ライフサイエンスコーパス: ESA

1 ESA decay kinetics were oxidation-state dependent and co

2 ESA dose adjustments were allowed after 4 weeks.

3 ESA dose was negatively associated with achieved hemoglo

4 ESA fluorescence was monitored in animals for more than

5 ESA hyporesponsiveness may be useful in identifying pote

6 ESA hyporesponsiveness was primarily defined as a monthl

7 ESA induced greater chemotaxis of endothelial progenitor

8 ESA release was sustained for 4 weeks in vitro, remained

9 ESA requirements are independent of age when dose is sca

10 ESA response was positively associated with arsenic.

11 ESA sensitivity was positively associated with residual

12 ESA treatment of anemia to obtain higher hemoglobin targ

13 ESA treats RNA structures as 3D curves with sequence inf

14 ESA treats RNA structures as three dimensional curves wi

15 ESA use decreased from 25.6% at 1 month to 8.23% at 24 m

16 ESA was encapsulated in hyaluronic acid hydrogels during

17 ESAs (including biosimilars) may be offered to patients

18 ESAs did not affect SVR or discontinuation rates among p

19 ESAs have also been reported to promote angiogenesis.

20 ESAs have effects beyond erythropoiesis.

21 ESAs should be avoided in patients with cancer not recei

22 ESAs should be discontinued after 6 to 8 weeks in nonres

23 ESAs show great promise in preventing and treating brain

24 ESAs were permitted for anemic patients (hemoglobin [Hb]

25 (ESA) of the ligand-centered S(1) state; (2) ESA of a receiver ligand-to-metal or metal-to-ligand cha

26 nsfer triplet state (tau(1) </= 300 fs); (3) ESA of the vibrationally excited, ligand-centered T(1) s

27 tered T(1) state (tau(3) = 7-10 ps); and (4) ESA of the relaxed T(1) state.

28 e in Arabidopsis produced approximately 7.5% ESA in seed lipids.

29 re assigned to (1) excited state absorption (ESA) of the ligand-centered S(1) state; (2) ESA of a rec

30 a S(1) and Zea(*+) excited-state absorption (ESA) signals, respectively, after Chl excitation.

31 (2) broad visible excited-state absorption (ESA), and (3) stimulated emission (SE) at 670 nm.

32 l as a new signal excited-stated absorption (ESA) at signal wavelengths around 5.5 mum.

33 ur knowledge, this is the first time an ACFC-ESA system has been used to capture, recover, and liquef

34 ts of a gas recovery system (GRS) using ACFC-ESA for three adsorbates with relative pressures between

35 ated polyenoic FAs (alpha-eleostearic acids [ESAs]) using Arabidopsis (Arabidopsis thaliana) as a mod

36 rovision of the U.S. Endangered Species Act (ESA) is implemented: consultation to ensure federal acti

37 the habitat needs of Endangered Species Act (ESA)-listed salmonids relative to climate change in the

38 the influence of: (1) each-step activation (ESA) of NADH supply (including glycolysis) and oxidative

39 quence that is essential for Sirt1 activity (ESA).

40 tions (SCOs), and electrical spike activity (ESA) functions critical to neuronal network formation.

41 In addition, ESA was detected in the rat heart >3 weeks when delivere

42 followed by electrothermal swing adsorption (ESA) and postdesorption pressure and temperature control

43 Electrothermal swing adsorption (ESA) of organic compounds from gas streams with activate

44 Here, we analyzed outcome after ESA failure and the effect of second-line treatments.

45 and investigational drugs, may be used after ESA failure in some countries, but their effect on disea

46 The Committee cautions against ESA use under other circumstances.

47 n Agency (JAXA F/NF), European Space Agency (ESA F/NF), Boston University (MCD12Q1 F/NF), Food and Ag

48 The European Space Agency (ESA) recently selected Comet Interceptor as its first 'f

49 data acquired by the European Space Agency (ESA) Sentinel-2 satellites and, furthermore, are disting

50 Erythropoiesis stimulating agent (ESA) administration may reduce mortality in severe traum

51 ne; use of erythropoiesis-stimulating agent (ESA) and iron; and immunosuppressive regimen data were o

52 mes in the erythropoiesis-stimulating agent (ESA) arm.

53 oaches for erythropoiesis stimulating agent (ESA) drug dosing guidelines or without consideration of

54 ime to the erythropoiesis stimulating agent (ESA) products, which facilitated novel, in-depth charact

55 tide-based erythropoiesis-stimulating agent (ESA) that may have therapeutic potential for anemia in p

56 tide-based erythropoiesis-stimulating agent (ESA), is a potential therapy for anemia in patients with

57 sponse to erythropoiesis-stimulating agents (ESA) is associated with morbidity and mortality among di

58 nders and erythropoiesis-stimulating agents (ESA) to receive 24 weeks of FC or to continue their non-

59 analogs [erythropoiesis-stimulating agents (ESA)] are clinically used to treat anemia in patients wi

60 al use of erythropoiesis-stimulating agents (ESAs) and intravenous iron in hemodialysis patients with

61 he use of erythropoiesis stimulating agents (ESAs) and iron.

62 Erythropoiesis-stimulating agents (ESAs) are commonly used to treat anemia in patients with

63 onsive to erythropoiesis-stimulating agents (ESAs) because of anemia of inflammation.

64 djunct to erythropoiesis-stimulating agents (ESAs) compared with ESA alone in the treatment of chemot

65 trials of erythropoiesis-stimulating agents (ESAs) comparing lower and higher hemoglobin targets in p

66 doses of erythropoiesis-stimulating agents (ESAs) during dialysis to manage anemia, but the influenc

67 ficacy of erythropoietin-stimulating agents (ESAs) for improving health-related quality of life (HRQO

68 Erythropoiesis stimulating agents (ESAs) have been reported to activate erythropoietin rece

69 ducts and erythropoiesis-stimulating agents (ESAs) have resulted in many patients with cancer receivi

70 owed that erythropoiesis-stimulating agents (ESAs) improve subjective measures of HF.

71 lines for erythropoiesis-stimulating agents (ESAs) in 2011 appear to have influenced use of injectabl

72 effect of erythropoiesis-stimulating agents (ESAs) in critically ill trauma patients.

73 sponse to erythropoiesis-stimulating agents (ESAs) in iron-replete patients with chemotherapy-associa

74 or use of erythropoiesis-stimulating agents (ESAs) in patients with cancer.

75 e dose of erythropoiesis-stimulating agents (ESAs) may contribute to cardiovascular events in patient

76 ment with erythropoiesis-stimulating agents (ESAs) may result in undesired patterns of hemoglobin var

77 ssued for erythropoietin-stimulating agents (ESAs) regarding serious adverse events, such as venous t

78 he use of erythropoiesis-stimulating agents (ESAs) such as erythropoietin and darbepoetin in preterm

79 Erythropoietin-stimulating agents (ESAs) were originally designed to replace endogenous ery

80 Erythropoiesis-stimulating agents (ESAs) were prescribed to 92% of patients, and neither th

81 required; erythropoiesis-stimulating agents (ESAs) were used at the investigator's discretion.

82 ated with erythropoiesis-stimulating agents (ESAs), with a response rate of approximately 50%.

83 iron and erythropoiesis-stimulating agents (ESAs).

84 tivity of erythropoiesis stimulating agents (ESAs).

85 of use of erythropoiesis-stimulating agents (ESAs).

86 on and/or erythropoiesis-stimulating agents (ESAs).

87 rom using erythropoiesis-stimulating agents (ESAs).

88 The binding modes to equine serum albumin (ESA) of two nonsteroidal anti-inflammatory drugs (NSAIDs

89 cid (RmA), and alpha-eleostearic acid (alpha-ESA)/punicic acid (PunA), are not currently combined in

90 of either Ricinodendron heudelotii, an alpha-ESA source, or Punica granatum, a PunA source, on the eg

91 g content in ALA, DHA, RmA, as well as alpha-ESA or PunA.

92 n eggs was largely higher than that of alpha-ESA.

93 ating an efficient conversion from the alpha-ESA or PunA precursors through a Delta-13 reductase acti

94 p we composed a survey of 29 questions among ESA members as well as collaborators from their institut

95 veraged ESA of ~8.86 x 10(-4) m(2)/g, and an ESA coefficient of 1.36 x 10(-2), indicating limited par

96 We discovered an ESA mutant peptide that can bind to the deacetylase core

97 7 critically ill patients after trauma to an ESA or placebo (or no ESA).

98 ggests that adding iron to treatment with an ESA may improve hematopoietic response and reduce the li

99 , a novel engineered SDF polypeptide analog (ESA) more efficiently induces EPC migration and improves

100 gineered stromal cell-derived factor analog [ESA]) induces continuous homing of endothelial progenito

101 F polypeptide analog (engineered SDF analog [ESA]) that splices the N-terminus (activation and bindin

102 new method based on elastic shape analysis (ESA) that compares RNA molecules by combining both seque

103 ment method based on elastic shape analysis (ESA).

104 In a multivariable analysis, ESA misuse was associated with MD degree, female sex of

105 ed of a miniaturized electrostatic analyzer (ESA) and a deflector, backed by a static, magnet-based,

106 (beta=-0.28, P=0.003, CI:-0.47 to -0.09) and ESA use (beta=-0.73, P<0.001, CI:-0.93 to -0.52), and pr

107 sessed based on decreases in Hb, anemia, and ESA use.

108 hen dose is scaled to body surface area, and ESA resistance is associated with inflammation, fluid re

109 ntified that surface markers CD49f, CD61 and ESA were aberrantly overexpressed in Her2-overexpressing

110 ed that posttransplant anemia is common, and ESA/iron use remains suboptimal, and Hb is independently

111 arent after 12 weeks and reduces iv iron and ESA use while maintaining hemoglobin over 52 weeks, with

112 cy of peginesatide, as compared with another ESA, darbepoetin, in 983 such patients who were not unde

113 gest that the environmentally suitable area (ESA) for An. dirus and An. minimus would increase by an

114 elineate the mineral effective surface area (ESA) evolution during a recycling reactive flow-through

115 tic Scoring System score, and progression at ESA failure, there was no significant OS difference amon

116 m(-3) s(-1), a corresponding sample-averaged ESA of ~8.86 x 10(-4) m(2)/g, and an ESA coefficient of

117 geting of a lower hemoglobin range may avoid ESA-associated risks.

118 A possible mechanism behind ESA-induced tumor progression is discussed.

119 For biosimilar ESAs, the literature search was expanded to include meta

120 More intensive use of both ESAs and iron was associated with increased mortality ri

121 -like cells (CSC) defined by CD44(+)/CD24(-)/ESA(+) phenotype, where it plays a critical role in the

122 ne using cell surface markers (CS24(-)CD44(+)ESA(+)) and found that this cell population has signific

123 report, we found that CSCs (CD24(-)/CD44(+)/ESA(+)) isolated from metastatic breast cell lines are s

124 In BCSCs sorted with CD44(+)/ESA(+)/CD24(-) markers, Gb3 activates c-Src/beta-catenin

125 with peginesatide relative to the comparator ESA in the four pooled studies (2591 patients) and 0.95

126 satide was similar to that of the comparator ESA in the pooled cohort.

127 with peginesatide relative to the comparator ESA of more than 1.3.

128 , for randomized controlled trials comparing ESAs to placebo (or no ESA).

129 The two structures of the ternary complex ESA/Dic/Nps, obtained by competitive cocrystallization (

130 Cumulative ESA over 52 weeks was lower with FC than AC (median [int

131 ted significant dose responses for decreased ESA resistance index and increased serum iron, total iro

132 5 DIV, reducing SCO amplitude and depressing ESA and burst frequencies by 60-70%.

133 nd the structure of the previously described ESA/Nps complex (2.42 A), it was found that both NSAIDs

134 Our previously designed ESA peptide was synthesized by the addition of a fluorop

135 , 1.12 to 1.42) predicted prolonged-duration ESA use, whereas female oncologists (OR, 0.79; 95% CI, 0

136 During ESA treatment, hemoglobin may be increased to the lowest

137 ntify patients likely to benefit from either ESAs or anti-hepcidin agents.

138 Chemotactic properties of the eluted ESA were assessed at multiple time points using rat endo

139 Compared with placebo (or no ESA), ESA therapy was associated with a substantial reduction

140 Experiments were performed examining ESA function on these cells.

141 Of 1,147 patients experiencing ESA failure, 653 experienced primary failure and 494 exp

142 Whether using a low fixed ESA dose versus dosing based on a hemoglobin-based, titr

143 ported the neuroprotective effects following ESA administration, and improved neurodevelopmental outc

144 ies to sustain critical instream habitat for ESA-listed salmonids.

145 s for initiating treatment or as targets for ESA therapy.

146 nt, and long-term regeneration technique for ESA systems.

147 Exploratory analyses for ESAs showed no association with DFS events (HR, 1.02; P

148 ts with cancer, which decreases the need for ESAs.

149 Greater ESA and iron use were associated with decreased mortalit

150 least in part, prior observations of greater ESA doses administered to African-American dialysis pati

151 Anemia and high ESA dose requirements independently predict mortality.

152 ents might reduce risks associated with high ESA doses and decrease the cumulative exposure-while red

153 One phenotype, termed CD44(high)ESA(high), was proliferative and retained epithelial cha

154 hereas the other phenotype, termed CD44(high)ESA(low), was migratory and had mesenchymal traits chara

155 Given historically higher ESA and vitamin D use among black patients, we assessed

156 s of SCOs using [Formula: see text] imaging, ESA using microelectrode array (MEA) technology, and den

157 coadministration of parenteral iron improves ESA efficacy in patients with CAA.

158 This change in ESA can be qualitatively reproduced employing scanning e

159 The primary endpoint was change in ESA dose from baseline to end of treatment.

160 Endothelial progenitor cells (EPCs) in ESA gradient, assayed by Boyden chamber, showed signific

161 sis of mRNA expression and protein levels in ESA-treated animals revealed reduced matrix metalloprote

162 an increase of 36% and 11%, respectively, in ESA of An. lesteri and An. sinensis, was estimated under

163 ed adverse events and/or reduced survival in ESA-treated patients, concerns have been raised about th

164 The trends in ESA use remained similar between the intervention and co

165 The two binary dependent variables included ESA use and hospitalized VTE.

166 mbined with suppression of AtDGAT1 increased ESA accumulation to 14% to 15%.

167 Coexpression of VfDGAT2 increased ESA levels to approximately 11%.

168 These results suggest that individualized ESA dosing decreases total hemoglobin variability compar

169 In patients with traumatic brain injury, ESA therapy did not increase the number of patients surv

170 s in iron/hematologic parameters and iv iron/ESA use at time points throughout the active control per

171 However, centers that used larger ESA doses in patients with hematocrit between 33% and 35

172 fferences, dialysis centers that used larger ESA doses in patients with hematocrit less than 30% had

173 Median ESA usage decreased by 15,000, 15,000, or 33,000 IU/wk p

174 The median ESA dosage per patient was 2000 IU/wk in both groups.

175 aline, hydrogel alone, or hydrogel+25 microg ESA was injected into the borderzone.

176 nsiveness was primarily defined as a monthly ESA dose of 75,000 units or higher and hematocrit 33% or

177 obinopathy traits associated with 13.2% more ESA per treatment (P=0.001).

178 Compared with placebo (or no ESA), ESA therapy was associated with a substantial redu

179 nts after trauma to an ESA or placebo (or no ESA).

180 lled trials comparing ESAs to placebo (or no ESA).

181 8 to -1.27] for heart failure), although non-ESA-related changes in practice and Medicare payment pen

182 alysis patients associated with the observed ESA response variability and with consideration to ESA d

183 recovery kinetics, and the time constant of ESA decay was slower following severe (180 s) than moder

184 In addition, slow decay of ESA was required to fit phosphocreatine recovery kinetic

185 to the time from admission to first dose of ESA.

186 pathy traits received higher median doses of ESA than patients with normal hemoglobin (4737.4 versus

187 the hypothesis that individualized dosing of ESA improves hemoglobin variability over a standard popu

188 both NSAIDs bind within drug site 2 (DS2) of ESA and both occupy secondary binding sites in separate

189 ntly shown a potential detrimental effect of ESA administration on tumor progression and survival in

190 methods were used to estimate the effect of ESA hyporesponsiveness on allograft failure and all-caus

191 natural experiment to examine the effects of ESA boxed warnings on utilization and risk of VTE.

192 nical data showed neuroprotective effects of ESA, however, the literature regarding impact on outcome

193 human Epo (rHuEpo), none showed evidence of ESA-induced EpoR activation.

194 There was no evidence of ESA-induced intracellular signaling in endothelial cells

195 nd peri-infarct intramyocardial injection of ESA, SDF-1alpha, or saline.

196 5) were less likely to use 1 week or less of ESA treatment.

197 We compared these data to three measures of ESA dose response, sex, and dialysis incidence versus di

198 ession to correlate center-level patterns of ESA and iron use with 1-year mortality risk in 269,717 i

199 isozyme competition influenced production of ESA.

200 Although early studies showed promise of ESA administration in reducing the need for transfusions

201 On the basis of the crystal structure of ESA/Dic determined to a resolution of 1.92 A and the str

202 to 92% of patients, and neither the type of ESA nor the dosing interval appeared to affect efficacy.

203 re likely to prescribe more than 24 weeks of ESA treatment.

204 s exploring direct, "pleiotropic" actions of ESAs.

205 The administration of ESAs to critically ill trauma patients is associated wit

206 The effect of ESAs varied by time to anemia; patients with early-onset

207 red the potential neuroprotective effects of ESAs.

208 Primary failure of ESAs was associated with a higher risk of acute myeloid

209 Early failure of ESAs was associated with a higher risk of AML progressio

210 t reduction ( P < .001) in the likelihood of ESAs being used to treat cancers targeted by the warning

211 confirmed the neuroprotective properties of ESAs, including promotion of oligodendrocyte development

212 nd physician-related factors with receipt of ESAs were analyzed.

213 Receipt of ESAs while not actively receiving chemotherapy (off labe

214 hese preliminary studies, the future role of ESAs and iron replacement will be determined by ongoing

215 tive trials are needed to assess the role of ESAs in HCV treatment.

216 have been raised about the potential role of ESAs in promoting tumor progression, possibly through tu

217 dies have called into question the safety of ESAs as supportive therapy in patients being treated for

218 and benefits (eg, decreased transfusions) of ESAs and compare these with potential harms (eg, serious

219 and benefits (eg, decreased transfusions) of ESAs and compare these with potential harms (eg, serious

220 lity risk was associated with greater use of ESAs and iron in these patients.

221 strated widespread variability in the use of ESAs.

222 d and Drug Administration's boxed warning of ESAs used to treat chemotherapy-induced anemia because e

223 Based on ESA, a rigorous mathematical framework can be built for

224 pathy traits and quantify their influence on ESA dosing.

225 acteristics exerted substantial influence on ESA use.

226 diagnosed between 1995 and 2005 who had one ESA and chemotherapy claim.

227 to borderzone injection of saline (n=18) or ESA (n=18).

228 isolated with CD44(+)CD24(-/lo)SSEA-3(+) or ESA(hi)PROCR(hi)SSEA-3(+) markers had higher tumorigenic

229 resulting from implementation of the PPS or ESA label change.

230 The novel, biomolecularly designed peptide ESA induces chemotaxis of endothelial progenitor stem ce

231 43-1.81), respectively, supporting that poor ESA response during hemodialysis is associated with adve

232 nclear whether the risk associated with poor ESA response during dialysis extends beyond kidney trans

233 We examined pretransplantation ESA response and its effect on allograft failure and mor

234 .93) were less likely to prescribe prolonged ESA treatment.

235 (3)H(6) -> ((3)F(4), (3)F(3)) after the pump ESA ((3)H(5) -> (3)H(6)) at a pump wavelength of 4.1 mum

236 Patients were randomly assigned to receive ESA doses guided by the Smart Anemia Manager algorithm (

237 91 patients analyzed, 5,099 (24.2%) received ESAs for 1 week or less (misuse), and 1,601 (7.6%) recei

238 or less (misuse), and 1,601 (7.6%) received ESAs for more than 14 weeks (prolonged use).

239 eviated Injury Scale (AIS), >or=3] receiving ESA while in the surgical intensive care unit from Janua

240 duce RBC transfusions for patients receiving ESA with or without iron deficiency.

241 trait and 2.4% hemoglobin C trait) receiving ESAs, demographic and clinical variables were similar ac

242 Compared with control, FC reduced ESA dose [mean change (SD), -1211.8 (3609.5) versus +119

243 phosphate and haemoglobin levels, FC reduced ESA dose, RDW, and C-terminal FGF23 compared with contro

244 ly improved markers of inflammation, reduced ESA requirements, and increased serum albumin in patient

245 d that the warning was effective in reducing ESA utilization.

246 ization of exponential spectral analysis (RS-ESA).

247 Voxelwise RS-ESA yielded similar V(T)s and coefficients of variation.

248 The signal ESA of the fibre is attributed to the transition (3)H(6)

249 Thus, this signal ESA should be suppressed in a resonantly pumped Pr(3+)-d

250 Similarly, ESAs did not reproducibly provide cytoprotection to neur

251 After a screening period documenting stable ESA and iron dosing, we randomized 61 patients with elev

252 g regimens employed in the included studies, ESA therapy did not increase the risk of lower limb prox

253 llel activation of ATP usage and ATP supply (ESA), and a strong inhibition of ATP supply by anaerobic

254 ted patients with myelodysplastic syndromes, ESAs should not be offered to most patients with nonchem

255 A potential explanation was that ESA-activated erythropoietin (Epo) receptors (EpoRs) pro

256 Although the ESA+ patients experienced protracted hospital length of

257 verestimates the size of the infarct and the ESA-based area at risk.

258 ased capillary and arteriolar density in the ESA group (P<0.01).

259 Animals in the ESA treatment group also had significant reductions in i

260 increase in angiopoietin-1 expression in the ESA- and SDF-treated hearts.

261 etylase core, competes with and inhibits the ESA region from interacting with the deacetylase core.

262 The administration of the ESA epoetin alfa to critically ill trauma patients has b

263 ng the ACS and NOMAD instruments onboard the ESA-Roscosmos ExoMars Trace Gas Orbiter from April to Au

264 As the dissolution reaction progressed, the ESA is observed to first increase and then decrease.

265 We tested the ESA and deflector, magnet-based mass spectrometer, and a

266 Regressions showed that the ESA boxed warning was associated with a 20.2-percentage-

267 a large pivotal outcome trial found that the ESA darbepoetin alfa did not improve long-term outcomes

268 Our results indicate that the ESA region interacts with and functions as an "on switch

269 Therefore, the ESA region is a potential target for development of ther

270 de a new approach to analyze and upscale the ESA during geochemical reactions, which are involved in

271 with the area at risk as determined with the ESA method and is localized in the perfusion territory o

272 cid hydrogels during gel formation, and then ESA release, along with gel degradation, was monitored f

273 n and LacNAc extension patterns of the three ESAs were similar, with a maximum of four N-acetyl-neura

274 P < .0001) and the area at risk according to ESA (17% +/- 13, P < .0001).

275 FDG uptake and the area at risk according to ESA was observed (r = .70, P = .001).

276 dely used pharmaceutical drugs in binding to ESA.

277 sponse variability and with consideration to ESA dose response, hepcidin, and high sensitivity C-reac

278 with inflammation and hyporesponsiveness to ESA therapy.

279 Bottom Line: Addition of iron to ESAs improves hematopoietic response, reduces the need f

280 Results Erythroid response to ESAs was 61.5%, and median response duration was 17 mont

281 rly-onset anemia (</= 8 weeks of treatment), ESAs were associated with higher SVR rate (45.0% vs 25.9

282 r or angiotensin receptor blocker (ARB) use, ESA use, dialysis access type, dialysis access change, a

283 patients (28.6%); 449 of these (51.9%) used ESAs.

284 If used, ESAs should be administered at the lowest dose possible

285 ls that provide evidence in support of using ESA to improve the neurodevelopmental outcomes in term a

286 Caution should be exercised when using ESAs with chemotherapeutic agents in diseases associated

287 The weekly ESA dose inversely correlated with age when scaled to we

288 Hemoglobin was negatively associated with ESA dose and cadmium while positively associated with an

289 um albumin and was inversely associated with ESA dose.

290 tion taken to mitigate risks associated with ESA use and changes in payment policy did not result in

291 trials have identified risks associated with ESA use.

292 esis-stimulating agents (ESAs) compared with ESA alone in the treatment of chemotherapy-induced anemi

293 enting 16 tumor types were low compared with ESA-responsive positive controls.

294 ion and the area at risk, as determined with ESA, were assessed and compared with the area of reduced

295 ly-onset anemia had higher rates of SVR with ESA use, whereas no effect was observed in those with la

296 fractional area change in mice treated with ESA compared with controls.

297 f phosphorylated AKT, and cells treated with ESA yielded significantly greater phosphorylated AKT lev

298 with non-del(5q) lower-risk MDS treated with ESAs, none of the most commonly used second-line treatme

299 with non-del(5q) lower-risk MDS treated with ESAs.

300 s and lacked detectable Zea S(1) and Zea(*+) ESA signals in vivo, which strongly suggests that the ac