ライフサイエンスコーパス: fludarabine

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

2 hemoresistance of activated CLL cells toward fludarabine.

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

4 randomly assigned to receive chlorambucil or fludarabine.

5 en without irradiation, the latter including fludarabine.

6 paration combining thiotepa, treosulfan, and fludarabine.

7 cell chimerism was significantly better with fludarabine.

8 e and total body irradiation with or without fludarabine.

9 drugs, including cytarabine, cladribine, and fludarabine.

10 ing regimen of low-dose cyclophosphamide and fludarabine.

11 were suppressed by chronic administration of fludarabine.

12 onditioning regimen of cyclophosphamide plus fludarabine.

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

14 hesis induced by bendamustine was blocked by fludarabine.

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

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

17 e survival time was observed (19 months with fludarabine, 18 months with chlorambucil; P = .7).

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

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

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

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

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

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

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

33 Patients received a conditioning regimen of fludarabine (30 mg/m(2) daily for 3 days), cyclophospham

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

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

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

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

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

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

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

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

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

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

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

45 5 showed a higher therapeutic potential than fludarabine, a drug already in use in lymphoma treatment

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

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

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

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

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

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

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

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

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

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

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

57 A regimen of fludarabine and 200 cGy total body irradiation was follo

58 6 cycles (25 mg/m(2) per day for 5 days) of fludarabine and 8 infusions (375 mg/m(2) per week) of ri

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

60 The combination of fludarabine and alemtuzumab is another treatment option

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

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

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

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

65 -4 induced resistance to the cytotoxic drugs fludarabine and chlorambucil and to the novel p53-elevat

66 re to achieve remission after treatment with fludarabine and chlorambucil in patients with chronic ly

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

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

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

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

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

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

73 reduce the toxicity of FCR by decreasing the fludarabine and cyclophosphamide (FCR-Lite).

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

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

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

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

78 All patients received fludarabine and cyclophosphamide before a single infusio

79 The fludarabine and cyclophosphamide couplet has become the

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

81 100% in the subset of patients who received fludarabine and cyclophosphamide lymphodepletion.

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

83 When combined with fludarabine and cyclophosphamide, subcutaneous rituximab

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

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

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

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

88 ll killing by oxaliplatin in the presence of fludarabine and cytarabine.

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

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

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

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

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

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

95 15 patients treated in British Columbia with fludarabine and rituximab (FR) from 2004 to 2010 for rel

96 IL-21 might enhance the apoptosis induced by fludarabine and rituximab and also play a role in augmen

97 totic proteins associated with resistance to fludarabine and rituximab and is effective against p53-m

98 The results of this study demonstrate that fludarabine and rituximab are highly active in WM, altho

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

100 cation for combination studies of IL-21 with fludarabine and rituximab in CLL and suggest that BIM up

101 f a multicenter, prospective study examining fludarabine and rituximab in Waldenstrom macroglobulinem

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

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

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

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

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

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

108 2-Gy total body irradiation, with or without fludarabine, and alloHCT from human leukocyte antigen-id

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

110 prognostic markers, in vitro sensitivity to fludarabine, and clinical outcome.

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

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

113 01 sensitizes CLL cells toward bendamustine, fludarabine, and dexamethasone.

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

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

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

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

118 Conditioning was with alemtuzumab, fludarabine, and melphalan, and additional graft-versus-

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

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

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

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

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

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

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

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

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

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

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

130 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

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

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

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

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

135 ost common adult leukemia, and resistance to fludarabine-based therapies is a major challenge in CLL

136 multivariate analysis of patients receiving fludarabine-based therapy at our center, FCR therapy eme

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 177 patients enrolled in a phase 2 study of fludarabine, cyclophosphamide, and rituximab (FCR) and i

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

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 r

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

164 Chemoimmunotherapy combining fludarabine, cyclophosphamide, and rituximab (FCR) is an

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

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

167 Early results of the fludarabine, cyclophosphamide, and rituximab (FCR) regim

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

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

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

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

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

183 A randomized trial of oblimersen plus fludarabine/cyclophosphamide (OBL-FC; n = 120) versus FC

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

185 conducted a phase I-II trial of oxaliplatin, fludarabine, cytarabine, and rituximab (OFAR) in these d

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

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

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

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

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

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

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

193 eviously, we studied sequential therapy with fludarabine followed by cyclophosphamide (F-->C).

194 otal-body irradiation alone or combined with fludarabine followed by HCT from related (n = 52) or unr

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

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

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

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

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

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

201 s protected CLL B cells from spontaneous and fludarabine-induced apoptosis (P = .003) by increasing t

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

203 ually effective in protecting CLL cells from 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 n contrast, FR improved outcomes relative to fludarabine, irrespective of age (PFS: HR = 0.6, 95% CI,

208 Fludarabine is another purine analog widely used in indo

209 eated with alkylating agents or single-agent fludarabine, its significance in the era of chemoimmunot

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 ent of CLL cells but not normal T cells with fludarabine or rituximab additively enhanced the direct

225 i-CD23 monoclonal antibody, is combined with fludarabine or rituximab.

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

227 ong correlations with in vitro resistance to fludarabine (P = .005 and P < .001, respectively).

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

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

230 Patients in the fludarabine plus alemtuzumab group had more cytomegalovi

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

232 Fludarabine plus cyclophosphamide (FC) is the chemothera

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

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

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

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

237 Patients treated with fludarabine plus rituximab administered concurrently or

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

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

240 Fludarabine refractoriness (FR) represents an unsolved c

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

242 gic category, number of prior therapies, and fludarabine refractoriness did not influence the respons

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

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

245 Responders included 17 (40%) of 43 fludarabine refractory patients, 7 (39%) of 18 patients

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

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

248 Richter's syndrome (RS) and fludarabine-refractory chronic lymphocytic leukemia (CLL

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

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

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

252 ty-two patients, age 42 to 72 years, who had fludarabine-refractory CLL were conditioned with 2 Gy to

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

254 ian survival of 5 years for patients who had fludarabine-refractory CLL with sustained remissions and

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

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

257 all response rates were 50% in RS and 33% in fludarabine-refractory CLL.

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

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

260 unmutated V(H), and of 25% in patients with fludarabine-refractory disease.

261 n is highly active in RS and has activity in fludarabine-refractory patients with CLL.

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

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

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

265 althy subjects (n = 12), we showed that both fludarabine-resistant and -sensitive CLL cells were high

266 t a novel ROS-mediated strategy to eliminate fludarabine-resistant CLL cells based on this redox alte

267 l compound PEITC is effective in eliminating fludarabine-resistant CLL cells through a redox-mediated

268 Fludarabine resulted in a significantly higher overall a

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

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

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

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

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

285 Addition of fludarabine to the lymphodepletion regimen improved CAR-

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

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

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

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

290 dule C was similar to schedule B except that fludarabine was also infused.

291 st indolent leukemias, and combining it with fludarabine was most promising.

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

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

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

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

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

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

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

299 depletion consisting of cyclophosphamide and fludarabine with either 2 (25 patients) or 12 Gy (25 pat

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