ライフサイエンスコーパス: hydroxyurea

1 vera who were resistant to or intolerant of hydroxyurea.

2 nse to or had unacceptable side effects from hydroxyurea.

3 d sensitivity to the DNA synthesis inhibitor hydroxyurea.

4 global loss of histone H3 and sensitivity to hydroxyurea.

5 esponse to the replication stress induced by hydroxyurea.

6 wered by treatment with either anagrelide or hydroxyurea.

7 ymerase movement for mutant cells exposed to hydroxyurea.

8 a vera who are resistant to or intolerant of hydroxyurea.

9 duces the mutagenic profile as compared with hydroxyurea.

10 e to killing by the DNA replication stressor hydroxyurea.

11 eplisome becomes unstable in the presence of hydroxyurea.

12 talizations and transfusions if treated with hydroxyurea.

13 st increases of HbF with similar efficacy as hydroxyurea.

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

15 on as we have additionally demonstrated with hydroxyurea.

16 ed in the range of 0.62-102.33 ng mL(-1) for hydroxyurea.

17 for the detection of an anticancerous drug, hydroxyurea.

18 ing for mutants with enhanced sensitivity to hydroxyurea.

19 vera who were resistant to or intolerant of hydroxyurea.

20 megaly who were inadequately controlled with hydroxyurea.

21 ed to the ribonucleotide reductase inhibitor hydroxyurea.

22 vation of ATM in response to aphidicolin and hydroxyurea.

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

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

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

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

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

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

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

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

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

32 Because hydroxyurea also reduces leukocytosis, an understanding

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

34 rcome this, we use DNA synthesis inhibitors (hydroxyurea and 1-beta-d-arabinofuranosyl cytosine) to t

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

36 t not Ubp8, confers increased sensitivity to hydroxyurea and activates a cryptic transcription report

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

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

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

40 me-internal DNA replication, is sensitive to hydroxyurea and dependent on 9-1-1 activity.

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

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

43 COH29 overcame hydroxyurea and gemcitabine resistance in cancer cells.

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

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

46 ed blood cells, only two therapies for SCD - hydroxyurea and L-glutamine - are approved by the US Foo

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

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

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

50 und including long-established drugs such as hydroxyurea and new compounds in development such as epa

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

52 ribe a single-arm trial using dose-escalated hydroxyurea and regular transfusions to prevent complica

53 Hydroxyurea and transfusion therapy are strongly recomme

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

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

56 = 5.5 x 10 - 8 adjusted for haemoglobin and hydroxyurea) and validated it in independent SCD patient

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

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

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

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

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

62 hey accelerate centrosome reduplication upon hydroxyurea arrest.

63 Using hydroxyurea as a radical scavenger, the spin-coupled hid

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

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

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

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

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

69 Children received hydroxyurea at a dose of 15 to 20 mg per kilogram of bod

70 Children received hydroxyurea at a fixed dose (94 children; mean [+/-SD] a

71 randomized, double-blind trial, we compared hydroxyurea at a fixed dose (approximately 20 mg per kil

72 dren completed screening and began receiving hydroxyurea at a mean (+/-SD) dose of 17.5+/-1.8 mg per

73 Hydroxyurea at a relatively low dose is frequently presc

74 and approximately two thirds were receiving hydroxyurea at baseline.

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

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

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

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

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

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

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

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

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

84 o DNA damaging agents such as gemcitabine or hydroxyurea by inhibition of HR.

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

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

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

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

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

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

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

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

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

94 fraction is considerably increased following hydroxyurea exposure.

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

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

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

98 ascade, which in the presence of glucose and hydroxyurea generates a protocell-mediated flux of nitri

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

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

101 Children receiving hydroxyurea had significantly increased hemoglobin conce

102 Although hydroxyurea has become the standard of care for young ch

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

104 Hydroxyurea has proven safety, feasibility, and efficacy

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

106 t patients with sickle cell disease (SCD) on hydroxyurea have lower cerebral oxygen extraction fracti

107 Budding yeast treated with hydroxyurea (HU) activate the S phase checkpoint kinase

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

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

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

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

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

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

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

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

116 The neuroprotective efficacy of hydroxyurea (HU) remains unclear.

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

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

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

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

121 tients before and 2 years after the onset of hydroxyurea (HU) treatment or during a vaso-occlusive cr

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

123 ents (HbSS) of which 11 were on, and 12, off hydroxyurea (HU) treatment, and 5 ethnic matched control

124 n response to methyl methanesulfate (MMS) or hydroxyurea (HU) treatment, and its depletion partially

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

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

132 e impact of ectopic RNF168 overexpression on hydroxyurea (HU)-induced stalled replication forks in th

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

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

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

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

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

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

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

140 m nucleolytic degradation during response to hydroxyurea (HU).

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

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

143 n ET and PV patients previously treated with 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 -blind, placebo-controlled clinical trial of hydroxyurea in infants (beginning at 9-18 months of age)

148 ect the feasibility, safety, and benefits of hydroxyurea in low-resource settings.

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 With the increasing use of hydroxyurea, in lieu of transfusion therapy, for SCD pat

154 Hydroxyurea increased haemoglobin and fetal haemoglobin,

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 ollowing NS depletion and are protected from hydroxyurea-induced damage by NS overexpression.

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 TP)-producing pathways and shields them from hydroxyurea-induced loss of dNTPs.

165 9,195 compounds for their ability to inhibit hydroxyurea-induced phosphorylation of Ser345 on Chk1, k

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

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

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

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

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

171 ingle-agent best available therapy comprised hydroxyurea, interferon or pegylated interferon, pipobro

172 Hydroxyurea is an effective treatment for sickle cell an

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

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

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

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

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

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

179 ll disease (SCD); however, only 4 therapies (hydroxyurea, l-glutamine, crizanlizumab, and voxeletor)

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

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

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

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

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

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

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

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

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

189 Ps in CEM-SS leukemia cells with and without hydroxyurea or auranofin treatment.

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

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

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

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

194 ditions or after treatment with HbF inducers hydroxyurea or pomalidomide.

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

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

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

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

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

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

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

202 proved therapeutic alternative for this post-hydroxyurea patient population.

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

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

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

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

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

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

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

210 Robust activation of Cds1 in response to hydroxyurea prevents the endonuclease Mus81 from cleavin

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

212 Hydroxyurea provides SCA-related laboratory and clinical

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

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

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

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

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

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

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

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

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

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

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

224 results, there is appropriate anxiety about hydroxyurea's cerebral protection.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

240 Hydroxyurea therapy is strongly recommended for adults w

241 Hydroxyurea therapy led to significant increases in both

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

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

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

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

246 ns for crises, number of blood transfusions, hydroxyurea therapy, transcranial Doppler-confirmed cere

247 set of patients from chronic transfusions to hydroxyurea therapy.

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

249 dent in human sickle cell patients receiving hydroxyurea therapy.

250 usions for >=1 year with potential switch to hydroxyurea thereafter), using propensity score matching

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

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

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

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

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

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

257 ISC1 deletion prevents spindle elongation in hydroxyurea-treated cells.

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

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

260 Utilizing data from both wild-type and hydroxyurea-treated yeast cells, we show that our model

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

262 Hydroxyurea treatment appears safe for children with SCA

263 Hydroxyurea treatment decreased neutrophil extravasation

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

265 Centrosome amplification after hydroxyurea treatment increases significantly in Cep135-

266 Hydroxyurea treatment is recommended for children with s

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

268 Hydroxyurea treatment of sickle cell mice improved their

269 Hydroxyurea treatment reduces haemolysis and anaemia by

270 Hydroxyurea treatment was feasible and safe in children

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

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

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

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

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

276 ease symptoms and provides an alternative to hydroxyurea treatment.

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

278 tressors such as rapamycin, fluconazole, and hydroxyurea treatment.

279 ression defect upon checkpoint activation by hydroxyurea treatment.

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

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

282 Hydroxyurea use reduced the incidence of vaso-occlusive

283 es of clinical adverse events decreased with hydroxyurea use, including rates of vaso-occlusive pain

284 SdhX overproduction confers resistance to hydroxyurea, via regulation of ackA SdhX abundance is ti

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

286 Hydroxyurea was associated with statistically significan

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

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

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

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

291 ss to regular TCD screening since birth, and hydroxyurea was routinely administered to children with

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

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

294 vera who were resistant to or intolerant of hydroxyurea were randomly assigned 1:1 to receive either

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

296 th sickle cell anemia in sub-Saharan Africa, hydroxyurea with dose escalation had superior clinical e

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

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

299 rior clinical efficacy to that of fixed-dose hydroxyurea, with equivalent safety.

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