ライフサイエンスコーパス: fludarabine

1 ), DAC (DA plus cladribine), or DAF (DA plus fludarabine).

2 were suppressed by chronic administration of fludarabine.

3 g with total body irradiation, thiotepa, and fludarabine.

4 hesis induced by bendamustine was blocked by fludarabine.

5 hemoresistance of activated CLL cells toward fludarabine.

6 atio 0.27; P = .004) but not chlorambucil or fludarabine.

7 randomly assigned to receive chlorambucil or fludarabine.

8 en without irradiation, the latter including fludarabine.

9 paration combining thiotepa, treosulfan, and fludarabine.

10 cell chimerism was significantly better with fludarabine.

11 e and total body irradiation with or without fludarabine.

12 ine and fludarabine, or cyclophosphamide and fludarabine.

13 ing regimen of low-dose cyclophosphamide and fludarabine.

14 onditioning regimen of cyclophosphamide plus fludarabine.

15 drugs, including cytarabine, cladribine, and fludarabine.

16 Sixteen patients were conditioned with fludarabine (125 mg/m(2)) and melphalan (140 mg/m(2)) pl

17 with cyclophosphamide 200 mg/kg (n = 30) or fludarabine 150 mg/m(2) (n = 40), with alemtuzumab in mo

18 mg (n = 31) or 1000 mg (n = 30) day 1, with fludarabine 25 mg/m(2) and cyclophosphamide 250 mg/m(2)

19 Patients (n = 102) received fludarabine 25 mg/m(2) intravenously days 1 to 5 and rit

20 b 30 mg per day on days 1-3) or monotherapy (fludarabine 25 mg/m(2) on days 1-5) by use of an interac

21 The regimen consisted of fludarabine 25 mg/m(2) per day for 5 days, melphalan 140

22 mg/m2 on day 1 (375 mg/m2 the first cycle), fludarabine 25 mg/m2 on days 1 to 3, cyclophosphamide 20

23 n age of 70 years were randomized to receive fludarabine (25 mg/m(2) for 5 days intravenously, every

24 located to receive six cycles of intravenous fludarabine (25 mg/m(2) per day) and cyclophosphamide (2

25 yclophosphamide (60 mg/kg, days 1 and 2) and fludarabine (25 mg/m(2), day 3 through 7) followed by tw

26 ay cycles were administered intravenously of fludarabine (25 mg/m(2), days 1-3), cyclophosphamide (25

27 ed cyclophosphamide (60 mg/kg on day -7) and fludarabine (25 mg/m(2)/d on days -6 through -2), follow

28 mide [60 mg/kg] daily for 2 days followed by fludarabine [25 mg/m(2)] daily for 5 days, followed by a

29 een May 2013 and March 2015 and who received fludarabine 30 mg/m day (D)-7 to -3, melphalan 140 mg/m

30 Fludarabine 30 mg/m(2) and cytarabine 2 g/m(2) were admi

31 21) and unrelated donors (UD; n = 29), using fludarabine 30 mg/m(2) for 4 days, cyclophosphamide 300

32 9 and 2 mg/kg on days -8 and -7, intravenous fludarabine 30 mg/m(2) on days -6 to -2, intravenous cyc

33 chedule to open-label combination treatment (fludarabine 30 mg/m(2) per day and alemtuzumab 30 mg per

34 re offered (cycle 1: CPX-351; cycle 2: FLAG [fludarabine 30 mg/m(2)/dose on days 1-5; cytarabine 2,00

35 ntensity conditioning consisted of high-dose fludarabine (30 mg/m(2) [infants <9 kg 1.2 mg/kg]; one d

36 r conditioning chemotherapy with intravenous fludarabine (30 mg/m(2) body-surface area) and cyclophos

37 All patients were prepared for HSCT with fludarabine (30 mg/m(2) per day) 4, 3, and 2 days before

38 g per day, intravenously, on days -4 to -2), fludarabine (30 mg/m(2) per day, intravenously, on days

39 regimen composed of treosulfan (14 g/m) and fludarabine (30 mg/m) started on day -6 and given for 3

40 ificantly higher among patients treated with fludarabine (36%) compared with patients treated with ch

41 radiation [TBI] 200 cGy + cyclophosphamide + fludarabine), 4-6 of 6 matched dUCB-other (n = 40; alkyl

42 s of oral FC chemotherapy (days 1 through 3: fludarabine 40 mg/m(2) per day and cyclophosphamide 250

43 After a uniform preparative regimen (fludarabine 40 mg/m(2) x 5, cyclophosphamide 50 mg/kg, 2

44 patients received a conditioning regimen of fludarabine (40 mg/m(2) daily for 4 days) and busulfan (

45 -anti-CD45 antibody (30F11), with or without fludarabine (5 days starting day -8), with cyclophospham

46 roblasts with specific inhibitors for STAT1 (fludarabine, 50 muM), STAT3 (S31-201, 10 muM), p38 MAPK

47 All patients received alkylating agent plus fludarabine; 792 received allografts from a human leukoc

48 Conditioning consisted of fludarabine (90 mg/m2) and 2 to 3 Gy total body irradiat

49 otal body irradiation alone or combined with fludarabine, 90 mg/m(2), before related (n = 184) or unr

50 5 showed a higher therapeutic potential than fludarabine, a drug already in use in lymphoma treatment

51 nistration of STAT1 small interfering RNA or fludarabine, a selective STAT1 inhibitor.

52 d busulfan, cyclophosphamide, cytarabine, or fludarabine according to the donor used.

53 lled in a phase 2 study of cyclophosphamide, fludarabine, alemtuzumab, and rituximab (CFAR).

54 at 7 years were 8.2% after FC and 4.6% after fludarabine alone (P = .09).

55 rly CLL patients the first-line therapy with fludarabine alone does not result in a major clinical be

56 treatment group and 149 (90%) of 165 in the fludarabine alone group.

57 ine plus cyclophosphamide (FC) compared with fludarabine alone yielded higher complete and overall re

58 lymphocytic leukemia, 9 after FC and 4 after fludarabine alone.

59 ta suggest that FC may induce more t-MN than fludarabine alone.

60 d]; 0.65 [0.45-0.94]; p=0.021) compared with fludarabine alone.

61 comes using a sequential transplant regimen, fludarabine/amsacrine/cytarabine-busulphan (FLAMSA-Bu),

62 tched-related and -unrelated donors received fludarabine and 200 cGy of total body irradiation (TBI);

63 h chronic lymphocytic leukemia refractory to fludarabine and alemtuzumab (FA-ref) and patients refrac

64 The combination of fludarabine and alemtuzumab is another treatment option

65 he efficacy and safety of the combination of fludarabine and alemtuzumab with fludarabine monotherapy

66 e treatment of CLL that is resistant to both fludarabine and alemtuzumab.

67 rst relapse, patients with prior exposure to fludarabine and alkylating agent combinations, and patie

68 CF-7.Hyor cells ( approximately 130-fold for fludarabine and approximately 45-fold for 6-methylpurine

69 -4 induced resistance to the cytotoxic drugs fludarabine and chlorambucil and to the novel p53-elevat

70 ezomib and carfilzomib), nucleoside analogs (fludarabine and cladribine), and ibrutinib.

71 Addition of rituximab (R) to fludarabine and cyclophosphamide (FC) has significantly

72 ndomly assigned to receive 6 courses of oral fludarabine and cyclophosphamide (FC) in combination wit

73 om 493 patients randomly assigned to receive fludarabine and cyclophosphamide (FC) or FC plus rituxim

74 LL8 study evaluating first-line therapy with fludarabine and cyclophosphamide (FC) or FC with rituxim

75 in the REACH trial, where patients received fludarabine and cyclophosphamide (FC) or rituximab plus

76 eeks for 6 to 8 cycles) or obinutuzumab plus fludarabine and cyclophosphamide (G-FC; every 4 weeks fo

77 ofatumumab, a human CD20 mAb, combined with fludarabine and cyclophosphamide (O-FC) as frontline the

78 trials of the German CLL Study Group (CLL8: fludarabine and cyclophosphamide [FC] v FC plus rituxima

79 domisation was stratified by Binet stage and fludarabine and cyclophosphamide administration route (o

80 All patients received fludarabine and cyclophosphamide before a single infusio

81 The fludarabine and cyclophosphamide couplet has become the

82 mg or intravenous rituximab 500 mg/m(2) plus fludarabine and cyclophosphamide every 4 weeks for up to

83 100% in the subset of patients who received fludarabine and cyclophosphamide lymphodepletion.

84 All patients underwent lymphodepletion with fludarabine and cyclophosphamide with or without alemtuz

85 Finally, we found that fludarabine and cyclophosphamide, frequently used before

86 When combined with fludarabine and cyclophosphamide, subcutaneous rituximab

87 were enrolled in the SELHEM (Selinexor With Fludarabine and Cytarabine for Treatment of Refractory o

88 bitors (TKIs) imatinib and dasatinib inhibit fludarabine and cytarabine uptake.

89 ibitor of nuclear export, when combined with fludarabine and cytarabine, in children with relapsed or

90 Conclusion Selinexor, in combination with fludarabine and cytarabine, is tolerable at doses up to

91 A reduced-intensity regimen using fludarabine and low-dose cyclophosphamide might be effec

92 oing transplantation for PIDs using RIC with fludarabine and melphalan (Flu/Melph) and to study the e

93 erred option with recent evidence suggesting fludarabine and melphalan as the optimal conditioning re

94 ne, and prednisone) and R-FM (rituximab plus fludarabine and mitoxantrone) regimens without rituximab

95 lpha inhibitors enhanced the cytotoxicity of fludarabine and reversed the protective effect of MSC on

96 , coupled with our historical fixed doses of fludarabine and rituximab (BFR), as a nonmyeloablative a

97 15 patients treated in British Columbia with fludarabine and rituximab (FR) from 2004 to 2010 for rel

98 ble in some patients who receive combination fludarabine and rituximab for chronic cold agglutinin di

99 Pretransplant conditioning consisted of fludarabine and targeted busulfan (n = 25) or total body

100 nts received cyclophosphamide in addition to fludarabine and TBI as conditioning.

101 phagy-activating therapeutic agents, such as fludarabine and the BCL2 homology domain 3 mimetic ABT-7

102 d by CC-115, and CD40-mediated resistance to fludarabine and venetoclax could be reverted by CC-115.

103 otal-body irradiation, cyclophosphamide, and fludarabine) and graft-versus-host disease prophylaxis (

104 um, 32 mCi/kg) (9)(0)Y-ibritumomab tiuxetan, fludarabine, and 2 Gy total body irradiation and matched

105 oning regimen incorporated cyclophosphamide, fludarabine, and 200 cGy of total body irradiation.

106 ide at 50 mg/kg and 100 mg/kg with TBI 2 Gy, fludarabine, and anti-thymocyte globulin results in effe

107 igh-dose therapy to six cycles of rituximab, fludarabine, and cyclophosphamide (R-FC) every 28 days o

108 higher than that associated with rituximab, fludarabine, and cyclophosphamide.

109 01 sensitizes CLL cells toward bendamustine, fludarabine, and dexamethasone.

110 LRF CLL4 trial, which compared chlorambucil, fludarabine, and FC, were screened by TaqMan real-time p

111 egimens consisted of an alkylating agent and fludarabine, and GVHD prophylaxis involved a calcineurin

112 suppression, and alemtuzumab (anti-CD52) and fludarabine, and low dose cyclophosphamide for immunosup

113 cell transplantation (HCT) with alemtuzumab, fludarabine, and melphalan is an effective approach for

114 ens predominantly consisting of alemtuzumab, fludarabine, and melphalan.

115 e conditioning regimen included alemtuzumab, fludarabine, and melphalan.

116 recovery following RIC HCT with alemtuzumab, fludarabine, and melphalan.

117 regimen included busulfan, cyclophosphamide, fludarabine, and rabbit anti-thymocyte globulin.

118 e conducted a phase I study of flavopiridol, fludarabine, and rituximab (FFR) in patients with mantle

119 New treatments are needed for patients with fludarabine- and alemtuzumab-refractory (FA-ref) chronic

120 analyses, cladribine compared favorably with fludarabine, another purine nucleoside analog that is mo

121 We investigated whether the combination of fludarabine, anti-thymocyte globulin, and total body irr

122 To define the efficacy of a busulfan/fludarabine/antithymocyte globulin RIC regimen in pediat

123 e incidence rate of 20.6% versus 3.7% in the fludarabine arm (P = .001).

124 onse (DR) were significantly improved in the fludarabine arm compared with the chlorambucil arm: PFS,

125 RR was 47.8% (95% CI, 40.9% to 54.8%) in the fludarabine arm versus 38.6% (95% CI, 32.0% to 45.7%) in

126 overall survival (OS) was not reached in the fludarabine arm versus 69.8 months in the chlorambucil a

127 or to busulfan when used in combination with fludarabine as a conditioning regimen for allogeneic HSC

128 stine, and prednisone, 23.1%; rituximab plus fludarabine based, 15.5%; other, 6.4%.

129 ho have comorbidities is challenging because fludarabine-based chemoimmunotherapies are mostly not su

130 with relapsed or refractory HL who received fludarabine-based lymphodepletion followed by CD30.CAR-T

131 32 patients with active disease who received fludarabine-based lymphodepletion was 72%, including 19

132 The addition of rituximab to fludarabine-based regimens in chronic lymphocytic leukem

133 MDS (n = 80) were randomly assigned 1:1 to a fludarabine-based RIC regimen or FLAMSA-Bu.

134 Patients had received prior fludarabine-based therapy or chemoimmunotherapy.

135 ic leukemia (CLL) with primary resistance to fludarabine-based therapy or with progressive disease we

136 ctive disease needing treatment, but in whom fludarabine-based treatment was not possible.

137 orbidities that may make them ineligible for fludarabine-based treatment.

138 outcome for patients who are ineligible for fludarabine-based treatments.

139 drugs have been approved for CLL treatment (fludarabine, bendamustine, and the monoclonal antibodies

140 quent AML/MDS patients who received busulfan-fludarabine (Bu-Flu).

141 d retrospectively) and 92 receiving busulfan/fludarabine (BuFlu) conditioning (data collected prospec

142 treatment with therapeutic agents, including fludarabine, CAL-101, and flavopiridol as well as the en

143 r's choice of either rituximab, gemcitabine, fludarabine, chlorambucil, or cytarabine.

144 safety of conditioning with treosulfan plus fludarabine compared with reduced-intensity busulfan plu

145 Cyclophosphamide plus fludarabine conditioning chemotherapy was administered b

146 After treatment with fludarabine containing regimens UGT2B17 was up-regulated

147 ncreased among patients who received infused fludarabine-containing chemotherapy with or without ritu

148 We investigated whether a fludarabine-containing induction regimen improved the co

149 depleting conditioning with cyclophosphamide/fludarabine (Cy/Flu).

150 ody irradiation (TBI), cyclophosphamide, and fludarabine (Cy/Flu/TBI200).

151 nutuzumab-bendamustine (G-B) or obinutuzumab fludarabine cyclophosphamide (G-FC) for the therapy of p

152 with targeted drugs, chemoimmunotherapy with fludarabine, cyclophosphamide (FC), and rituximab (R) re

153 momab tiuxetan (0.4 mCi/kg) was added to the fludarabine, cyclophosphamide conditioning regimen ((90)

154 pients underwent low-intensity conditioning (fludarabine, cyclophosphamide, 200 cGy TBI), received a

155 LL) patients after treatment with rituximab, fludarabine, cyclophosphamide, and mitoxantrone (R-FCM).

156 nfections were more frequently observed with fludarabine, cyclophosphamide, and rituximab (235 [84%]

157 Fludarabine, cyclophosphamide, and rituximab (FCR) achie

158 lete remission rate with first-line combined fludarabine, cyclophosphamide, and rituximab (FCR) begs

159 Fludarabine, cyclophosphamide, and rituximab (FCR) can i

160 We report the final analysis of combined fludarabine, cyclophosphamide, and rituximab (FCR) for p

161 received bendamustine and rituximab (BR) or fludarabine, cyclophosphamide, and rituximab (FCR) for u

162 Fludarabine, cyclophosphamide, and rituximab (FCR) has b

163 Fludarabine, cyclophosphamide, and rituximab (FCR) has r

164 dual disease (U-MRD) status after first-line fludarabine, cyclophosphamide, and rituximab (FCR) have

165 ose-escalation study of lumiliximab added to fludarabine, cyclophosphamide, and rituximab (FCR) in pr

166 Frontline chemoimmunotherapy with fludarabine, cyclophosphamide, and rituximab (FCR) is as

167 Fludarabine, cyclophosphamide, and rituximab (FCR) is fi

168 Although fludarabine, cyclophosphamide, and rituximab (FCR) toget

169 g front-line therapy with the combination of fludarabine, cyclophosphamide, and rituximab (FCR).

170 and 55.2 months (95% CI not evaluable) with fludarabine, cyclophosphamide, and rituximab (HR 1.643,

171 d with a similar population who had received fludarabine, cyclophosphamide, and rituximab as salvage

172 ion-to-treat population: 282 patients in the fludarabine, cyclophosphamide, and rituximab group and 2

173 Chemoimmunotherapy with fludarabine, cyclophosphamide, and rituximab is the stan

174 leukemia and being treated with prednisone, fludarabine, cyclophosphamide, and rituximab presented w

175 The combination of fludarabine, cyclophosphamide, and rituximab remains the

176 d frequency of infectious complications with fludarabine, cyclophosphamide, and rituximab was more pr

177 FCR (fludarabine, cyclophosphamide, and rituximab) is the cur

178 mpared with standard chemoimmunotherapy with fludarabine, cyclophosphamide, and rituximab, in patient

179 e chemoimmunotherapy (CIT), such as combined fludarabine, cyclophosphamide, and rituximab, in the maj

180 on, or six cycles of chemoimmunotherapy with fludarabine, cyclophosphamide, and rituximab.

181 regimen consisted of antithymocyte globulin, fludarabine, cyclophosphamide, and total body irradiatio

182 recipients, 5 of whom were conditioned with fludarabine, cyclophosphamide, and total-body irradiatio

183 e allogeneic stem cell transplantation after fludarabine, cyclophosphamide, rituximab (FCR) condition

184 rospective comparison with patients from the fludarabine-cyclophosphamide-rituximab (FCR) arm of the

185 ion-free survival (PFS) after treatment with fludarabine-cyclophosphamide-rituximab (FCR) chemoimmuno

186 Patients were randomly assigned to fludarabine, cytarabine, and granulocyte colony-stimulat

187 hout etoposide (ADE; n = 1983) or ADE versus fludarabine, cytarabine, granulocyte colony-stimulating

188 cytarabine, daunorubicin, and etoposide; or fludarabine, cytarabine, granulocyte colony-stimulating

189 Both groups received 30 mg/m(2) intravenous fludarabine daily for 5 days (days -6 to -2).

190 Moreover, fludarabine did not increase the overall survival time (

191 ed in subsequent patients who received lower fludarabine doses and more intense postfludarabine dialy

192 antithymocyte globulin (ATG) with or without fludarabine (FLU), followed by T-cell-depleted bone marr

193 educed-intensity conditioning (RIC) included fludarabine (Flu)/melphalan/alemtuzumab (n = 20), Flu/bu

194 Regimens included chlorambucil, fludarabine, fludarabine plus rituximab (FR), fludarabin

195 chemotherapy regimen of cyclophosphamide and fludarabine followed by a single infusion of anti-CD19 C

196 ts with lymphodepleting cyclophosphamide and fludarabine followed by NK cell infusion and interleukin

197 rine starting at -45 days pretransplant, and fludarabine from days -16 to -12.

198 , lymphodepletion using cyclophosphamide and fludarabine, higher CAR T-cell dose, thrombocytopenia be

199 sensitizes CLL cells toward bendamustine and fludarabine in BMSC cocultures.

200 d WM1 study (Trial Comparing Chlorambucil to Fludarabine in Patients With Advanced Waldenstrom Macrog

201 The major change was the use of fludarabine in the conditioning, with decreased doses of

202 ompared with reduced-intensity busulfan plus fludarabine in this population.

203 and reversed the protective effect of MSC on fludarabine-induced apoptosis.

204 down-regulation, and enhanced sensitivity to fludarabine-induced cytotoxicity.

205 and protected CLL cells from spontaneous and fludarabine-induced Mcl-1 and PARP cleavage.

206 us busulfan formulation and combined it with fludarabine instead of cyclophosphamide in preparation f

207 00/muL increment increase), incorporation of fludarabine into the lymphodepletion regimen (HR, 0.25),

208 mug/kg per day subcutaneously on days 1-5), fludarabine (intravenous infusion 30 mg/m(2) per day on

209 n contrast, FR improved outcomes relative to fludarabine, irrespective of age (PFS: HR = 0.6, 95% CI,

210 Fludarabine is another purine analog widely used in indo

211 ety and efficacy of intravenous busulfan and fludarabine (IV Bu/Flu) myeloablative conditioning as we

212 fludarabine+melphalan 140 mg/m2 (FM140), (3) fludarabine+IV busulfan AUC >= 5000/d x 4 d (Bu>=20000),

213 fan AUC >= 5000/d x 4 d (Bu>=20000), and (4) fludarabine+IV busulfan AUC 4000/d x 4 d (Bu16000).

214 i (90)Y-anti-CD45 RIT and CY, without TBI or fludarabine, led to mixed chimeras with 81.3 +/- 10.6% m

215 of 24 patients received cyclophosphamide and fludarabine lymphodepletion and CD19 CAR-T cells at or b

216 essive NHL treated with cyclophosphamide and fludarabine lymphodepletion followed by 2 x 10(6) CD19-d

217 1/2 clinical trial with cyclophosphamide and fludarabine lymphodepletion followed by infusion of 2 x

218 and higher intensity of cyclophosphamide and fludarabine lymphodepletion was associated with higher p

219 of the following conditioning regimens: (1) fludarabine+melphalan 100 mg/m2 (FM100), (2) fludarabine

220 fludarabine+melphalan 100 mg/m2 (FM100), (2) fludarabine+melphalan 140 mg/m2 (FM140), (3) fludarabine

221 s, we have added 4 Gy TBI to the widely used fludarabine, melphalan conditioning regimen, in hopes of

222 enty-six patients received RIC consisting of fludarabine, melphalan, and alemtuzumab.

223 e, chronic graft-versus-host disease; use of fludarabine, melphalan, and thiotepa; and receiving no p

224 splant conditioned with 3 different regimens:fludarabine-melphalan (n = 46); total body irradiation-e

225 mtuzumab dose deescalation in the context of fludarabine-melphalan conditioning and human leukocyte a

226 Overall, combination fludarabine-melphalan with low-dose TBI after haplocord

227 ed acute myeloid leukemia patients receiving fludarabine-melphalan without TBI.

228 ients with sibling donors (n = 32) receiving fludarabine/melphalan (FluMel) as a preparative regimen

229 Specifically, patients who received fludarabine/melphalan-based reduced-intensity regimens w

230 umab (n=168) resulted in better PFS than did fludarabine monotherapy (n=167; median 23.7 months [95%

231 bination of fludarabine and alemtuzumab with fludarabine monotherapy in previously treated patients w

232 FCR-ibrutinib closed early due to a lack of fludarabine-naive previously treated patients.

233 patient died as a result of complications of fludarabine neurological toxicity.

234 into BALB.B (H-2) recipients after RIC with fludarabine of 100 mg/kg per day for 5 days, cyclophosph

235 either bendamustine alone, bendamustine and fludarabine, or cyclophosphamide and fludarabine.

236 than 70 years, PFS and OS was improved with fludarabine over chlorambucil (PFS: hazard ratio [HR] =

237 tensity conditioning regimen of busulfan and fludarabine, patients received one intravenous infusion

238 me (MDS) were treated with (131)I-BC8 Ab and fludarabine plus 2 Gy total body irradiation.

239 Fludarabine plus alemtuzumab (n=168) resulted in better

240 Patients in the fludarabine plus alemtuzumab group had more cytomegalovi

241 therapy of chronic lymphocytic leukemia with fludarabine plus cyclophosphamide (FC) compared with flu

242 Fludarabine plus cyclophosphamide (FC) is the chemothera

243 Choice of chemotherapy (fludarabine plus cyclophosphamide, bendamustine, or chlo

244 e for </=6 cycles]) or standard care (either fludarabine plus cytarabine plus granulocyte colony-stim

245 and then 375 mg/m(2) day 1 of cycles 2 to 6; fludarabine plus rituximab (FR) administration was repea

246 Regimens included chlorambucil, fludarabine, fludarabine plus rituximab (FR), fludarabine with consol

247 Patients treated with fludarabine plus rituximab administered concurrently or

248 These long-term data support fludarabine plus rituximab as one acceptable first-line

249 B 9712 demonstrates extended OS and PFS with fludarabine plus rituximab.

250 Fludarabine refractoriness (FR) represents an unsolved c

251 dose of venetoclax or higher (>/=400 mg/d), fludarabine refractoriness and complex karyotype were as

252 ukemia (CLL) and high-risk features, such as fludarabine refractoriness, complex karyotype, or abnorm

253 Patients with disease that is fludarabine refractory or who have complex cytogenetics

254 human anti-CD20 Ab approved for treatment of fludarabine-refractory B chronic lymphocytic leukemia (B

255 ), SF3B1(mut)) as compared with TP53(mut) in fludarabine-refractory chronic lymphocytic leukemia (CLL

256 ffective and well tolerated in patients with fludarabine-refractory chronic lymphocytic leukemia, inc

257 sruption selectively affected 12 of 49 (24%) fludarabine-refractory CLL cases by inactivating mutatio

258 itutive noncanonical NF-kappaB activation in fludarabine-refractory CLL patients harboring molecular

259 lymphocytic leukemia (CLL) or patients with fludarabine-refractory CLL with bulky (> 5 cm) lymphaden

260 In contrast to fludarabine-refractory CLL, progressive but fludarabine-

261 r an ongoing clinical trial in patients with fludarabine-refractory CLL.

262 antibody with activity in CLL patients with fludarabine-refractory disease and 17p deletion.

263 Activity was observed in patients with fludarabine-refractory disease, bulky adenopathy, and de

264 nt providing clear clinical improvements for fludarabine-refractory patients with very poor-prognosis

265 omes in patients treated with the treosulfan-fludarabine regimen suggest its potential to become a st

266 tuximab plus bendamustine and rituximab plus fludarabine regimens.

267 ors after conditioning with low-dose TBI and fludarabine, relying almost exclusively on graft-versus-

268 The STAT1 inhibitor, fludarabine, rescues the effect of E3B-14.7K deletion by

269 tine-induced DNA damage will be inhibited by fludarabine, resulting in increased cytotoxicity.

270 Rituximab monotherapy and fludarabine-rituximab in combination are documented trea

271 atients previously treated with rituximab or fludarabine-rituximab, 7 (50%) responded to bendamustine

272 Among patients with fludarabine-sensitive disease who had previously demonst

273 partial remission, as well as those who have fludarabine-sensitive disease, a significant survival be

274 .53; P = .05), was observed in patients with fludarabine-sensitive disease.

275 ent: patients with up to 3 prior treatments, fludarabine-sensitive patients irrespective of prior rit

276 fludarabine-refractory CLL, progressive but fludarabine-sensitive patients were consistently devoid

277 lly, combined treatment with mafosfamide and fludarabine showed that these therapeutic drugs are syne

278 e complete intent-to-treat study population, fludarabine significantly improved PFS compared with chl

279 tched dUCB-other (n = 40; alkylating agent + fludarabine +/- TBI), and 8 of 8 (n = 313) and 7 of 8 HL

280 Rituximab plus fludarabine therapy seems to carry a higher risk of long

281 Treosulfan (busulfan in 1 patient), fludarabine, thiotepa, and anti-thymocyte globulin or al

282 fractionated 12 Gy TBI and etoposide versus fludarabine, thiotepa, and either busulfan or treosulfan

283 and protected CLL cells from the toxicity of fludarabine, this induction was reversed by HHT, which o

284 rognosis, including those with resistance to fludarabine, those with chromosome 17p deletions (deleti

285 Simultaneous or prior addition of fludarabine to bendamustine resulted in maximum cytotoxi

286 end, we developed a novel regimen by adding fludarabine to dose-adjusted continuous-infusion etoposi

287 Addition of fludarabine to the lymphodepletion regimen improved CAR-

288 e addition of a purine analog, cladribine or fludarabine, to the standard induction regimen affects t

289 llow-up is required, but in combination with fludarabine, treosulfan is a good choice of conditioning

290 All patients received a fludarabine-/treosulfan-based conditioning regimen, with

291 Interaction effects of fludarabine versus chlorambucil by age group (PFS, P = .

292 the overall survival time (46 months in the fludarabine vs 64 months in the chlorambucil arm; P = .1

293 [(3)H]cytarabine, [(3)H]cladribine, or [(3)H]fludarabine was reduced by each of the five TKIs, and al

294 nt front-line regimes include agents such as fludarabine, which act primarily via the DNA damage resp

295 F CCL4) trial that compared chlorambucil and fludarabine with and without cyclophosphamide in previou

296 These data provide a rationale for combining fludarabine with bendamustine for patients with CLL.

297 mtuzumab (FA-ref) and patients refractory to fludarabine with bulky (> 5 cm) lymph nodes (BF-ref).

298 n 65 years comparing first-line therapy with fludarabine with chlorambucil.

299 ludarabine, fludarabine plus rituximab (FR), fludarabine with consolidation alemtuzumab, and FR with

300 ta suggest that the addition of rituximab to fludarabine with or without cyclophosphamide prolongs su