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1 e) proceeded to alloSCT after treatment with bendamustine.
2 phosphamide, vincristine, and prednisone, or bendamustine.
3 ed), BV plus dacarbazine (DTIC), and BV plus bendamustine.
4 s who received any amount of obinutuzumab or bendamustine.
5 of ibrutinib combined with rituximab (R) and bendamustine.
6 or for whom this treatment failed, received bendamustine 120 mg/m(2) as a 30-minute infusion on days
7 eived rituximab (44% versus 9%; P < 0.0001), bendamustine (22% versus 0%; P < 0.001), high-dose stero
9 on day 1 of a 21 day cycle, plus one dose of bendamustine (70 mg/m(2), 80 mg/m(2), or 90 mg/m(2)) on
10 e safety and efficacy of escalating doses of bendamustine (70, 90, 110, and 130 mg/m2 per day for 3 d
11 plus rituximab for a maximum of six cycles (bendamustine: 70 mg/m(2) intravenously on days 1 and 2 f
12 uximab given in cycles of 4 weeks' duration (bendamustine: 70 mg/m(2) intravenously on days 2-3 in cy
14 nts received rituximab 375 mg/m(2) day 1 and bendamustine 90 mg/m(2) days 1 and 2 for 4 cycles at a 2
15 th adequate organ function were treated with bendamustine 90 mg/m(2) days 1 and 4; rituximab 375 mg/m
16 8, and 15, cycle 1; day 1, cycles 2-6) plus bendamustine 90 mg/m(2) per day (days 1 and 2, cycles 1-
18 day) for the first 3 days or to intravenous bendamustine (90 mg/m(2) per day) for the first 2 days o
19 Patients received R (375 mg/m(2)) on day 1, bendamustine (90 mg/m(2)) on days 1 and 2, and ibrutinib
20 d peripheral T-cell lymphoma, treatment with bendamustine alone only achieves modest improvements in
23 alone or rituximab combined with alkylators (bendamustine and cyclophosphamide), proteasome inhibitor
26 We investigated the safety and efficacy of bendamustine and rituximab (BR) in previously untreated
27 actory chronic lymphocytic leukemia received bendamustine and rituximab (BR) or fludarabine, cyclopho
28 ival was 41.7 months (95% CI 34.9-45.3) with bendamustine and rituximab and 55.2 months (95% CI not e
30 ents with chronic lymphocytic leukaemia, but bendamustine and rituximab is associated with less toxic
33 at the 2-year progression-free survival with bendamustine and rituximab was not 67.5% or less with a
38 d toxicity of the combination of bortezomib, bendamustine, and rituximab in patients with follicular
40 een approved for CLL treatment (fludarabine, bendamustine, and the monoclonal antibodies alemtuzumab,
41 ne therapy); had received a purine analogue, bendamustine, anti-CD20 antibody, chlorambucil, or alemt
42 assigned to receive brentuximab vedotin plus bendamustine at the recommended phase 2 dose from phase
44 tment agents (interferon-alpha, alemtuzumab, bendamustine, bortezomib, dasatinib, imatinib, lenalidom
47 upport current and future studies evaluating bendamustine combinations in relapsed and refractory HL.
48 atforms have changed in the past 5 years, as bendamustine combined with rituximab has rapidly become
49 or relapse within 24 months with a previous bendamustine-containing regimen, or haemopoietic stem-ce
50 nib treatment, and subsequent treatment with bendamustine, cytarabine, or lenalidomide failed to reve
55 received 1.8 mg/kg BV plus 90 or 70 mg/m(2) bendamustine for up to 6 cycles (dose reduced due to tox
56 ety and preliminary efficacy of obinutuzumab-bendamustine (G-B) or obinutuzumab fludarabine cyclophos
57 phase II study evaluated the combination of bendamustine, gemcitabine, and vinorelbine (BeGEV) as in
58 ths (IQR 12.1-31.0) in the obinutuzumab plus bendamustine group and 20.3 months (9.5-29.7) in the ben
59 vent-related deaths in the obinutuzumab plus bendamustine group and five (42%) of 12 in the bendamust
60 8%) of 194 patients in the obinutuzumab plus bendamustine group and in 123 (62%) of 198 patients in t
61 n 74 patients (38%) in the obinutuzumab plus bendamustine group and in 65 patients (33%) in the benda
62 rogressing patients in the obinutuzumab plus bendamustine group received obinutuzumab maintenance (10
63 utropenia (64 [33%] in the obinutuzumab plus bendamustine group vs 52 [26%] in the bendamustine monot
64 ximately 30 patients were to receive BV plus bendamustine; however, the incidence of serious adverse
67 the combination of brentuximab vedotin plus bendamustine in heavily pretreated patients with relapse
71 study evaluated the efficacy and toxicity of bendamustine in patients with B-cell non-Hodgkin's lymph
75 mg/kg brentuximab vedotin plus 80 mg/m(2) of bendamustine in two (7%) patients and diffuse rash at 1.
76 pothesized that similar to cyclophosphamide, bendamustine-induced DNA damage will be inhibited by flu
82 se 1/2 trial investigated the combination of bendamustine, lenalidomide, and dexamethasone in repeati
83 ituximab-refractory disease, suggesting that bendamustine may be the most effective drug available fo
84 significantly longer with obinutuzumab plus bendamustine (median not reached [95% CI 22.5 months-not
85 95% CI 22.5 months-not estimable]) than with bendamustine monotherapy (14.9 months [12.8-16.6]; hazar
86 m(2) per day (days 1 and 2, cycles 1-6), and bendamustine monotherapy dosing was 120 mg/m(2) per day
87 ndamustine group and five (42%) of 12 in the bendamustine monotherapy group were treatment related.
88 b plus bendamustine group vs 52 [26%] in the bendamustine monotherapy group), thrombocytopenia (21 [1
89 ustine group and in 65 patients (33%) in the bendamustine monotherapy group, and deaths due to advers
90 tine group and 20.3 months (9.5-29.7) in the bendamustine monotherapy group, progression-free surviva
92 zumab maintenance has improved efficacy over bendamustine monotherapy in rituximab-refractory patient
95 ts (33%) received fewer than three cycles of bendamustine, mostly because of disease progression.
96 t (six 28-day cycles) with obinutuzumab plus bendamustine or bendamustine monotherapy, both given int
97 ituximab and cyclophosphamide-dexamethasone, bendamustine, or bortezomib-dexamethasone provide durabl
98 nations with cyclophosphamide/dexamethasone, bendamustine, or bortezomib/dexamethasone provided durab
99 otherapy (fludarabine plus cyclophosphamide, bendamustine, or chlorambucil) and anti-CD20 antibody (r
102 3 study evaluated the efficacy and safety of bendamustine plus rituximab (BR) vs a standard rituximab
103 oved progression-free survival compared with bendamustine plus rituximab alone in patients with relap
104 l interactive web response system to receive bendamustine plus rituximab for a maximum of six cycles
105 igned (1:1) by a web-based system to receive bendamustine plus rituximab given in cycles of 4 weeks'
106 TERPRETATION: Idelalisib in combination with bendamustine plus rituximab improved progression-free su
107 ibitor of Bruton's tyrosine kinase (BTK), to bendamustine plus rituximab in patients with previously
112 C plus rituximab; CLL10: FC plus rituximab v bendamustine plus rituximab) were analyzed according to
117 addition of lenalidomide (LEN) to rituximab-bendamustine (R-B) as first-line treatment for elderly p
119 ltaneous or prior addition of fludarabine to bendamustine resulted in maximum cytotoxicity assayed by
120 the significant activity and tolerability of bendamustine, rituximab, and bortezomib in patients with
122 r phase 3 clinical trial NHL1-2003 comparing bendamustine-rituximab (B-R) with rituximab, cyclophosph
123 In a single-arm, phase 2 clinical trial, bendamustine-rituximab (BR) demonstrated an overall resp
124 ynthesis of available evidence, we recommend bendamustine-rituximab as primary therapy for bulky dise
130 Questions related to the optimization of bendamustine therapy, including dose and schedule, role
131 cells display resistance to doxorubicin and bendamustine, two drugs largely used in FL therapy, comp
134 lation phase, the maximum-tolerated dose for bendamustine was not reached; the 90 mg/m(2) dose level
135 /kg of brentuximab vedotin and 90 mg/m(2) of bendamustine, which are the standard doses of the drugs
137 is study shows that brentuximab vedotin plus bendamustine, with a favourable safety profile, is an ac
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