth in vivo and shi

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

85 Surface marker expression of CD11b+ myeloid cells was also assessed.

86 e pattern of involvement of peripheral blood myeloid cells was indistinguishable between LCH and ECD,

87 Primary ex vivo myeloid cells were isolated from heterozygous patients a

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

93 nodeficiency virus of macaques) infection of myeloid cells, even in the presence of Vpx.

94 understood interaction among megakaryocytes, myeloid cells, fibroblasts, and endothelial cells.

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

100 ransforming different types of lung-resident myeloid cells.

101 ulator of many facets of immune responses by myeloid cells.

102 turbations to prothrombotic TF activation on myeloid cells.

103 p of HIV-1 replication in T cells but not in myeloid cells.

104 he type I interferon receptor in a subset of myeloid cells.

105 urface expression of PD-L1 in epithelial and myeloid cells.

106 ring viral and bacterial infections in human myeloid cells.

107 ls and significantly decreased percentage of myeloid cells.

108 atory molecules, IL-1beta and S100A9, by the myeloid cells.

109 nd TNF (tumor necrosis factor) production by myeloid cells.

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

114 In spite of prominent changes in the myeloid compartment, the anti-CCR4 antibody did not affe

115 indicating a novel role for TREM2 in the non-myeloid compartment.

116 , unlike shown previously for the hemITAM of myeloid CTLR.

117 nt mutation, JAK2V617F, activates the 3 main myeloid cytokine receptors (erythropoietin receptor, gra

118 NOX5 was expressed in circulating myeloid DC, and at a lower level in plasmacytoid DC.

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

121 tions of tumor-infiltrating murine and human myeloid dendritic cells (TIDC) in ovarian cancer.

122 erferon (IFN-gamma), TNF-alpha, and IL-12 in myeloid dendritic cells are of importance in generating

123 Targeting of myeloid-dendritic cell receptor DC-SIGN by numerous chro

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

126 onstitutive NLRP3 inflammasome activation in myeloid-derived cells.

127 In myeloid-derived dendritic cells and macrophages as well

128 This myeloid-derived IL-1beta did not vitally contribute to t

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

131 Accumulation of myeloid-derived suppressor cells (MDSC) in melanoma micr

132 arrier to efficacy may be the recruitment of myeloid-derived suppressor cells (MDSC) into the tumor m

133 Myeloid-derived suppressor cells (MDSC), which expand du

134 KDR expression increased in myeloid cells as myeloid-derived suppressor cells (MDSCs) accumulated, wh

135 Myeloid-derived suppressor cells (MDSCs) described in ca

136 Human monocytic myeloid-derived suppressor cells (MO-MDSCs) within the h

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

141 g macrophages and granulocytic and monocytic myeloid-derived suppressor cells.

142 ing Tol-DC, Rapa-DC, DC-10, and PGE2-induced myeloid-derived suppressor cells.

143 , we reevaluated the role of RelB in cDC and myeloid development using a series of radiation chimeras

144 odeficient NSGS mice, which strongly promote myeloid development.

145 expansion of hematopoietic progenitors, and myeloid differentiation bias.

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

151 In the absence of TLR2, TLR4, myeloid differentiation response gene 88, or TRIF, the c

152 Here, we report that the myeloid differentiation-related transcription factor nuc

153 ;17), or t(8;21) and is downregulated during myeloid differentiation.

154 Myc function or sterol biosynthesis impaired myeloid differentiation.

155 atenin in hematopoietic cells yielded lethal myeloid disease in a NUP98-HOXD13 mouse model of MDS, co

156 ver hematopoietic progenitors give rise to a myeloid disease upon transplantation.

157 Mice lacking myeloid Drp1 showed defective efferocytosis and its path

158 tested post-HSCT (7/7), as early as day +14 (myeloid engraftment).

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

161 factor (IRF)-5 is an important modulator of myeloid function and programming.

162 220 cell types implicated the regulation of myeloid gene expression in AD risk.

163 m cell (HSC)-enriched LSK population but not myeloid-granulocyte progenitors.

164 SIGLEC5 is expressed in various myeloid immune cells and classified as an inhibitory rec

165 hese organelles in inflammatory responses of myeloid immune cells is largely unknown.

166 cancer cells, and its counter-receptor, the myeloid inhibitory immunoreceptor SIRPalpha.

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

171 The outcome acute myeloid leukaemia evolution or disease progression occur

172 5 years) patients with treatment-naive acute myeloid leukaemia who were not candidates for intensive

173 had a treatment-related adverse event (acute myeloid leukaemia) with an outcome of death.

174 icacy in myelodysplastic syndromes and acute myeloid leukaemia, but complete tumour responses are inf

175 y METTL3 in this way are necessary for acute myeloid leukaemia.

176 n patients with relapsed or refractory acute myeloid leukaemia.

177 as a potential therapeutic target for acute myeloid leukaemia.

178 ncephalopathy, neutropenic sepsis, and acute myeloid leukaemia]).

179 Patients with acute myeloid leukemia (AML) and a FLT3 mutation have poor out

180 The heterogeneous nature of acute myeloid leukemia (AML) and its poor prognosis necessitat

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)

185 Acute myeloid leukemia (AML) cells have increased mitochondria

186 Adults with acute myeloid leukemia (AML) commonly require support in the i

187 herapies, most patients diagnosed with acute myeloid leukemia (AML) die of their disease.

188 Purpose Elderly patients with acute myeloid leukemia (AML) have a poor prognosis, and innova

189 Previous studies in childhood acute myeloid leukemia (AML) have shown a negative correlation

190 In this study, using acute myeloid leukemia (AML) human cell lines and a custom CRI

191 Acute myeloid leukemia (AML) is a disease associated with epig

192 Acute myeloid leukemia (AML) is a major unmet medical need.

193 Childhood acute myeloid leukemia (AML) is frequently characterized by ch

194 tor (CAR) T cells in preclinical human acute myeloid leukemia (AML) models at the cost of severe hema

195 which is expressed in the majority of acute myeloid leukemia (AML) patients.

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

201 Purpose Children with acute myeloid leukemia (AML) whose disease is refractory to st

202 Patients with SCN are predisposed to acute myeloid leukemia (AML), and progression from SCN to AML

203 FLT3-mutated acute myeloid leukemia (AML), despite not being recognized as

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

206 Acute myeloid leukemia (AML), the most common adult acute leuk

207 In acute myeloid leukemia (AML), therapy resistance frequently oc

208 and salvage chemotherapy regimens for acute myeloid leukemia (AML).

209 ancers, including approximately 12% of acute myeloid leukemia (AML).

210 acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).

211 s of myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML).

212 therapeutic approach for patients with acute myeloid leukemia (AML).

213 chemotherapy in younger patients with acute myeloid leukemia (AML).

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

218 rotein kinase-induced mouse model of chronic myeloid leukemia (CML).

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

224 driven antiproliferative activities in acute myeloid leukemia cell lines.

225 7f inhibited the growth of acute and chronic myeloid leukemia cells and the phosphorylation and trans

226 ploited to kill chemotherapy-resistant acute myeloid leukemia cells.

227 These include new subtypes of acute myeloid leukemia defined by mutations in RUNX1 or BCR-AB

228 on of the BCR-ABL1 fusion delineates chronic myeloid leukemia from classic BCR-ABL1(-) MPNs, which ar

229 -MYC, BCL2 and PTEN mRNAs in the human acute myeloid leukemia MOLM-13 cell line.

230 Patients with myeloid leukemia of Down syndrome (ML-DS) have favorable

231 ailed picture of the BM vasculature in acute myeloid leukemia using intravital two-photon microscopy.

232 a, and blast cells, and a diagnosis of acute myeloid leukemia was made.

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

236 omegaly, and a propensity to evolve to acute myeloid leukemia.

237 nd its inactivation is associated with acute myeloid leukemia.

238 hematological malignancies, including acute myeloid leukemia.

239 linically related diagnosis atypical chronic myeloid leukemia.

240 ivation in mice is sufficient to drive acute myeloid leukemia.

241 ineages and a tendency to transform to acute myeloid leukemia.

242 MAC in patients with MDS or secondary acute myeloid leukemia.

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

245 al effectors of tyrosine kinase oncogenes in myeloid leukemias.

246 Moreover, we found that PUM1/2 sustain myeloid leukemic cell growth.

247 The transcription factor Meis1 drives myeloid leukemogenesis in the context of Hox gene overex

248 f NK-like cells, and a smaller population of myeloid-like cells.

249 Both global and transgenic hCD39- and myeloid lineage CD39-overexpressing mice (transgenic, n=

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

253 ene was specifically deleted in cells of the myeloid lineage, including macrophages.

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

256 rome is composed mostly of immature cells of myeloid lineage.

257 , leading to inhibition of lymphoid, but not myeloid, lineage potential.

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.

262 elated inflammatory gene signature for human myeloid malignancies.

263 idenib in patients with mutant-IDH2 advanced myeloid malignancies.

264 and after haploidentical HSCT for high-risk myeloid malignancies.

265 therapeutic strategies for treating CBL(mut) myeloid malignancies.

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

270 Myeloid mutation panels have identified somatic variants

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

273 cted before the diagnosis of therapy-related myeloid neoplasm.

274 therapy, and did not develop therapy-related myeloid neoplasms after at least 5 years of follow-up.

275 Therapy-related myeloid neoplasms are a potentially life-threatening con

276 the cumulative incidence of therapy-related myeloid neoplasms at 10 years was significantly higher i

277 oiesis to the development of therapy-related myeloid neoplasms.

278 For cells of myeloid origin, while integrins function at the level of

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

283 EBPA overlapped an enhancer active in common myeloid progenitors and influenced its activity.

284 In contrast, ectopic expression of NFI-A in myeloid progenitors from NFI-A myeloid cell-deficient mi

285 that function with short-term, and primarily myeloid, regenerative potential.

286 Engrafted cells were myeloid-restricted and matched the immunophenotype, morp

287 le of filopodia-inducing Cdc42, we generated myeloid-restricted Cdc42 knock-out mice.

288 ther manipulations, Dnmt3a+/- mice developed myeloid skewing over time, and their hematopoietic stem/

289 ietic stem cell (HSC) self-renewal capacity, myeloid skewing, and immune cell depletion.

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

292 Myeloid-specific deletion of Hif1a, Epas1, or both toget

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

296 We used a myeloid-specific Mll1 knockout (Mll1(f/f)Lyz2(Cre+) ) to

297 Meanwhile, the myeloid-specific transcription factor C/EBPalpha, usuall

298 D) expression in hematopoietic cells induced myeloid transformation, with a fully penetrant, lethal c

299 renewal or cooperate with Flt3-ITD to induce myeloid transformation.

300 Comutated, myeloid tumor-suppressor genes contribute to phenotypic