ライフサイエンスコーパス: hydroxyurea

1 megaly who were inadequately controlled with hydroxyurea.

2 wered by treatment with either anagrelide or hydroxyurea.

3 ymerase movement for mutant cells exposed to hydroxyurea.

4 duces the mutagenic profile as compared with hydroxyurea.

5 e to killing by the DNA replication stressor hydroxyurea.

6 eplisome becomes unstable in the presence of hydroxyurea.

7 talizations and transfusions if treated with hydroxyurea.

8 st increases of HbF with similar efficacy as hydroxyurea.

9 atment with low-dose aspirin, phlebotomy, or hydroxyurea.

10 nomic consequences of the therapeutic use of hydroxyurea.

11 iron depletion and the Tyr(*)-reducing agent hydroxyurea.

12 ed to the ribonucleotide reductase inhibitor hydroxyurea.

13 mosome bipolar attachment in the presence of hydroxyurea.

14 microtubule interaction after treatment with hydroxyurea.

15 e-wide screen for yeast mutants sensitive to hydroxyurea.

16 vation of ATM in response to aphidicolin and hydroxyurea.

17 nse to or had unacceptable side effects from hydroxyurea.

18 d sensitivity to the DNA synthesis inhibitor hydroxyurea.

19 global loss of histone H3 and sensitivity to hydroxyurea.

20 incidence did not differ between children on hydroxyurea (0.05 episodes per child per year; 95% confi

21 Three deaths occurred (2 hydroxyurea, 1 placebo, and none from malaria).

22 and ninety-three subjects were randomized to hydroxyurea (20 mg/kg/d) or placebo; there were 374 pati

23 ndomisation, best available therapy included hydroxyurea (37 [49%] of 75 in the best available therap

24 or blood transfusion) was less frequent with hydroxyurea (45%) than placebo (69%; P = .001).

25 tyrate (2), valproic acid (3), riluzole (6), hydroxyurea (7), and albuterol (9), none of which has de

26 lta, crb2Delta, chk1Delta, and rad3Delta, to hydroxyurea, a compound that stalls replication forks an

27 chore assembly is delayed in the presence of hydroxyurea, a DNA synthesis inhibitor, presumably due t

28 g 0.5 G y gamma-irradiation daily or 150 muM hydroxyurea, a replication stress inducer.

29 Pre-arresting cells in G(1) phase by hydroxyurea abrogated both AITC-induced mitotic arrest a

30 Because hydroxyurea also reduces leukocytosis, an understanding

31 ually relies on cytoreductive agents such as hydroxyurea, although ongoing studies will help delineat

32 Here we report that low doses of hydroxyurea, an inhibitor of ribonucleotide reductase an

33 on alternative treatment (N = 67) initiated hydroxyurea and 60 (90%) reached MTD at 26.2 +/- 4.9 mg/

34 in the presence of the replication inhibitor hydroxyurea and accumulate multiple Rad52 foci.

35 Using hydroxyurea and aspirin to treat patients with BCS cause

36 f catalase deficiency likewise affected both hydroxyurea and avrRpm1 sensitivity, we selected mutants

37 comprised preconditioning cytoreduction with hydroxyurea and azathioprine starting at -45 days pretra

38 nd that deletion of UBP7 sensitizes cells to hydroxyurea and cisplatin and demonstrate that factors t

39 it, rsc4-K25R mutants display sensitivity to hydroxyurea and delayed S-phase progression under DNA da

40 eotide homeostasis through other mechanisms (hydroxyurea and floxuridine) also act synergistically wi

41 arget of established clinical agents such as hydroxyurea and gemcitabine because of its critical role

42 COH29 overcame hydroxyurea and gemcitabine resistance in cancer cells.

43 Hydroxyurea and interferon may be used as first-line tre

44 nt options for MPNs include cytoreduction by hydroxyurea and JAK1/2 inhibition by ruxolitinib, both o

45 Two disease-modifying therapies, hydroxyurea and long-term blood transfusions, are availa

46 lls, amplified the cGMP-elevating effects of hydroxyurea and may represent a promising and more tissu

47 epistatic with dph1Delta for sensitivity to hydroxyurea and methyl methanesulfonate, and with elp3De

48 y was to compare clinical events between the hydroxyurea and placebo groups.

49 Hydroxyurea and transfusion therapy are strongly recomme

50 n compromised CHK1 activation in response to hydroxyurea and UV, thus promoting hypersensitivity to d

51 prevented activation of Chk1 in response to hydroxyurea and various other drug treatments.

52 = 5.5 x 10 - 8 adjusted for haemoglobin and hydroxyurea) and validated it in independent SCD patient

53 onstrated increased sensitivity to UV light, hydroxyurea, and camptothecin, which are known activator

54 in the S phase and had reduced expression in hydroxyurea, and H3.2 protein was not incorporated into

55 le therapies, including aspirin, phlebotomy, hydroxyurea, and interferon.

56 e trials of agents, including 5-azacytidine, hydroxyurea, and short-chain fatty acids.

57 iagent chemotherapy, hypomethylating agents, hydroxyurea, and supportive care.

58 sing the fetal hemoglobin-reactivating agent hydroxyurea are currently the mainstay of treatment.

59 ion tracts created before fork stalling with hydroxyurea are degraded in the absence of BRCA2 but are

60 hey accelerate centrosome reduplication upon hydroxyurea arrest.

61 otic benefit from cytoreductive therapy with hydroxyurea as first-line and interferon-alfa and busulf

62 ty risk, we make a strong recommendation for hydroxyurea as first-line therapy and a weak recommendat

63 volvement and a low threshold for the use of hydroxyurea as preventative measures for end-stage renal

64 Patients who were receiving concomitant hydroxyurea as well as those not receiving hydroxyurea w

65 cause of BCS: 17 patients with MPDs received hydroxyurea/aspirin; 5 received warfarin; and 3 (2 whose

66 oxyurea could increase malaria severity, and hydroxyurea-associated neutropenia could worsen infectio

67 Hydroxyurea at a relatively low dose is frequently presc

68 nvestigator-selected best available therapy (hydroxyurea [at the maximum tolerated dose], interferon

69 ication, but their fragility is increased by hydroxyurea, ATR inhibition, or deregulated c-Myc expres

70 n addition to induction of fetal hemoglobin, hydroxyurea attenuates leukocyte-endothelial interaction

71 Among a subset of children on hydroxyurea, baseline fetal hemoglobin levels explained

72 ing of strokes in 7 of 67 children receiving hydroxyurea but none in 66 children who received transfu

73 lex dissociated when cells were treated with hydroxyurea but not methyl-methane-sulfonate, suggesting

74 ecin and methyl methanesulfonate, as well as hydroxyurea but not to UV light.

75 omycin C (MMC) and the replication inhibitor hydroxyurea, but not the DSB inducer ionizing radiation.

76 d tolerance to replicative stress induced by hydroxyurea, but result in enhanced sensitivity to a wid

77 ing agents methyl methanesulfonate (MMS) and hydroxyurea by a mechanism(s) that requires the copper-r

78 Limited support for hydroxyurea by lay organizations and inconsistent medica

79 However, the exact mechanisms by which hydroxyurea can induce HbF remain incompletely defined,

80 hesis, when elongation is largely blocked by hydroxyurea, can be readily detected by EdU incorporatio

81 expressed in budding yeast cells exposed to hydroxyurea, cell growth is severely inhibited, and exce

82 After exposure to hydroxyurea, cik1 and kar3 mutant cells exhibit normal D

83 M26, doxorubicin, camptothecin, aphidicolin, hydroxyurea, cisplatin, mechlorethamine and x-rays) on k

84 In vitro studies suggest hydroxyurea could increase malaria severity, and hydroxy

85 iber track assays with HeLa cells exposed to hydroxyurea demonstrated that Tim or DDX11 depletion sig

86 Remarkably, these low hydroxyurea doses generated the same mitotic defects (an

87 Gemcitabine, 5-fluorouracil, hydroxyurea, doxorubicin and paclitaxel have no measurab

88 he A17 protein, similar to the resistance to hydroxyurea enabled by duplication of the gene encoding

89 gh aphidicolin, gemcitabine, camptothecin or hydroxyurea exposure, activates transcription of APOBEC3

90 nfluenced serum hydroxyurea levels and total hydroxyurea exposure.

91 notoxicity or carcinogenicity with long-term hydroxyurea exposure.

92 fraction is considerably increased following hydroxyurea exposure.

93 fety and efficacy of a regimen consisting of hydroxyurea followed by azacitidine, 75 mg/m(2) for 7 da

94 The potential utility of hydroxyurea for all patients with SCA is clear and indis

95 ents for anemia, cytoreductive drugs such as hydroxyurea for the splenomegaly and constitutional symp

96 rboxylate, hydroxypyridinonate, thiol, and N-hydroxyurea functional groups.

97 n is under challenge induced by ultraviolet, hydroxyurea, gemcitabine, or aphidicolin treatment.

98 from 31 thalassemic patients mobilized with hydroxyurea+granulocyte colony-stimulating factor (G-CSF

99 ficant difference between the anagrelide and hydroxyurea group regarding incidences of major arterial

100 Children receiving hydroxyurea had significantly increased hemoglobin conce

101 Hydroxyurea has been shown to be efficacious for the tre

102 Based on this cumulative experience, hydroxyurea has emerged as an important therapeutic opti

103 Our findings indicate that hydroxyurea has immediate beneficial effects on the micr

104 Hydroxyurea has many characteristics of an ideal drug fo

105 abundant evidence for its efficacy, however, hydroxyurea has not yet translated into effective therap

106 MCM9L, while the replication fork inhibitor, hydroxyurea, has no effect.

107 , Almeida et al report immediate benefits of hydroxyurea (HU) acute administration in diminishing vas

108 es cerevisiae, replication stress induced by hydroxyurea (HU) and methyl methanesulfonate (MMS) activ

109 rect histone deacetylase inhibitor activity, hydroxyurea (HU) and sulforaphane.

110 Hydroxyurea (HU) depletes the cells of dNTPs, which init

111 Hydroxyurea (HU) has a long history of clinical and scie

112 definition of resistance and intolerance to hydroxyurea (HU) in polycythemia vera (PV) were proposed

113 The drug hydroxyurea (HU) inactivates both Ia/b and Ic beta(2) su

114 Hydroxyurea (HU) inhibits ribonucleotide reductase (RNR)

115 Hydroxyurea (HU) is effectively used in the management o

116 The effect of hydroxyurea (HU) on urine albumin-to-creatinine ratio (A

117 treated with methyl methane sulfonate (MMS), hydroxyurea (HU) or camptothecin (CPT), we show that gen

118 Ablating neuroblasts with hydroxyurea (HU) prior to onset of larval proliferation

119 lling of the replication of MVM genomes with hydroxyurea (HU) resulted in Chk1 phosphorylation in a v

120 eplication in human cells in the presence of hydroxyurea (HU) revealed that only the earliest origins

121 ith hematological parameters, HbS level, and hydroxyurea (HU) therapy.

122 When yeast cells were treated with hydroxyurea (HU) to block DNA synthesis and induce repli

123 Hydroxyurea (HU) treatment activates the intra-S phase c

124 oom bodies (MBs) of the fly brain via larval hydroxyurea (HU) treatment results in a loss of olfactio

125 Hydroxyurea (HU), a common therapy for sickle cell disea

126 ction mechanism in Escherichia coli beta2 by hydroxyurea (HU), a radical scavenger and cancer therape

127 Although hydroxyurea (HU), an inducer of fetal hemoglobin, is the

128 ally all origins after transient exposure to hydroxyurea (HU), an inhibitor of ribonucleotide reducta

129 s (AGAs), and toxic small molecules, such as hydroxyurea (HU), kill bacteria the same way, namely, by

130 We found that hydroxyurea (HU), which depletes dNTP pools, slightly el

131 Here, we demonstrate that hSSB1 relocates to hydroxyurea (HU)-damaged replication forks where it is r

132 is required for DNA-PKcs-dependent repair of hydroxyurea (HU)-induced DSBs but dispensable for RPA/RA

133 ole in genome-wide replication restart after hydroxyurea (HU)-induced replication fork stalling.

134 in Mcm2-deficient cells under conditions of hydroxyurea (HU)-mediated replication stress.

135 eatment with the replication inhibitory drug hydroxyurea (HU).

136 uxolitinib), a dual Jak1/Jak2 inhibitor, and hydroxyurea (HU).

137 ase, resulted in an increased sensitivity to hydroxyurea (HU).

138 r hypersensitivity to the DNA-damaging agent hydroxyurea (HU).

139 on and recovery of DNA replication following hydroxyurea (HU).

140 rosslinkers and replication blockers such as hydroxyurea (HU).

141 the ribonucleotide reductase (RNR) inhibitor hydroxyurea (HU).

142 by NO donors and the NO-donor properties of hydroxyurea (HU).

143 eus during the stalled replication caused by hydroxyurea (HU).

144 NOHARM (Novel use Of Hydroxyurea in an African Region with Malaria) was a ran

145 resolved within a month after discontinuing hydroxyurea in April 2010 and have not recurred since.

146 n in response to fork-stalling agents UV and hydroxyurea in cultured cells.

147 The phase III study of hydroxyurea in infants (BABY HUG) has just been complete

148 -blind, placebo-controlled clinical trial of hydroxyurea in infants (beginning at 9-18 months of age)

149 e demonstrate that plasma EPO elevation with hydroxyurea in SCD is independent of hypoxic responses a

150 The findings suggested role of hydroxyurea in the pathogenesis of these ulcers, and tha

151 lowering agent is not inferior compared with hydroxyurea in the prevention of thrombotic complication

152 The efficacy of hydroxycarbamide (hydroxyurea) in this setting is unknown; we performed th

153 Hydroxyurea increased haemoglobin and fetal haemoglobin,

154 dministered at maximum tolerated dose (MTD), hydroxyurea increases fetal hemoglobin (HbF) to levels r

155 reased when dNTP synthesis was suppressed by hydroxyurea, indicating that Polzeta function does not r

156 replication forks active during a transient hydroxyurea-induced arrest.

157 mutants (cat2) in a screen for resistance to hydroxyurea-induced cell death.

158 intra-S-phase checkpoint in the presence of hydroxyurea-induced DNA damage and are unable to survive

159 cleostemin shows a protective effect against hydroxyurea-induced DNA damage.

160 ts SET domain is essential for recovery from hydroxyurea-induced DNA damage.

161 ion forks, reduced repair of spontaneous and hydroxyurea-induced DNA double strand breaks (DSBs), and

162 ngs clarify the overlap between baseline and hydroxyurea-induced fetal hemoglobin levels in pediatric

163 itment of the core repair protein, RAD51, to hydroxyurea-induced foci.

164 9,195 compounds for their ability to inhibit hydroxyurea-induced phosphorylation of Ser345 on Chk1, k

165 ntaining Bloom syndrome helicase (BLM) after hydroxyurea-induced replication fork stalling.

166 Similarly, following hydroxyurea-induced replication stress, lamin A/C-defici

167 stability and functionality at forks during hydroxyurea-induced replication stress.

168 delayed resumption of DNA replication after hydroxyurea-induced stalling of replication forks, reduc

169 exposure to UV irradiation, camptothecin, or hydroxyurea induces accumulation of HDHB on chromatin in

170 he introduction of DNA replication stress by hydroxyurea induces the HTA2-HTB2 amplification event.

171 Since hydroxyurea inhibits ribonucleotide reductase and reduce

172 Hydroxyurea is a potent inducer of fetal hemoglobin, and

173 (SWiTCH) study designed to determine whether hydroxyurea is as effective as transfusions in preventin

174 The urease-catalyzed hydrolysis of hydroxyurea is known to exhibit biphasic kinetics, showi

175 ransfusions led the authors to conclude that hydroxyurea is not effective in mitigating strokes.1

176 In my practice, hydroxyurea is still the "gold standard" when cytoreduct

177 se is polymerization of a hemoglobin mutant, hydroxyurea is the only drug approved for treatment by t

178 e to DNA damage and apoptosis in response to hydroxyurea, its restoration resulted in less DNA damage

179 th chromatin-modifying agents (CMAs) but not hydroxyurea, Janus kinase 2 (JAK2) inhibitors, or low do

180 velocities and no stenosis were treated with hydroxyurea, known to decrease anemia and hemolytic rate

181 notype (rapid or slow) that influenced serum hydroxyurea levels and total hydroxyurea exposure.

182 Currently used cytoreductive drugs include hydroxyurea, mainly used in older patients, and interfer

183 etic and alternative molecular mechanisms of hydroxyurea-mediated HbF induction by examining methylat

184 s in miRNA expression may be associated with hydroxyurea-mediated HbF induction.

185 ole for lysine 4 on H3 and the H2A N-tail in hydroxyurea-mediated response.

186 Children received either hydroxyurea (N = 104) or placebo (N = 103).

187 HeLa cells to paraquat and H2O2, but not to hydroxyurea, neocarzinostatin, or camptothecin.

188 as hydroxamic acids, N-hydroxy carbamates, N-hydroxyureas, nitrile oxides, and 1,2,4-oxadiazole-4-oxi

189 Three new reports document the benefits of hydroxyurea on reducing mortality in SCA: two adult tria

190 FANCJ helicase depleted cells, we show that hydroxyurea or aphidicolin treatment leads to loss of mi

191 After exposure of cells to hydroxyurea or aphidicolin, APRIN and other cohesin comp

192 icantly modified in ET patients treated with hydroxyurea or aspirin only.

193 als investigating optimal frontline therapy (hydroxyurea or IFN) and second-line therapy for hydroxyu

194 exacerbated by exposing the cells to either hydroxyurea or methyl methanesulfonate, lending support

195 When replication elongation was blocked by hydroxyurea or nalidixic acid, arrested cells contained

196 Combined treatment with MI-223 and hydroxyurea or olaparib exhibited a strong synergy again

197 ing that short-term administration of either hydroxyurea or the phosphodiesterase 9 (PDE9) inhibitor,

198 th postcapillary pulmonary hypertension; and hydroxyurea or transfusions to raise the hemoglobin conc

199 ptothecin, cis-diamminedichloroplatinum(II), hydroxyurea, or 5-fluorouracil.

200 vera who were being treated with phlebotomy, hydroxyurea, or both to receive either more intensive tr

201 at comparable phases using serum starvation, hydroxyurea, or RO-3306.

202 NA damage by the replication stress inducer, hydroxyurea, or the radiomimetic antibiotic, neocarzinos

203 leading to sensitization of cancer cells to hydroxyurea- or olaparib-induced DNA replication stress.

204 of care for second-line therapy in this post-hydroxyurea patient population.

205 re providers have inadequate knowledge about hydroxyurea, patients and families are not offered treat

206 The Pediatric Hydroxyurea Phase 3 Clinical Trial (BABY HUG) was a phas

207 fusions/chelation) to alternative treatment (hydroxyurea/phlebotomy) for children with SCA, stroke, a

208 ard (transfusions/chelation) to alternative (hydroxyurea/phlebotomy) treatment to prevent recurrent s

209 kes on transfusions/chelation but 7 (10%) on hydroxyurea/phlebotomy, still within the noninferiority

210 isodes per child per year [0.03, 0.16]); the hydroxyurea/placebo malaria incidence rate ratio was 0.7

211 Subjects on alternative treatment received hydroxyurea plus overlap transfusions during dose escala

212 alone (CRT arm; docetaxel, fluorouracil, and hydroxyurea plus radiotherapy 0.15 Gy twice per day ever

213 but also in a subset of patients switched to hydroxyurea, provided trimestrial Doppler follow-up and

214 Hydroxyurea provides SCA-related laboratory and clinical

215 ients with SCD, we investigated how the drug hydroxyurea quantitatively affects microvascular obstruc

216 roxyurea or IFN) and second-line therapy for hydroxyurea-refractory or intolerant PV with JAK inhibit

217 tion of dNTP pools through pretreatment with hydroxyurea renders tel1-Delta cells (but not wild type)

218 th BLM exerted a dominant negative effect on hydroxyurea resistance by interfering with the FANCJ-BLM

219 ythaemia vera, no palpable splenomegaly, and hydroxyurea resistance or intolerance were stratified by

220 ofibrosis (MF), and its use in patients with hydroxyurea resistant or intolerant polycythemia vera (P

221 Here, we identify an Arabidopsis thaliana hydroxyurea-resistant autophagy mutant, atg2, which also

222 ruxolitinib was recently approved for use in hydroxyurea-resistant PV, its role in routine clinical p

223 ic loci in larger populations and in unusual hydroxyurea responders are needed to further understand

224 self is variable, and accurate predictors of hydroxyurea responses do not currently exist.

225 Inhibition of D. discoideum class I RNR by hydroxyurea resulted in a 90% reduction in spore formati

226 nse to or had unacceptable side effects from hydroxyurea, ruxolitinib was superior to standard therap

227 However, in stark contrast to hydroxyurea's myelosuppressive effects, pomalidomide aug

228 y therapy with both drugs failed to mitigate hydroxyurea's myelotoxic effects and caused loss of HbF

229 n functional domains of Sgs1, suppressed the hydroxyurea sensitivity of BLM-overexpressing cells, sug

230 We also show that hydroxyurea sensitivity of mrc1Delta and swi1Delta was s

231 homologous recombination intermediates, and hydroxyurea sensitivity that is additive with mms21-11.

232 On recovery, treatment with hydroxyurea should be discussed to reduce the likelihood

233 ermediate effect whereas tranylcypromine and hydroxyurea showed relatively low HbF reactivation.

234 Notwithstanding limited data, hydroxyurea, somatostatin analogues and interferon-alpha

235 ocessing of newly synthesized DNA strands in hydroxyurea-stalled forks.

236 of Cdc17 turnover resulted in sensitivity to hydroxyurea, suggesting that this pathway is important f

237 rom the Stroke With Transfusions Changing To Hydroxyurea (SWiTCH) study designed to determine whether

238 The Stroke With Transfusions Changing to Hydroxyurea (SWiTCH) trial compared standard (transfusio

239 Stroke With Transfusions Changing to Hydroxyurea (SWiTCH) was a multicenter phase 3 randomize

240 trokes (Stroke With Transfusions Changing to Hydroxyurea [SWiTCH]) or silent cerebral infarcts (Silen

241 ower p53 levels after activation of ATR with hydroxyurea than did normal control fibroblasts.

242 First, we determined low doses of hydroxyurea that did not affect the cell cycle distribut

243 with SCA, both at baseline before beginning hydroxyurea therapy and after reaching maximum tolerated

244 icacy information for clinicians considering hydroxyurea therapy for very young children with sickle

245 Focus is placed on hydroxyurea therapy given its benefits and increasing us

246 Hydroxyurea therapy has proven laboratory and clinical e

247 Hydroxyurea therapy is strongly recommended for adults w

248 ell transfusions can be safely replaced with hydroxyurea therapy or bone marrow transplantation for a

249 ance or intolerance were stratified by their hydroxyurea therapy status (resistance vs intolerance) a

250 vaso-occlusive complications include chronic hydroxyurea therapy to induce fetal hemoglobin.

251 s (PK) data for children with SCA initiating hydroxyurea therapy, to investigate pharmacodynamics (PD

252 mined in children at baseline and induced by hydroxyurea therapy.

253 dent in human sickle cell patients receiving hydroxyurea therapy.

254 set of patients from chronic transfusions to hydroxyurea therapy.

255 Exporting our knowledge and experience with hydroxyurea to developing nations with large medical bur

256 , and were more strongly stimulated by using hydroxyurea to induce DNA replication stress than by the

257 E/beta-thalassemia disease was treated with hydroxyurea to induce hemoglobin F production since 2007

258 nducted in malaria-endemic Uganda, comparing hydroxyurea to placebo at 20 +/- 2.5 mg/kg per day for 1

259 od and Drug Administration (FDA) approval of hydroxyurea to reduce the frequency of vaso-occlusive ep

260 In UV (ultraviolet light)- or HU (hydroxyurea)-treated cells, PIAS3 is required for effici

261 sumption of stalled DNA replication forks in hydroxyurea-treated cells.

262 Furthermore, we found that SS-RBCs from hydroxyurea-treated patients show a lower expression of

263 l factor affecting S phase progression after hydroxyurea treatment and demonstrate an evolutionary an

264 Hydroxyurea treatment appears safe for children with SCA

265 Hydroxyurea treatment decreased neutrophil extravasation

266 be phosphorylated upon ultraviolet light or hydroxyurea treatment in ERH knocked-down HepG2 cells.

267 Centrosome amplification after hydroxyurea treatment increases significantly in Cep135-

268 Hydroxyurea treatment is recommended for children with s

269 s in fork reactivation and progression after hydroxyurea treatment observed in WRN- or RAD51-deficien

270 Hydroxyurea treatment of sickle cell mice improved their

271 Hydroxyurea treatment reduces haemolysis and anaemia by

272 Accurate prediction of hydroxyurea treatment responses for SCA remains a worthy

273 -term safety profile, it is time to consider hydroxyurea treatment the standard of care for all young

274 fic miRNAs was significantly increased after hydroxyurea treatment, and expression of miR-26b and miR

275 ed for viability of WRN-depleted cells after hydroxyurea treatment, and identified HDAC1, a member of

276 n of Akt inhibits Chk1 phosphorylation after hydroxyurea treatment, and this effect is dependent on T

277 detected after replicative stress induced by hydroxyurea treatment, suggesting it may be a dormant or

278 or regulation of baseline HbF, but not after hydroxyurea treatment, whereas changes in miRNA expressi

279 phosphorylate RxxS sites preferentially upon hydroxyurea treatment, whereas Pmk1 and Cdk1 preferentia

280 reduced in patients on long-term (>5 months) hydroxyurea treatment.

281 ease symptoms and provides an alternative to hydroxyurea treatment.

282 ine HbF levels, but only slightly altered by hydroxyurea treatment.

283 This in vivo repression was reversed by hydroxyurea treatment.

284 many young patients with SCA should receive hydroxyurea treatment.

285 ression defect upon checkpoint activation by hydroxyurea treatment.

286 ood Institute-sponsored Multicenter Study of Hydroxyurea trial proved clinical efficacy for preventin

287 ulticenter TCD With Transfusions Changing to Hydroxyurea (TWiTCH) study and suggest that it may be sa

288 bstituted (TCD With Transfusions Changing to Hydroxyurea [TWiTCH]).

289 The protective effect of hydroxyurea was abrogated in mice deficient in E-selecti

290 Hydroxyurea was associated with statistically significan

291 ccal pneumonia and sepsis, administration of hydroxyurea was found to significantly improve survival.

292 the combination of BMN673, ruxolitinib, and hydroxyurea was highly effective in vivo against JAK2(V6

293 Despite expected mild myelosuppression, hydroxyurea was not associated with an increased risk of

294 Switch from transfusions to hydroxyurea was prescribed for 45 patients, with a mean

295 t hydroxyurea as well as those not receiving hydroxyurea were included in the study.

296 and tolerability of anagrelide compared with hydroxyurea were investigated in a prospective randomize

297 erance to the deoxynucleotide-depleting drug hydroxyurea, which could be mimicked by DNA cross-linkin

298 wn; we performed the TWiTCH trial to compare hydroxyurea with standard transfusions.

299 ed pharmacologic therapy for this disease is hydroxyurea, with effects largely attributable to induct

300 te strength suggests offering treatment with hydroxyurea without regard to the presence of symptoms f