ライフサイエンスコーパス: G-CSF

1 G-CSF and M-CSF are two lineage-specific cytokines that

2 G-CSF did not improve mRS (ordinal regression), odds rat

3 G-CSF induces the expansion of hematopoietic progenitors

4 G-CSF is a hemopoietic growth factor that has a role in

5 G-CSF or CSF-3, originally defined as a regulator of gra

6 G-CSF was found to play a key role in MDSC mobilization

7 G-CSF- and G-CSF receptor-deficient mice are profoundly

8 ammatory mediators such as IL-1beta, Cxcl-1, G-CSF, and IL-6 are increased.

9 10 RCTs comprising 196 stroke patients (116 G-CSF, 80 placebo), mean age 67.1 (SD 12.9), 92% ischaem

10 ition of neutrophil production via the IL-17/G-CSF axis, and rhythmic modulation of the haematopoieti

11 nt bone marrow niche signals (SCF, IL-1beta, G-CSF, TGFbeta and CXCL4) and activation of an inducible

12 ty was comparable between the groups (21.4%, G-CSF; 28.6%, placebo; P = 0.69).

13 fically responsible for T(h)17 (IL-17, IL-6, G-CSF) and T(h)1 differentiation and expression (IL-12,

14 In 119 patients (61 G-CSF and 58 SOC, respectively), CMR was available at ba

15 dards (ranging from 1.5-25 ng/muL) and 6XHis-G-CSF (ranging from 0.1-100 ng/muL) expressed in cell-fr

16 terleukin-1RA, interleukin-6, interleukin-8, G-CSF, and M-CSF (p < 0.001).

17 elayed, in vitro proliferative activity in a G-CSF-dependent cell line.

18 In addition, G-CSF leads to downregulation of synaptic glutamatergic

19 In addition, G-CSF treatment reduced the levels of four of five measu

20 that high-dose cyclophosphamide given after G-CSF-mobilized blood cell transplantation would reduce

21 poiesis and impaired HSPC mobilization after G-CSF stimulation was confirmed in human diabetes.

22 ioglitazone therapy, HSPC mobilization after G-CSF was partially rescued.

23 s negatively impacted HSC mobilization after G-CSF with or without chemotherapy but had no effect on

24 on of downstream Stat3 phosphorylation after G-CSF treatment, and impaired G-CSF-mediated differentia

25 istration of neutralizing antibodies against G-CSF only partially restored the myeloproliferation, su

26 the galectin-3-induced secretion of IL-6 and G-CSF cytokines from the endothelial cells.

27 intestine and increased circulatory IL-6 and G-CSF, along with a hematopoietic shift toward granulocy

28 ytokines (IL-12p40, IL-1beta, TNF-alpha, and G-CSF) and chemokines (CXCL2, CCL5) were significantly e

29 G-CSF- and G-CSF receptor-deficient mice are profoundly protected i

30 n, and also increased keratinocyte CXCL1 and G-CSF production.

31 ing G-CSF treatment reduces excitability and G-CSF-induced visceral pain in vivo.

32 markers (IL-6, nCD64, IL-1ra, PCT, MCP1, and G-CSF) yielded the same predictive power as collecting a

33 d thereby inhibits STAT3 phosphorylation and G-CSF receptor signaling.

34 sults suggest that the combination of RT and G-CSF should be further evaluated in preclinical and cli

35 ch as hematopoietic cell transplantation and G-CSF- or inflammation-induced stress myelopoiesis.

36 Anti-G-CSF receptor rapidly halted the progression of establi

37 The eyes of G-CSF-deficient and anti-G-CSF monoclonal antibody-treated WT mice had minimal ne

38 G-CSF-STAT3 signaling loop with either anti-G-CSF antibody or STAT3 inhibitor depleted the CSC subpo

39 rom an inflammatory phenotype following anti-G-CSF receptor therapy in collagen Ab-induced arthritis.

40 reduced in G-CSF-deficient mice and in anti-G-CSF monoclonal antibody-treated, wild-type (WT) mice.

41 ollowing administration of neutralizing anti-G-CSF antiserum.

42 ls in the blood and arthritic joints of anti-G-CSF receptor-treated mice showed alterations in cell a

43 e, blocking neutrophil trafficking with anti-G-CSF receptor suppressed local production of proinflamm

44 e U.S. Food and Drug Administration approved G-CSF (filgrastim) for the treatment of congenital and a

45 As G-CSF treatment also induces HSC proliferation, we sough

46 Primary prophylaxis (PP) was defined as G-CSF administration within 5 days of beginning chemothe

47 that directly stimulate myelopoiesis such as G-CSF or GM-CSF.

48 randomised controlled trials (RCT) assessing G-CSF in patients with hyperacute, acute, subacute or ch

49 e randomized to ATG and pegylated G-CSF (ATG+G-CSF) (N = 17) or placebo (N = 8).

50 ptide was not significantly different in ATG+G-CSF (0.49 nmol/L/min) versus placebo (0.29 nmol/L/min)

51 gulatory T cells (Treg) were elevated in ATG+G-CSF subjects at 6, 12, and 18 but not 24 months.

52 A phase II study of ATG+G-CSF in patients with new-onset type 1 diabetes is ongo

53 pe 1 diabetes is ongoing and may support ATG+G-CSF as a prevention strategy in high-risk subjects.

54 Subjects treated with ATG+G-CSF demonstrated reduced CD4(+) T cells and CD4(+)/CD8

55 ATG/G-CSF therapy was associated with relative preservation

56 Combination ATG/G-CSF treatment tended to preserve beta cell function in

57 We herein report that commercially available G-CSF and PEG ELISA detection kits have different capaci

58 animal models of TRL-positive cancer bearing G-CSF expressing cervical cancer cells.

59 s with the mutated truncated receptor before G-CSF treatment begins.

60 further investigate the actions of blocking G-CSF/G-CSF receptor signaling in inflammatory disease,

61 Both G-CSF and SCF had pronounced effects on frataxin levels

62 A new G-CSF-driven (methylated BSA/G-CSF) arthritis model was established enabling us to de

63 but had no effect on mobilization induced by G-CSF with plerixafor.

64 Mobilization induced by G-CSF, AMD3100 or ischemia was evaluated by flow cytomet

65 ing molecular mechanism of MTA1 induction by G-CSF was proved to be through induction of c-Fos and it

66 In db/db mice, mobilization by G-CSF or AMD3100 was either increased or unaffected (P <

67 graftment efficiency than those mobilized by G-CSF.

68 Signaling by G-CSF, a regulator of neutrophil development, traffickin

69 IL-13, IL-17, CCL2, CCL3, CCL4, CCL5, CCL11, G-CSF, GM-CSF and TNF-alpha.

70 This drug combination (AraC+CHK1i+G-CSF) will open the doors for a more efficient treatmen

71 positive selection of mutants due to chronic G-CSF therapy to reverse the severe neutropenia.

72 matory cytokines, including granulocyte CSF (G-CSF) and chemokines.

73 lobulin (ATG) and pegylated granulocyte CSF (G-CSF) would preserve beta cell function in patients wit

74 It was more efficient than granulocyte CSF (G-CSF), a common treatment of severe neutropenia, which

75 acrophage colony-stimulating factor (GM-CSF)/G-CSF in vitro, inhibited GVHD-induced death and attenua

76 f central nervous system ECs produce GM-CSF, G-CSF, IL-6, Cxcl1, and Cxcl2.

77 on, through increased plasma levels of CSF3 (G-CSF; beta = 0.29; P = 0.002), and an increased inflamm

78 These data suggest that G-CSFR/G-CSF targeting may be a safe therapeutic strategy for a

79 L3, CCL4, CCL11, CXCL1, CXCL2, CXCL5, CXCL9, G-CSF, GM-CSF, VEGF, and M-CSF) and chemokine receptors

80 -6 and IL-1beta), and chemotactic cytokines (G-CSF, CXCL12, CXCL1, and CX3CL1).

81 Five cytokines (G-CSF, GM-CSF, IL-1-ra, IL-2 and IL-16) were significant

82 Taken together, our results define G-CSF as a CSC-activating factor in neuroblastoma, sugge

83 nts, we demonstrate that bone marrow-derived G-CSF-responsive cells home to the injured brain and are

84 ersistent pancytopenia despite moderate-dose G-CSF treatment.

85 the increased demand for neutrophils during G-CSF-induced emergency granulopoiesis in humans.

86 ing CX3CR1 or nitric oxide production during G-CSF treatment reduces excitability and G-CSF-induced v

87 effects of G-CSF on myelopoiesis, endogenous G-CSF suppressed development of marrow adipocytes and hi

88 ril reduced radiation-induced cytokines EPO, G-CSF, and SAA in the plasma.

89 Exogenous G-CSF enhances tumor growth and metastasis in human xeno

90 okine granulocyte-colony-stimulating factor (G-CSF or Csf-3) as a key mediator of visceral sensitizat

91 eutic granulocyte colony-stimulating factor (G-CSF) administration early in life exerts a strong sele

92 e via granulocyte colony-stimulating factor (G-CSF) administration.

93 otein granulocyte colony-stimulating factor (G-CSF) against storage at 4 degrees C and shipping tempe

94 okine granulocyte-colony stimulating factor (G-CSF) alters cocaine reward and reinforcement and can e

95 en by granulocyte colony-stimulating factor (G-CSF) and administration of neutralizing antibodies aga

96 izing granulocyte colony-stimulating factor (G-CSF) and chemokine receptor-mediated signals.

97 cy of granulocyte colony-stimulating factor (G-CSF) and haemopoietic stem-cell infusions in patients

98 ts of granulocyte colony-stimulating factor (G-CSF) and of nitric oxide (NO) upon challenge with cory

99 ines, granulocyte-colony stimulating factor (G-CSF) and stem cell factor (SCF) in a humanized murine

100 on of granulocyte colony-stimulating factor (G-CSF) and the ELR(+) CXC chemokine CXCL1.

101 ified granulocyte-colony stimulating factor (G-CSF) as a neuroactive cytokine that alters behavioral

102 se of granulocyte colony stimulating factor (G-CSF) as the most common regimen used for HSPC mobiliza

103 on of granulocyte colony-stimulating factor (G-CSF) enhanced RT-mediated antitumor activity by activa

104 using granulocyte colony-stimulating factor (G-CSF) for hematopoietic stem cell (HSC) mobilization ha

105 that granulocyte-colony stimulating factor (G-CSF) in patients with glycogenosis-related pancytopeni

106 ty of granulocyte colony-stimulating factor (G-CSF) in steroid nonresponders.

107 Granulocyte colony-stimulating factor (G-CSF) is a regulator of neutrophil production, function

108 Granulocyte colony-stimulating factor (G-CSF) is used clinically to treat leukopenia and to enf

109 , and granulocyte colony-stimulating factor (G-CSF) levels in the amniotic fluid of ZIKV-positive pre

110 Granulocyte colony stimulating factor (G-CSF) may enhance recovery from stroke through neuropro

111 lated granulocyte colony-stimulating factor (G-CSF) preserves beta-cell function for at least 12 mont

112 human granulocyte-colony stimulating factor (G-CSF) prior to MS/MS and MS(3) analysis to specifically

113 after granulocyte colony-stimulating factor (G-CSF) prophylaxis in patients with breast cancer who re

114 o the granulocyte colony-stimulating factor (G-CSF) receptor and exhibited potent, but delayed, in vi

115 ing a granulocyte-colony stimulating factor (G-CSF) receptor knockout mouse model in combination with

116 duced granulocyte colony-stimulating factor (G-CSF) receptor levels, attenuation of downstream Stat3

117 after granulocyte colony-stimulating factor (G-CSF) stimulation.

118 okine granulocyte colony-stimulating factor (G-CSF) through complex mechanisms.

119 ty of granulocyte colony-stimulating factor (G-CSF) to mobilize endogenous cells have attracted the m

120 , and granulocyte colony-stimulating factor (G-CSF) was chosen, due to its clinically proven neurogen

121 ating granulocyte-colony stimulating factor (G-CSF) was increased in mice, and was transiently elevat

122 ATG), granulocyte-colony stimulating factor (G-CSF), a dipeptidyl peptidase IV inhibitor (DPP-4i), an

123 a2m), granulocyte colony stimulating factor (G-CSF), and three monoclonal antibodies (mAbs).

124 -78), granulocyte colony stimulating factor (G-CSF), granulocyte macrophage colony stimulating factor

125 IL-8, granulocyte-colony stimulating factor (G-CSF), IL-33, IL-11, IL-1alpha, and IL-1beta.

126 ls of granulocyte colony-stimulating factor (G-CSF), interleukin 1alpha (IL-1alpha), IL-6, IL-9, RANT

127 beta, granulocyte colony-stimulating factor (G-CSF), interleukin-12/23 (IL-12/23), and IL-13 trended

128 mma), granulocyte colony-stimulating factor (G-CSF), monocyte chemoattractant protein 1 (MCP-1), macr

129 with granulocyte colony-stimulating factor (G-CSF), which can increase neutrophil counts but does no

130 upon granulocyte-colony stimulating factor (G-CSF)- mediated granulocytic differentiation of 32Dcl3

131 drive granulocyte colony-stimulating factor (G-CSF)-induced HSC mobilization via the secretion of cal

132 on of granulocyte colony-stimulating factor (G-CSF)-mobilized blood cells from HLA-matched related or

133 on of granulocyte colony-stimulating factor (G-CSF)-treated donors (GDs) consists of mature CD66b(+)C

134 en of granulocyte colony-stimulating factor (G-CSF).

135 se to granulocyte colony-stimulating factor (G-CSF).

136 eased granulocyte-colony stimulating factor (G-CSF).

137 on of granulocyte-colony stimulating factor (G-CSF); these effects are reversed following administrat

138 ts of granulocyte-colony stimulation factor (G-CSF), and partially rescued HSPC mobilization, but it

139 beta, granulocyte colony stimulating factor (G.CSF), IL-13, IL-6, IL-12, interferon (IFN)-gamma, IFN-

140 ophil numbers after IR, as well as following G-CSF-mediated bone marrow mobilization, which was indep

141 n resulted in monocyte development following G-CSF induction whereas inhibition of Erk1/2 signaling p

142 al latency that can be reactivated following G-CSF treatment.

143 ilization to refrigeration, but critical for G-CSF stabilization at elevated temperatures.

144 adiposity were reduced in mice deficient for G-CSF; however, bone mass was not influenced.

145 Several studies point to a critical role for G-CSF as the main mediator of emergency granulopoiesis.

146 these data demonstrate an important role for G-CSF in invoking autophagy within hematopoietic and mye

147 These data reveal an integral role for G-CSF-driven neutrophil responses in ocular autoimmunity

148 fter transplantation with splenic cells from G-CSF-treated donors blocks suppression of aGVHD, sugges

149 understand which patients benefit most from G-CSF prophylaxis in this setting.

150 relies on incoming IL-10(+) neutrophils from G-CSF-treated donor spleen (G-Neutrophils).

151 was completely deficient in neutrophils from G-CSF-treated donors.

152 Furthermore, G-CSF-induced neutrophil and HSC mobilization is impaire

153 drinking-resilient males showed the highest G-CSF, IL-13, and leptin levels.

154 However, G-CSF is also produced in response to infection, and exc

155 utside of the bone marrow, and also identify G-CSF as a potential therapeutic target in the treatment

156 rylation after G-CSF treatment, and impaired G-CSF-mediated differentiation.

157 Importantly, G-CSF receptor blockade did not adversely affect viral c

158 ly, dorsal root ganglion neurons cultured in G-CSF failed to respond to G-CSF in vitro, and Csf3r gen

159 inium enhancement significantly decreased in G-CSF group only (P=0.04).

160 from baseline to 6 months was 5.1% higher in G-CSF patients versus SOC (P=0.01); concurrently, there

161 lobal longitudinal strain was 2.4% higher in G-CSF patients versus SOC (P=0.04).

162 umferential strain significantly improved in G-CSF group only (P=0.006).

163 ne uveoretinitis was dramatically reduced in G-CSF-deficient mice and in anti-G-CSF monoclonal antibo

164 ous adverse events were more frequent the in G-CSF and stem-cell infusion group (12 [43%] patients) t

165 t size and longer symptom-to-balloon time in G-CSF patients.

166 hese MSCs by various interventions including G-CSF administration diminished cancer cell homing.

167 tin receptor antagonist, PESLAN-1, increased G-CSF- or AMD3100-mobilization of WBCs and LSKs, compare

168 tained neutrophilia accompanied by increased G-CSF signaling and testicular vacuolation associated wi

169 ssion in the CeA, and a profile of increased G-CSF, GM-CSF, IL-13, IL-6, IL-17a, leptin, and IL-4 tha

170 The increased G-CSF was accompanied by an increased activation of the

171 CBD administration in mice induced G-CSF, CXCL1, and M-CSF, but not GM-CSF.

172 d715, derived from an SCN patient inhibited G-CSF-induced expression of NE in a dominant negative ma

173 Interestingly, G-CSF- and M-CSF-stimulated activation of Erk1/2 was aug

174 INTERPRETATION: G-CSF with or without haemopoietic stem-cell infusion di

175 IL-5, IL-7, IL-12p70, IL-13, IL-17F, leptin, G-CSF, GM-CSF, LIF, NGF, SCF, and TGF-alpha.

176 2(-/-) mice also produced significantly less G-CSF, IL-6, and MCP-1 in the serum, spleen, and liver o

177 gnificant difference in all-cause mortality (G-CSF 11.2%, placebo 7.6%, p = 0.4).

178 which potently antagonizes binding of murine G-CSF and thereby inhibits STAT3 phosphorylation and G-C

179 e developed a neutralizing mAb to the murine G-CSF receptor, which potently antagonizes binding of mu

180 ncy hematopoiesis and identify an IL-1/MyD88/G-CSF-dependent pathway as the key regulator of emergenc

181 n MDSC mobilization inasmuch as neutralizing G-CSF caused a significant decrease in MDSC.

182 A new G-CSF-driven (methylated BSA/G-CSF) arthritis model was

183 We also show that M-CSF, but not G-CSF, stimulated strong and sustained activation of Erk

184 We find that administration of G-CSF accelerates extinction and reduces cue-induced dru

185 Administration of G-CSF during extinction accelerated the rate of extincti

186 Early administration of G-CSF exerted a beneficial effect on top of SOC in patie

187 tion, the effects of early administration of G-CSF in terms of LV remodeling and function, infarct si

188 mRNA expression induced by administration of G-CSF in vivo, as a model of emergency granulopoiesis in

189 Administration of G-CSF is safe and helps to reduce the disease severity a

190 Finally, administration of G-CSF-neutralizing antibody can prevent the establishmen

191 of rheumatoid arthritis, and Ab blockade of G-CSF also protects against disease.

192 Blockade of G-CSF restored normal granulopoiesis in DeltaNC16A mice.

193 However, the consequences of G-CSF stimulation on the transcriptome of neutrophils an

194 lected from healthy individuals after 5 d of G-CSF administration.

195 e therapeutic responses using lower doses of G-CSF combined with targeting to correct NE mislocalizat

196 we describe for the first time the effect of G-CSF receptor blockade in a therapeutic model of inflam

197 animals neutropenic, suggesting an effect of G-CSF receptor blockade on neutrophil homing to inflamma

198 In addition to stimulatory effects of G-CSF on myelopoiesis, endogenous G-CSF suppressed devel

199 basis of evidence we studied the effects of G-CSF treatment on extinction and reinstatement of cocai

200 Elevation of G-CSF was found to recapitulate many effects of VSG on b

201 The eyes of G-CSF-deficient and anti-G-CSF monoclonal antibody-treat

202 f indexed LV end-systolic volume in favor of G-CSF group (P=0.02).

203 diabetes (>/=20 weeks) induced impairment of G-CSF- or AMD3100-mobilization (P < 0.01, n = 8).

204 y mice subjected to intrathecal injection of G-CSF exhibit pronounced visceral hypersensitivity, an e

205 Furthermore, the level of G-CSF in bone marrow and circulation were significantly

206 rthermic, fast resolvers" had high levels of G-CSF, CCL2, and interleukin-10 compared with the "hypot

207 driven by IL-1/MyD88-dependent production of G-CSF.

208 t a validated short transduction protocol of G-CSF plus plerixafor-mobilized CD34(+) cells from FA-A

209 pathway significantly reduces the release of G-CSF from DeltaNC16A BM-MSC in vitro and the level of s

210 Herein, we investigated the role of G-CSF in a murine model of human uveitis-experimental au

211 Here, we investigate the role of G-CSF in affecting extinction and reinstatement of cocai

212 it enabled the convergent total synthesis of G-CSF aglycone.

213 ehensive reevaluation of the clinical use of G-CSF in these patients to support white blood cell coun

214 00-mobilized LSK cells, and had no effect on G-CSF.

215 Cs are preferentially mobilized to the PB on G-CSF treatment.

216 topoiesis and EMH in response to bleeding or G-CSF treatment.

217 prague Dawley rats were injected with PBS or G-CSF during (1) extinction or (2) abstinence from cocai

218 Overall, G-CSF did not improve stroke outcome in this individual

219 months) were randomized to ATG and pegylated G-CSF (ATG+G-CSF) (N = 17) or placebo (N = 8).

220 5 mg/kg intravenously) followed by pegylated G-CSF (6 mg subcutaneously every 2 weeks for 6 doses) an

221 d in all xenografted groups, with Plerixafor+G-CSF-mobilized cells achieving superior short-term engr

222 and assigned to standard of care (SOC) plus G-CSF or SOC alone.

223 Conclusion Primary G-CSF prophylaxis was associated with low-to-modest bene

224 can prolong neutrophil survival by producing G-CSF and GM-CSF, delaying the mitochondrial outer membr

225 hrm1) signaling in the hypothalamus promotes G-CSF-elicited HSC mobilization via hormonal priming of

226 nts with WHIM syndrome who could not receive G-CSF were treated with low-dose plerixafor, a CXCR4 ant

227 ith untreated animals, animals that received G-CSF following radiation injury exhibited enhanced func

228 whereas it was not in patients who received G-CSF plus plerixafor.

229 poorer mobilization in patients who received G-CSF with/without chemotherapy, whereas it was not in p

230 Patients with diabetes who received G-CSF without plerixafor had a lower probability of reac

231 poorer mobilization in patients who received G-CSF.

232 On Cox regression analysis, receiving G-CSF (hazard ratio, 0.37; SD, 0.14-0.98; P = 0.04), and

233 Furthermore, recombinant G-CSF or adoptive transfer of granulocytic-MDSCs isolate

234 Importantly, recombinant G-CSF exists as an FDA-approved medication which may fac

235 ity disrupted CEBPbeta induction and reduced G-CSF expression in CRTC2/3m stromal cells, our results

236 a-catenin-TCF/LEF complex directly regulates G-CSF receptor levels, and consequently controls proper

237 ytokines that discriminated high responders (G-CSF, IFN-gamma, TNF-alpha) correlated with both egress

238 ppaB pathway in CAIX-depleted cells restored G-CSF secretion.

239 ghtened IL-4 activity, with IL-4 restricting G-CSF-induced neutrophil expansion and migration to tiss

240 nsistent with a key role for pegfilgrastim's G-CSF moiety in driving formation of inactive aggregates

241 l T-cell expressed and presumably secreted), G-CSF (granulocyte-colony-stimulating factor) and MMP2 (

242 NC16A BM-MSC in vitro and the level of serum G-CSF in DeltaNC16A mice.

243 nic inflammation, thereby identifying spinal G-CSF as a target for treating chronic abdominal pain.

244 ndomly assigned to groups given subcutaneous G-CSF (5 mug/kg/d) for 5 days and then every third day (

245 care (control), treatment with subcutaneous G-CSF (lenograstim) 15 mug/kg for 5 days, or treatment w

246 Taken together, these findings support G-CSF as a viable translational research target with the

247 icroglia express the G-CSF receptor and that G-CSF signaling mediates microglial activation following

248 o G-CSF treatment without dividing, and that G-CSF-mediated proliferation is restricted to cells with

249 We conclude that G-CSF treatment generates a population of activated and

250 Mechanistically, we demonstrate that G-CSF injection increases Cathepsin S activity in spinal

251 global protein expression demonstrated that G-CSF regulated proteins primarily in mPFC that are crit

252 We showed previously that G-CSF treatment generates low-density splenic granulocyt

253 We report that G-CSF is specifically up-regulated in the thoracolumbar

254 We show that G-CSF controls the ocular neutrophil infiltrate by modul

255 el dilution of dormant HSCs, suggesting that G-CSF does not stimulate dormant HSC proliferation.

256 al prefrontal cortex (mPFC), suggesting that G-CSF influences drug seeking via glutamatergic mechanis

257 w that resident spinal microglia express the G-CSF receptor and that G-CSF signaling mediates microgl

258 nds of MELD change over time (p=0.55 for the G-CSF group vs standard care and p=0.75 for the G-CSF pl

259 SF group vs standard care and p=0.75 for the G-CSF plus stem-cell infusion group vs standard care).

260 hat tumor-expressed CAIX is required for the G-CSF-driven mobilization of granulocytic myeloid-derive

261 fusion group (12 [43%] patients) than in the G-CSF (three [11%] patients) and standard care (three [1

262 d care group (variceal bleed) and two in the G-CSF and stem-cell infusion group (one myocardial infar

263 At 90 days, in the G-CSF but not in the placebo group, the Model for End-St

264 patients with a serious adverse event in the G-CSF group (29.6% versus 7.5%, p = 0.07) with no signif

265 rse events were ascites (two patients in the G-CSF group and two patients in the G-CSF plus stem-cell

266 andard care group, -0.5 (-1.7 to 0.5) in the G-CSF group, and -0.5 (-1.3 to 1.0) in the G-CSF plus st

267 ascites twice), sepsis (four patients in the G-CSF plus stem-cell infusion group), and encephalopathy

268 s in the G-CSF group and two patients in the G-CSF plus stem-cell infusion group, one of whom was adm

269 ), and encephalopathy (three patients in the G-CSF plus stem-cell infusion group, one of whom was adm

270 e G-CSF group, and -0.5 (-1.3 to 1.0) in the G-CSF plus stem-cell infusion group.

271 tality (35.7% versus 71.4%; P = 0.04) in the G-CSF than in the placebo group.

272 nduction of CEBPbeta, a key regulator of the G-CSF gene.

273 mutations in the extracellular domain of the G-CSF receptor (CSF3R) have been reported only in severe

274 a is known to be marked by expression of the G-CSF receptor (G-CSFR).

275 ts, and suggest that direct targeting of the G-CSF-STAT3 signaling represents a novel therapeutic app

276 mly assigned to the standard care, 26 to the G-CSF group, and 28 to the G-CSF plus stem-cell infusion

277 d care, 26 to the G-CSF group, and 28 to the G-CSF plus stem-cell infusion group.

278 r stabilization of the important therapeutic G-CSF, as well as a general platform for the future disc

279 Blockade of this G-CSF-STAT3 signaling loop with either anti-G-CSF antibo

280 ultured with microglia BV-2 cells exposed to G-CSF, dorsal root ganglion (DRG) nociceptors become hyp

281 40 mg/day of prednisolone were randomized to G-CSF (12 doses, 300 mug each in 28 days) or placebo.

282 %) were nonresponders and were randomized to G-CSF or placebo (14 in each group after exclusions).

283 urons cultured in G-CSF failed to respond to G-CSF in vitro, and Csf3r gene expression could not be d

284 euron-microglia interaction that responds to G-CSF by engaging Cathepsin S-CX3CR1-inducible NOS signa

285 te that dormant HSCs mobilize in response to G-CSF treatment without dividing, and that G-CSF-mediate

286 within the BM HSC compartment in response to G-CSF treatment.

287 In response to G-CSF, STAT3 acts in a feed-forward loop to transcriptio

288 system to track HSC divisions in response to G-CSF.

289 Patients tolerated G-CSF without any major adverse events.

290 not require increase in mutation rate under G-CSF treatment and agrees with age distribution of sMDS

291 tudies identify a novel mechanism underlying G-CSF effects on behavioral plasticity.SIGNIFICANCE STAT

292 ntribution or stem cell activity and, unlike G-CSF, did not impede recovery of HS/PCs, thrombocyte nu

293 a primary mechanism for bone loss with VSG, G-CSF plays an intermediary role for effects of VSG on t

294 proliferation, we sought to examine whether G-CSF-mediated repopulation defects are a result of incr

295 sults reveal an important mechanism by which G-CSF and M-CSF instruct neutrophil versus monocyte line

296 n effectively out-competes PB mobilized with G-CSF.

297 -1,2,3,6-tetrahydropyridine mouse model with G-CSF showed significant induction of MTA1 and TH with r

298 al autoimmune uveoretinitis was reduced with G-CSF deficiency.

299 In phase 1 dose expansion studies with G-CSF support, 23r has shown promising single agent acti

300 tim) 15 mug/kg for 5 days, or treatment with G-CSF for 5 days followed by leukapheresis and intraveno