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1 relapse can be successfully re-treated with cladribine.
2 rferon alfa-2a and alfa-2b, pentostatin, and cladribine.
3 ens the duration of severe neutropenia after cladribine.
4 monocytes, we conducted a phase II trial of cladribine.
5 o relapse can be successfully retreated with cladribine.
6 to chlorambucil, cisplatin, carboplatin, and cladribine.
7 and on MRI findings in patients treated with cladribine.
8 iagnosis of hairy cell leukemia treated with cladribine.
9 nd poor response to standard treatments like cladribine.
10 stituent at the 2-position present in dG and cladribine.
11 erienced relapse after their first course of cladribine.
12 ended follow-up of HCL patients treated with cladribine.
19 rt efficient syntheses of the clinical agent cladribine (2-chloro-2'-deoxyadenosine, CldAdo), which i
24 ability (F value) of 2-chlorodeoxyadenosine (cladribine; 2-CdA) after multiple oral administrations,
25 Having relapsed after prior treatment with cladribine, 24 HCL pts (21 male, 3 female) with a median
26 d to evaluate the effectiveness of high-dose cladribine (2CDA) for treatment of chronic myelogenous l
28 lity to transport the nucleoside analog drug cladribine, 2CdA, (rCNT2 > > > hCNT2) to identify the cr
30 r 96 weeks, 178 (44%) of 402 patients in the cladribine 3.5 mg/kg group and 189 (46%) of 411 patients
31 r 48 weeks, 208 (54%) of 384 patients in the cladribine 3.5 mg/kg group and 222 (56%) of 396 patients
32 r 24 weeks, 266 (67%) of 395 patients in the cladribine 3.5 mg/kg group and 283 (70%) of 406 in the c
33 5.25 mg/kg group, 168 (82%) patients in the cladribine 3.5 mg/kg group, and 162 (79%) patients in th
34 other treatments; 5 pts were retreated with cladribine, 3 underwent splenectomy, and 1 received pent
35 essed for eligibility, 616 patients received cladribine 5.25 mg/kg (n=204), cladribine 3.5 mg/kg (n=2
36 g group and 189 (46%) of 411 patients in the cladribine 5.25 mg/kg group were free from disease activ
37 3.5 mg/kg group and 283 (70%) of 406 in the cladribine 5.25 mg/kg group were free from disease activ
38 g group and 222 (56%) of 396 patients in the cladribine 5.25 mg/kg group were free from disease activ
39 s were reported in 165 (81%) patients in the cladribine 5.25 mg/kg group, 168 (82%) patients in the c
41 ilure of one prior chemotherapy (n = 2) with cladribine (5.6 mg/m(2) given intravenously over 2 hours
42 day courses of Ara-C (1 g/m(2) per day) plus cladribine (9 mg/m(2) per day) followed by maintenance t
44 previous observations that single courses of cladribine administered to patients with HCL induce high
48 ssover study was started in 1992 to evaluate cladribine, an immunosuppressive drug, in the treatment
49 An international phase 2 study combining cladribine and cytarabine (Ara-C) was initiated for pati
52 eatment with the nucleoside purine analogues cladribine and pentostatin results in lengthy remissions
53 ed a study of priming filgrastim followed by cladribine and then filgrastim again to determine if fil
54 Thirty-five patients received filgrastim and cladribine and were compared with 105 historic controls
55 antineoplastic, 2-chloro-2'-deoxyadenosine (cladribine) and puromycin, a protein synthesis inhibitor
58 ssion-free survival (P = .007) after initial cladribine, and shorter overall survival from diagnosis
60 s with hairy cell leukemia were treated with cladribine at 0.087 or 0.1 mg/kg body weight per day by
61 showed that short-course oral treatment with cladribine at cumulative doses of 3.5 and 5.25 mg/kg ove
62 able patients treated with second courses of cladribine at first relapse, 33 (62%) achieved complete
63 f purine nucleoside analogs (pentostatin and cladribine) changed the natural history of this rare dis
64 of phase 3 trials and cross-study analyses, cladribine compared favorably with fludarabine, another
66 urvival for all patients following the first cladribine course was 231 months, and 251 months from di
68 le, has only modest single-agent activity in cladribine-failed HCL patients when compared with other
70 y to determine the feasibility and safety of cladribine followed by rituximab in patients with hairy
72 pproved novel agents may act in synergy with cladribine for these conditions and should be incorporat
73 /=40 years of age at diagnosis) treated with cladribine from the Scripps Clinic HCL Database, of whom
74 dverse events that were more frequent in the cladribine groups included lymphocytopenia (21.6% in the
82 ately 10-fold loss of cytostatic activity of cladribine in MCF-7.Hyor cells and observed a rapid and
83 he routine adjunctive use of filgrastim with cladribine in the treatment of HCL cannot be recommended
94 e analog 2-chloro-2'-deoxyadenosine (CldAdo; cladribine) is effective in the treatment of hairy cell
95 re stratified into three groups: response to cladribine less than 1 year, those with a response lasti
98 for relapsed/refractory HCL after first-line cladribine (n = 3) or after multiple lines of therapy (n
99 e 3 study we investigated the effect of oral cladribine on conversion to clinically definite MS in pa
100 we therefore aimed to assess the effects of cladribine on this composite outcome measure by doing a
101 ate whether the addition of a purine analog, cladribine or fludarabine, to the standard induction reg
103 T1), accumulation of [(3)H]cytarabine, [(3)H]cladribine, or [(3)H]fludarabine was reduced by each of
107 nfusions of 0.10 mg, 0.05 mg, and 0.05 mg of cladribine per kg of body weight per day for 7 consecuti
109 e analogues of medicinal importance, such as cladribine, require phosphorylation by deoxycytidine kin
111 single-arm phase 2 trials have demonstrated cladribine's potency across the full spectrum of lymphoi
115 io to receive one of two cumulative doses of cladribine tablets (either 3.5 mg or 5.25 mg per kilogra
116 ng were randomly assigned (1:1:1) to receive cladribine tablets at cumulative doses of 5.25 mg/kg or
120 s clinical and MRI measurements, the phase 3 Cladribine Tablets Treating Multiple Sclerosis Orally (C
122 .26 x 10(9)/L (2.5-fold increase), and after cladribine, the median nadir ANC in the filgrastim-treat
128 iency of PNPHyor-catalyzed phosphorolysis of cladribine to its less toxic base 2-chloroadenine (Km =
133 nd -1 and then again after the completion of cladribine until the absolute neutrophil count (ANC) was
136 small study of patients with de novo B-PLL, cladribine was an active agent that induced a high overa
138 ationally designed antineoplastic therapies, cladribine was identified as a lymphocyte-specific agent
143 nders subsequent to a single 7-day course of cladribine were without minimal residual disease (MRD) a
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