ライフサイエンスコーパス: cytarabine

1 , mitoxantrone plus cytarabine, or high-dose cytarabine).

2 tance to gemcitabine and cross-resistance to cytarabine.

3 on, or with secondary AML benefitted from HD cytarabine.

4 reached on the benefit of higher dosages of cytarabine.

5 for these exceptionally high-dose levels of cytarabine.

6 eive either imatinib or interferon alfa plus cytarabine.

7 mission (CR) received 3 courses of high-dose cytarabine.

8 ents who received rituximab and/or high-dose cytarabine.

9 3 weeks; and 4 weeks of cyclophosphamide and cytarabine.

10 in relationship with variable dose levels of cytarabine.

11 val advantage equivalent to doxorubicin plus cytarabine.

12 ombination with mitoxantrone, etoposide, and cytarabine.

13 ressing AML cells to treatment with ATRA and cytarabine.

14 I-AML3 to all-trans retinoic acid (ATRA) and cytarabine.

15 iving initial therapies that did not contain cytarabine.

16 rine, cytarabine, and etoposide or high-dose cytarabine.

17 e mechanism of action that is different from cytarabine.

18 ays of clofarabine with or without 7 days of cytarabine.

19 aliplatin in the presence of fludarabine and cytarabine.

20 sine nucleoside analogues, troxacitabine and cytarabine.

21 restored H3K36me3 levels and sensitivity to cytarabine.

22 median of 4 IT administrations of liposomal cytarabine.

23 est supportive care with or without low-dose cytarabine.

24 , gemcitabine, fludarabine, chlorambucil, or cytarabine.

25 atment with the cytidine nucleoside analogue cytarabine.

26 ilized the combination of anthracyclines and cytarabine.

27 e of anthracycline (or anthracenedione) plus cytarabine.

28 kemic activity, stronger than that caused by cytarabine.

29 ight (2%) of 350 patients given placebo plus cytarabine.

30 and acts synergistically in combination with cytarabine.

31 imab and four doses of intrathecal liposomal cytarabine.

32 ravenously (IV) daily x 3 (days 4 to 6), and cytarabine 1.5 g/m(2) IV as a continuous infusion daily

33 cycle; 70 mg/m(2) in subsequent cycles) plus cytarabine (1 g/m(2) intravenously on days 1-5) or place

34 ere similar between MACE/MidAc and high-dose cytarabine (1.5/3.0 g/m(2)), but cytarabine required les

35 nd one cycle of amsacrine (500 mg/m(2)) plus cytarabine (10 g/m(2); MAC/MAMAC/MAC).

36 ive two cycles of consolidation therapy with cytarabine 100 mg/m(2) daily for 5 days, etoposide 75 mg

37 , alternating idarubicin 8 mg/m(2) on day 1, cytarabine 100 mg/m(2) on days 1 to 5, and a regimen of

38 ncluded idarubicin 8 mg/m(2) on days 1 to 5, cytarabine 100 mg/m(2) on days 1 to 7, and lomustine 200

39 ) per day for 3 days and continuous-infusion cytarabine 100 mg/m(2) per day for 7 days.

40 ide 100 mg/m(2) twice daily (days -5 to -2), cytarabine 100 mg/m(2) twice daily (days -5 to -2), and

41 e meter), combined with seven daily doses of cytarabine (100 mg per square meter) by continuous intra

42 a single, standard induction with infusional cytarabine (100 mg/m(2) for 7 days) and daunorubicin (60

43 in (45 mg/m(2) per day on days 1, 2, and 3), cytarabine (100 mg/m(2) per day by continuous infusion o

44 In the second cycle, patients received cytarabine 1000 mg/m(2) twice daily on days 1-6 with or

45 two cycles of mitoxantrone (30 mg/m(2)) plus cytarabine (12 g/m(2)) and one cycle of amsacrine (500 m

46 ses of methotrexate 3.5 g/m(2) on day 1 plus cytarabine 2 g/m(2) twice daily on days 2 and 3 (group A

47 ses of methotrexate 3.5 g/m(2) on day 1 plus cytarabine 2 g/m(2) twice daily on days 2 and 3 (group A

48 Fludarabine 30 mg/m(2) and cytarabine 2 g/m(2) were administered on days 15 to 19.

49 o courses of consolidation chemotherapy with cytarabine 2 gm/m(2) on days 1 through 5 with bortezomib

50 f intravenous rituximab 375 mg/m(2) (day 1), cytarabine 3 g/m(2) (days 2 and 3), and thiotepa 40 mg/m

51 ngle hNT type (hENT1), accumulation of [(3)H]cytarabine, [(3)H]cladribine, or [(3)H]fludarabine was r

52 uded high-dose methotrexate (48%), high-dose cytarabine (33%), brain radiation (24%) and/or rituximab

53 18 showed association (P < .05) with either cytarabine 50% inhibitory concentration in leukemia cell

54 ontaining daunorubicin and intermediate-dose cytarabine (500 mg/m(2) every 12 hours for 6 days).

55 and prednisone) alternating with R-high-dose cytarabine (6 cycles total), followed by high-dose BEAM/

56 ns led to resistance to DNA-damaging agents, cytarabine, 6-thioguanine, doxorubicin, and etoposide, b

57 mly assigned to receive interferon alfa plus cytarabine (65.6%) and the short duration of therapy bef

58 stine-doxorubicin-dexamethasone-methotrexate/cytarabine, a cooperative group study of this regimen ap

59 h decitabine, a DNA demethylating agent, and cytarabine, a frontline cytotoxic agent used in the trea

60 (60 mg/m(2) per day on days 1, 2, and 3) and cytarabine alone (DA).

61 % (14-31) of those treated with methotrexate-cytarabine alone (hazard ratio 0.46, 95% CI 0.28-0.74) a

62 n reducing tumour burden than treatment with cytarabine alone suggesting that the sequential delivery

63 AEs were similar for decitabine and cytarabine, although patients received a median of four

64 s 38.7% for patients randomly assigned to SD cytarabine and 42.5% for those randomly assigned to HD c

65 onsolidation courses that included high-dose cytarabine and anthracycline, and maintenance therapy co

66 cell-differentiating drugs/compounds such as cytarabine and aphidicolin and found that they also prim

67 , the IC(50) of FdUMP[10] was lower than for cytarabine and approximately 1000 times lower than 5-flu

68 apy (induction therapy with daunorubicin and cytarabine and consolidation therapy with high-dose cyta

69 between patients receiving conventional-dose cytarabine and daunorubicin and either zosuquidar (550 m

70 re achieved among the 31 patients with prior cytarabine and daunorubicin treatment.

71 Adverse events were consistent with cytarabine and daunorubicin treatment.

72 sing a 3 + 7 regimen including standard-dose cytarabine and daunorubicin, complete remission was achi

73 treated patients with APL received 3 days of cytarabine and DRN followed by 30 doses of ATO beginning

74 llowed by intensification with high doses of cytarabine and etoposide combined with rituximab and fil

75 riple IT therapy (ie, methotrexate with both cytarabine and hydrocortisone).

76 osis and DNA damage following treatment with cytarabine and idarubicin.

77 20 (6%) of 355 patients given vosaroxin plus cytarabine and in eight (2%) of 350 patients given place

78 3 mg/m(2) while the MTD in combination with cytarabine and l-asparaginase was 2 mg/m(2).

79 les of alternating hyper-CVAD, and high-dose cytarabine and methotrexate.

80 The MTD for GMTZ in combination with cytarabine and mitoxantrone was 3 mg/m(2) while the MTD

81 We report results of a phase 2 trial using cytarabine and rituximab as induction regimen before aut

82 ents in first complete remission (CR1) after cytarabine and standard- or high-dose daunorubicin induc

83 tudies confirmed OCTN1-mediated transport of cytarabine and various structurally related cytidine ana

84 nvolving combinations of Mnk inhibitors with cytarabine and/or mTOR inhibitors for the treatment of A

85 Median half-life was 31.1 hours (cytarabine) and 21.9 hours (daunorubicin), with both dru

86 odeficient mouse response to combined Ara-C (cytarabine) and doxorubicin treatment.

87 sed by chemotherapeutic agents (thiopurines, cytarabine, and 5-fluorouracil), which acts at early ste

88 therapy induction (rituximab, dexamethasone, cytarabine, and a platinum derivative [R-DHAP]), the ove

89 receive 2 induction cycles with idarubicin, cytarabine, and all-trans retinoic acid either with VPA

90 Despite immunochemotherapy, high-dose cytarabine, and ASCT, younger MCL patients with deletion

91 one, and cisplatin (GDP) with dexamethasone, cytarabine, and cisplatin (DHAP) before ASCT.

92 latin, and etoposide (ICE) or dexamethasone, cytarabine, and cisplatin (DHAP), with autologous transp

93 r a standard induction regimen of tretinoin, cytarabine, and daunorubicin, followed by 2 courses of c

94 O in course 3 in combination with amsacrine, cytarabine, and etoposide or high-dose cytarabine.

95 to induction chemotherapy with mitoxantrone, cytarabine, and etoposide preceded, or not, by a course

96 rabine, followed by R-HDS (cyclophosphamide, cytarabine, and etoposide) supported by autologous stem-

97 ients were randomly assigned to fludarabine, cytarabine, and granulocyte colony-stimulating factor (F

98 r cells after administration of clofarabine, cytarabine, and granulocyte-colony stimulating factor pr

99 nd toxicity of the combination of sorafenib, cytarabine, and idarubicin in patients with acute myeloi

100 omparator group of supportive care, low-dose cytarabine, and intensive cytarabine plus anthracycline,

101 s were prepared using carmustine, etoposide, cytarabine, and melphalan and received consistent manage

102 h-dose treatment with carmustine, etoposide, cytarabine, and melphalan as well as rabbit antithymocyt

103 AM/C (bis-chloroethylnitrosourea, etoposide, cytarabine, and melphalan or cyclophosphamide) and autol

104 hase I-II trial of oxaliplatin, fludarabine, cytarabine, and rituximab (OFAR) in these diseases.

105 otrexate, most notably alkylators, high-dose cytarabine, and rituximab; and the use of myeloablative

106 tion stress and damage by ATR inhibition and cytarabine, and the ability of ATR inhibition to abrogat

107 ing tumor cells were also cross-resistant to cytarabine, another nucleoside analog commonly used in c

108 High-dose cytarabine applied during remission induction or as cons

109 e to docetaxel, paclitaxel, vincristine, and cytarabine (Ara-C) and exhibited increased cellular drug

110 The separation of cytarabine (ara-C) from the endogenous compounds in mous

111 The nucleoside analog cytarabine (Ara-C) is an essential component of primary

112 and enhanced the antileukemic properties of cytarabine (Ara-C) or mammalian target of rapamycin (mTO

113 from deep-sequencing of RNA derived from two cytarabine (Ara-C) resistance acute myeloid leukemia (AM

114 ional phase 2 study combining cladribine and cytarabine (Ara-C) was initiated for patients with refra

115 duction therapy commenced with daunorubicin, cytarabine (Ara-C), and all-trans retinoic acid (ATRA),

116 ntify rational therapeutic combinations with cytarabine (Ara-C), we developed a high-throughput, smal

117 g the effects of four CTNAs-acyclovir (ACV), cytarabine (Ara-C), zidovudine (AZT) and zalcitabine (dd

118 of acute myeloid leukaemia (AML) patients to cytarabine (Ara-C)-based therapies are often short lived

119 rapeutic agents, i.e., doxorubicin (DOX) and cytarabine (Ara-C).

120 in clinical therapy: daunorubicin (DNR) and cytarabine (ara-C).

121 eukemia (AML) cells for cytotoxic killing by cytarabine (Ara-C).

122 In vitro data suggested synergy with cytarabine (Ara-C).

123 ) plus imatinib/dasatinib or idarubicin plus cytarabine (Ara-C); 2 did not respond, 1 had CCyR, and 1

124 ine (AZA), but a good correlation to that of cytarabine (Ara-C; R = 0.89, P < .001).

125 e metabolite of cytosine arabinoside (ara-C, cytarabine), ara-CTP, has been investigated and verified

126 oxycytidine, dFdC) and cytosine arabinoside (cytarabine, ara-C) represent a class of nucleoside analo

127 duction (3 + 7) and consolidation (high-dose cytarabine; Ara-C) as the standard of care for acute mye

128 analogues 1-beta-d-arabinofuranosylcytosine (cytarabine; ara-C), gemcitabine, and troxacitabine, whic

129 Cytarabine arabinoside (ara-C) is an antimetabolite used

130 cells ex vivo have increased sensitivity to cytarabine (araC) and daunorubicin, suggesting that opti

131 The anticancer activity of cytarabine (AraC) and gemcitabine (dFdC) is thought to r

132 Cytarabine (AraC) represents the most effective single a

133 1-Beta-D-arabinofuranosylcytosine (cytarabine, araC) and 2',2'-difluoro-2'-deoxycytidine (g

134 motherapy, with usually an anthracycline and cytarabine as the foundation.

135 solidation with dasatinib, sequentially with cytarabine, asparaginase, and methotrexate for 6 months.

136 years) who had previously untreated AML with cytarabine at 1.5 g/m(2) by continuous intravenous (IV)

137 Cytarabine at 1.5 g/m(2) is equivalent to a 3 g/m(2) dos

138 Most centers use 7 to 10 days of cytarabine at a daily dose of 100 to 200 mg/m(2) for rem

139 If the same anthracycline/cytarabine-based approach is deployed, the remission rat

140 f age with AML (>/= 20% blasts) treated with cytarabine-based intensive chemotherapy between 1990 and

141 y confirms that induction with rituximab and cytarabine-based regimens is safe and effective in MCL p

142 At least 94% of patients receiving cytarabine-based therapy and surviving for more than 3 o

143 ade, there has been a widespread adoption of cytarabine-based therapy in younger patients, and the in

144 itive/synergistic effects when combined with cytarabine, bendamustine, or rituximab.

145 h MACE/MidAc is similar overall to high-dose cytarabine, but superior in high-risk patients.

146 inib and dasatinib and at least as potent as cytarabine; (c) APcK110 inhibits the phosphorylation of

147 lood-brain barrier such as high-dose MTX and cytarabine can result in significant neurotoxicity.

148 y used in cancer therapy, and 4-(N)-stearoyl cytarabine carried by solid lipid nanoparticles can also

149 When cytarabine chemotherapy was administered prior to vaccin

150 The combination of ADI-PEG 20 and cytarabine chemotherapy was more effective than either t

151 ux of anticancer nucleoside drugs, including cytarabine, cladribine, and fludarabine.

152 trexate/ifosfamide, etoposide, and high-dose cytarabine (CODOX-M/IVAC) for HIV-positive patients.

153 mab with or without thiotepa to methotrexate-cytarabine combination therapy (the MATRix regimen), fol

154 induction chemotherapy with an anthracycline/cytarabine combination, followed by either consolidation

155 reported the feasibility of clofarabine and cytarabine combinations in AML.

156 ngly enhanced the suppressive effects of low cytarabine concentrations on CFU-L.

157 sponded to the combination of bortezomib and cytarabine, concomitant with the re-establishment of EZH

158 rd induction course, followed by 3 high-dose cytarabine consolidation courses.

159 agnosis to receive either standard high-dose cytarabine consolidation with three cycles of 18 g/m(2)

160 Patients received 1.5 g/m(2) per day cytarabine continuous infusion for 3 days and laromustin

161 icities usually manifested after the MTX and cytarabine courses.

162 lodysplastic syndromes, that is, idarubicine-cytarabine (cycle I) and amsacrine-cytarabine (cycle II)

163 arubicine-cytarabine (cycle I) and amsacrine-cytarabine (cycle II) without or with clofarabine (10 mg

164 three induction schedules: daunorubicin and cytarabine; cytarabine, daunorubicin, and etoposide; or

165 Cytarabine (cytosine arabinoside) is one of the most eff

166 to two induction courses of daunorubicin and cytarabine (DA) with or without etoposide (ADE; n = 1983

167 ee induction regimens: DA (daunorubicin plus cytarabine), DAC (DA plus cladribine), or DAF (DA plus f

168 ednisone), CALGB C9710 (single arm of ATRA + cytarabine + daunorubicin), Eastern Cooperative Oncology

169 d SWOG S0521 (single-arm induction of ATRA + cytarabine + daunorubicin).

170 tion schedules: daunorubicin and cytarabine; cytarabine, daunorubicin, and etoposide; or fludarabine,

171 rapies for mutant FLT3 and IDH2, a liposomal cytarabine-daunorubicin formulation for therapy-related

172 60 years) de novo CN-AML patients treated on cytarabine/daunorubicin-based protocols.

173 C and ERG in 158 de novo patients treated on cytarabine/daunorubicin-based protocols.

174 CPX-351 is a liposomal formulation of cytarabine:daunorubicin designed to deliver synergistic

175 of dexamethasone, etoposide, cisplatin, and cytarabine (DECA).

176 he introduction of high-dose versus low-dose cytarabine did not significantly lower the rate of MRD-p

177 and amsacrine in combination with high-dose cytarabine does not improve treatment outcome and confer

178 seen in patients treated with escalated-dose cytarabine during remission induction.

179 high-dose consolidation with etoposide plus cytarabine (EA); three, progression-free survival (PFS);

180 higher remission and survival rates than SD cytarabine, especially in patients younger than age 46 y

181 itumomab tiuxetan with high-dose carmustine, cytarabine, etoposide, and melphalan (BEAM) and autologo

182 icin (FLAG-Ida; n = 1268), and to amsacrine, cytarabine, etoposide, and then mitoxantrone/cytarabine

183 cross-resistant to antileukemia agents (eg, cytarabine, etoposide, and TRAIL), HL-60/LR cells are co

184 alternating with high-dose methotrexate and cytarabine every 21 days.

185 ved 2 cycles of consolidation with high-dose cytarabine followed by peripheral blood progenitor cell

186 tine-prednisone with rituximab and high-dose cytarabine, followed by high-dose therapy appears quite

187 treated with high-doses of methotrexate and cytarabine, followed by R-HDS (cyclophosphamide, cytarab

188 a reappraisal of the usefulness of high-dose cytarabine for acute myeloid leukemia treatment.

189 n the SELHEM (Selinexor With Fludarabine and Cytarabine for Treatment of Refractory or Relapsed Leuke

190 f clinically used pyrimidine-based prodrugs (cytarabine, gemcitabine).

191 Liposomal cytarabine given via intrathecal route concomitantly wit

192 g/m(2), n=113) or low-dose (2 g/m(2), n=117) cytarabine given with daunorubicin and etoposide (ADE; i

193 In the presence of cytarabine, GM-CSF-Bcl-XL was able also to promote the d

194 e (ADE; n = 1983) or ADE versus fludarabine, cytarabine, granulocyte colony-stimulating factor, and i

195 daunorubicin, and etoposide; or fludarabine, cytarabine, granulocyte colony-stimulating factor, and i

196 us cytarabine group than in the placebo plus cytarabine group (107 [30%] of 356 patients vs 58 [16%]

197 and 6.1 months (5.2-7.1) in the placebo plus cytarabine group (hazard ratio 0.87, 95% CI 0.73-1.02; u

198 onths (95% CI 6.4-8.5) in the vosaroxin plus cytarabine group and 6.1 months (5.2-7.1) in the placebo

199 us cytarabine group than in the placebo plus cytarabine group included febrile neutropenia (167 [47%]

200 hat were more frequent in the vosaroxin plus cytarabine group than in the placebo plus cytarabine gro

201 ved complete remission in the vosaroxin plus cytarabine group than in the placebo plus cytarabine gro

202 8 [8%] of 355 patients in the vosaroxin plus cytarabine group vs 23 [7%] of 350 in the placebo plus c

203 group vs 23 [7%] of 350 in the placebo plus cytarabine group; 60-day: 70 [20%] vs 68 [19%]).

204 Clofarabine plus low-dose cytarabine has a higher response rate than clofarabine a

205 nation (CLARA) versus conventional high-dose cytarabine (HDAC) as postremission chemotherapy in young

206 (AML) treated with laromustine and high-dose cytarabine (HDAC) versus HDAC/placebo.

207 to either 5-drug reinduction or fludarabine/cytarabine/idarubicin.

208 cts of ATR inhibition alone or combined with cytarabine in AML cells.

209 tivity of ATR inhibition in combination with cytarabine in AML.

210 tients) versus escalated-dose (207 patients) cytarabine in cycles 1 and 2.

211 G2/M cell cycle arrest, and cooperated with cytarabine in inducing DNA replication stress and damage

212 ) the role of lower doses of clofarabine and cytarabine in older patients.

213 continuously exposed to increasing doses of cytarabine in order to establish equivalent resistant ce

214 ion with hypomethylating agents and low-dose cytarabine in patients with high-risk myelodysplastic sy

215 -class anticancer quinolone derivative, plus cytarabine in patients with relapsed or refractory acute

216 ortezomib was combined with daunorubicin and cytarabine in previously untreated older adults with acu

217 er-dose clofarabine with or without low-dose cytarabine in previously untreated patients with AML age

218 d-dose whole-brain radiotherapy (rdWBRT) and cytarabine in primary CNS lymphoma.

219 he standard combination of anthracycline and cytarabine in primary patient xenografts.

220 cs to matched patients treated with low-dose cytarabine in the United Kingdom AML14 trial, but had si

221 primary human AML cells after treatment with cytarabine in vitro Upon overexpression, RUNX1 restricte

222 nd autologous stem-cell rescue and high-dose cytarabine in younger patients and the benefits of maint

223 r export, when combined with fludarabine and cytarabine, in children with relapsed or refractory leuk

224 plantation (ASCT), with or without high-dose cytarabine, in the randomized European MCL Younger trial

225 Cytarabine induced phosphorylation/activation of Mnk and

226 ein, include tumor lysis, hyperleukocytosis, cytarabine-induced cellebellar toxicity, acute promyeloc

227 LCLs with AA genotype were more sensitive to cytarabine-induced cytotoxicity (P = 1.31 x 10(-6)) and

228 d to investigate the genetic determinants of cytarabine-induced cytotoxicity.

229 AZ20 synergistically enhanced cytarabine-induced proliferation inhibition and apoptosi

230 feration inhibition and apoptosis, abolished cytarabine-induced S and G2/M cell cycle arrest, and coo

231 To assess the functional relevance of cytarabine-inducible engagement of Mnk/eIF4E pathway, th

232 ortezomib to standard 3 + 7 daunorubicin and cytarabine induction chemotherapy for AML resulted in an

233 chemotherapy consisting of intermediate-dose cytarabine (Int-DAC).

234 After cytarabine intensification, patients randomized to inter

235 ed donor marrow transplantation or high-dose cytarabine intensification.

236 Cytarabine is a key constituent of remission induction c

237 R-MPV combined with consolidation rdWBRT and cytarabine is associated with high response rates, long-

238 ombination of vorinostat with idarubicin and cytarabine is safe and active in AML.

239 orafenib in combination with clofarabine and cytarabine is tolerable and shows activity in relapsed/r

240 linexor, in combination with fludarabine and cytarabine, is tolerable at doses up to 55 mg/m(2) in pe

241 ntensive induction therapy compared low-dose cytarabine (LDAC) with or without volasertib, a highly p

242 and 42.5% for those randomly assigned to HD cytarabine (log-rank test P = .06; multivariable analysi

243 cytarabine, etoposide, and then mitoxantrone/cytarabine (MACE-MidAC) or high-dose cytarabine (n = 1,4

244 ects of pharmacological inhibition of Mnk on cytarabine-mediated suppression of primitive leukemic pr

245 s suggests that the addition of vosaroxin to cytarabine might be of clinical benefit to some patients

246 The cytarabine MTD used in stage two was 800 mg/m(2), and R-

247 y 1), B (70 mg/m(2) IV on days 2 and 3), and cytarabine (MTD IV on days 2 to 4) every 28 days for fou

248 ed AML salvage regimens, including high-dose cytarabine, multiagent chemotherapy, hypomethylating age

249 antrone/cytarabine (MACE-MidAC) or high-dose cytarabine (n = 1,445) 3 g/m(2) or 1.5 g/m(2) (n = 657)

250 oxin plus cytarabine (n=356) or placebo plus cytarabine (n=355).

251 nts were randomly assigned to vosaroxin plus cytarabine (n=356) or placebo plus cytarabine (n=355).

252 ) including high-dose methotrexate (MTX) and cytarabine on alternating courses.

253 nduction chemotherapy with anthracycline and cytarabine on Southwest Oncology Group trials.

254 We determined the effects of chemotherapy (cytarabine) on the activation status of Mnk in AML cells

255 oxic activities of standard AML chemotherapy cytarabine or daunorubicin.

256 Consolidation with high-dose cytarabine or stem-cell transplantation in high-risk pat

257 onsolidation, and finally to a fifth course (cytarabine) or not (n = 227).

258 gimens contained busulfan, cyclophosphamide, cytarabine, or fludarabine according to the donor used.

259 colony-stimulating factor, mitoxantrone plus cytarabine, or high-dose cytarabine).

260 and subsequent treatment with bendamustine, cytarabine, or lenalidomide failed to reveal any associa

261 Cytarabine plays a pivotal role in the treatment of pati

262 alternating with methotrexate and high-dose cytarabine plus a tyrosine kinase inhibitor, had minimal

263 ive care, low-dose cytarabine, and intensive cytarabine plus anthracycline, while inducing trilineage

264 randomized to receive low-dose or high-dose cytarabine plus daunorubicin and etoposide; of these, 18

265 FdUMP[10] was better tolerated than 5-FU or cytarabine plus doxorubicin and did not affect normal HS

266 We evaluated the use of cytarabine plus either standard-dose or high-dose daunor

267 ]) or standard care (either fludarabine plus cytarabine plus granulocyte colony-stimulating factor, m

268 % (21-42) of those treated with methotrexate-cytarabine plus rituximab (0.61, 0.40-0.94).

269 equent in patients treated with methotrexate-cytarabine plus rituximab and thiotepa, but infective co

270 ine and consolidation therapy with high-dose cytarabine) plus either midostaurin or placebo; those wh

271 HD cytarabine produces higher remission and survival rates

272 jection of peg-Arg I plus chemotherapy agent Cytarabine prolonged survival in mice bearing T-ALL tumo

273 tions between treatment and demographics, or cytarabine randomization.

274 er, patients treated with the escalated-dose cytarabine regimen benefited from G-CSF priming, with im

275 406 patients were also randomized between 2 cytarabine regimens comparing conventional-dose (199 pat

276 d high-dose cytarabine (1.5/3.0 g/m(2)), but cytarabine required less supportive care.

277 ells, and predict relapse based on increased cytarabine resistance of a KRAS wild-type subclone.

278 Our data indicate that cytarabine-resistant cells are more susceptible to natur

279 arly, the combination of cercosporamide with cytarabine resulted in enhanced antileukemic responses i

280 ess let-7a exhibited enhanced sensitivity to cytarabine, resulting in greatly extended survival of im

281 th poor or no response to regimens including cytarabine, rituximab, and autologous stem-cell transpla

282 -5 and 0 (group B); or the same methotrexate-cytarabine-rituximab combination plus thiotepa 30 mg/m(2

283 -5 and 0 (group B); or the same methotrexate-cytarabine-rituximab combination plus thiotepa 30 mg/m(2

284 ediated cell lysis as compared with parental cytarabine-sensitive cells.

285 daily for 5 days with or without 20 mg/m(2) cytarabine subcutaneously daily for 14 days as induction

286 isation have demonstrated that methotrexate, cytarabine, thiotepa, and rituximab (called the MATRix r

287 ) intravenously on days 1-5) or placebo plus cytarabine through a central interactive voice system wi

288 MCC expression was induced by cytarabine treatment from 1.7- to 26.6-fold in LCLs.

289 F9-induced leukemia and caused resistance to cytarabine treatment in vivo, whereas homozygous loss de

290 The combination of CXCR4 silencing and cytarabine treatment resulted in more effective cytotoxi

291 ents without G-CSF undergoing escalated-dose cytarabine treatment.

292 atients receiving FLAG-Ida (two courses) and cytarabine (two courses), 8-year survival was 63% for pa

293 atinib and dasatinib inhibit fludarabine and cytarabine uptake.

294 elacytarabine, a novel elaidic acid ester of cytarabine, versus the investigator's choice of one of s

295 tergroup I0129, consisting of daunorubicin + cytarabine vs ATRA), and SWOG S0521 (single-arm inductio

296 Sequential treatment with decitabine and cytarabine was found to be more effective in reducing tu

297 Consolidation cytarabine was given after the radiotherapy.

298 Liposomal cytarabine was given for CNS prophylaxis to 31 patients

299 c antileukemic interactions between AZ20 and cytarabine were confirmed in primary AML patient samples

300 In this phase II study, we combined cytarabine with R and B (R-BAC) in patients with MCL age

301 ietic stem-cell transplantation or high-dose cytarabine, with or without a single dose of the monoclo