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1 rom toxicity or treatment abandonment during remission induction.
2 ived lipoATRA 90 mg/m(2) every other day for remission induction.
3 , prednisone, and asparaginase were used for remission induction.
4 ia niche to a fully reconstituted state upon remission induction.
5 rathecal therapy during the first 2 weeks of remission induction.
6 minimal residual disease (MRD) levels during remission induction.
7 ne at a daily dose of 100 to 200 mg/m(2) for remission induction.
8 n AML may provide improved outcome following remission induction.
9 reated with escalated-dose cytarabine during remission induction.
10 urnover rapidly, and disappear rapidly after remission induction.
11  genes at nephritis onset that reverses with remission induction.
12  mg per kilogram of body weight per day) for remission induction.
13 paraginase (2500 IU/m(2)) over 1 hour during remission induction.
14                                    Following remission induction, 1018 patients were randomized to re
15                                        After remission induction, 2027 patients were randomized to re
16 rituximab was a well-tolerated and effective remission induction agent for severe refractory Wegener'
17 s with detectable leukaemic cells was 23% at remission induction and 17% at week 14 of continuation t
18 ous complications of LP occurring during the remission induction and consolidation treatment periods
19 eatment regimen was highly effective in both remission induction and disease-free survival for patien
20 II (M2b)-activated macrophage as a marker of remission induction and impending relapse and suggest th
21 ) regimen alone or with chemosensitizers for remission induction and interferon (IFN) versus IFN plus
22  an up-to-date summary of MMF and its use as remission induction and maintenance therapy for lupus ne
23 pt given in addition to standard therapy for remission induction and maintenance, more solid malignan
24       The use of CYC and glucocorticoids for remission induction and MTX for remission maintenance re
25       The use of CYC and glucocorticoids for remission induction and MTX for remission maintenance wa
26  performed using CYC and glucocorticoids for remission induction and MTX for remission maintenance.
27 ed therapies most frequently employed during remission induction and remission maintenance, respectiv
28 ddress the distinction between therapies for remission induction and remission maintenance.
29 ents' minimal residual disease levels during remission induction and sequentially post-remission.
30 nal doses of intrathecal chemotherapy during remission induction and the first year of continuation t
31 l-depleting monoclonal antibody, in both the remission-induction and maintenance phases of the diseas
32 disease levels measured on days 19 and 46 of remission induction, and on week 7 of maintenance treatm
33 ients received CYC (n=161) or RTX (n=64) for remission-induction, and 51 were also treated with PLEX.
34 y APL were treated with arsenic trioxide for remission induction at daily doses that ranged from 0.06
35        Addition of PLEX showed no benefit on remission-induction at 6 months (IRR 0.73 [95% CI 0.44 t
36                 RTX was comparable to CYC in remission-induction (BVAS/WG=0) at 6 months (IRR 1.37 [9
37 n DADA2 and were significantly reduced after remission induction by anti-tumor necrosis factor (TNF)
38 with acute myeloid leukemia (AML) undergoing remission induction chemotherapy (RIC) given the recent
39 tophilia infection in AML patients receiving remission induction chemotherapy (RIC).
40 y, beginning 4 days after starting intensive remission induction chemotherapy and continuing until th
41 ngly recommend antifungal prophylaxis during remission induction chemotherapy for patients with acute
42 myelodysplasia-related) who had not received remission induction chemotherapy underwent allogeneic (n
43   The standard treatment paradigm for AML is remission induction chemotherapy with an anthracycline/c
44    All patients then received two courses of remission induction chemotherapy with daunorubicin, ara-
45 aluated angiogenesis after the completion of remission induction chemotherapy.
46           Cytarabine is a key constituent of remission induction chemotherapy.
47 sk myelodysplastic syndrome (MDS) undergoing remission-induction chemotherapy (RIC).
48 n bone marrow samples collected on day 19 of remission-induction chemotherapy from 248 children with
49 ance of leukemic cells after 2 to 3 weeks of remission-induction chemotherapy, and these patients hav
50 with newly diagnosed ALL received 6 weeks of remission-induction chemotherapy.
51 o a phase 3 AML trial using intensive-timing remission induction/consolidation and related donor marr
52         Therapy included four- or five-agent remission induction; consolidation therapy with doxorubi
53    Detectable residual disease at the end of remission induction correlated with adverse genetic abno
54 lophosphamide should be considered for rapid remission induction, corticosteroid reduction and long-t
55 cover neutrophils >/=1,000/microL during the remission induction course was 16 days (interquartile ra
56 as initiated that consisted of two cycles of remission induction (cytarabine, etoposide, and daunorub
57  minimal residual disease level of <0.01% on remission induction day 19.
58 of detectable residual disease at the end of remission induction (day 46).
59  residual disease (MRD) at day 22 of initial remission induction determined final risk classification
60 igh risk of life-threatening events, such as remission induction failure, is a high priority in APL,
61   The purpose of this study was to determine remission induction frequency when bortezomib was combin
62  healthy skin microbiome could contribute to remission induction in AD.
63 stent disease at day 15 and days 22 to 25 of remission induction in childhood acute lymphoblastic leu
64 ue to provide a valuable management tool for remission induction in mildly to moderately active dista
65 th autoimmune hepatitis (AIH) and results in remission induction in over 80% of patients.
66                                              Remission induction in patients with active primary SNV
67 effective differentiation-inducing agent for remission induction in patients with acute promyelocytic
68 X is the first proven alternative to CYC for remission induction in severe GPA and MPA.
69 ide (CYC) followed by azathioprine (AZA) for remission-induction in severe ANCA-associated vasculitis
70  of maintenance of glucocorticoids following remission induction is debatable.
71                                              Remission induction is the most important prognostic fac
72 The level of minimal residual disease during remission induction is the most important prognostic ind
73 al minimal residual disease monitoring after remission induction is warranted for patients with detec
74 he use of clofarabine with cytarabine during remission induction might reduce the need for anthracycl
75 gative minimal residual disease status after remission induction, minimal residual disease re-emerged
76 r minimal residual disease >1% at the end of remission induction (n = 5).
77            Carriers were more likely to fail remission induction (odds ratio = 4.22; 95% confidence i
78 DAC with standard-dose cytarabine (SDAC) for remission induction of previously untreated AML and to c
79 RD levels between 0.001% and <0.01% early in remission induction on the outcome of VLR ALL treated wi
80          High-dose cytarabine applied during remission induction or as consolidation after attainment
81          In our study of children undergoing remission induction or consolidation therapy for acute l
82                                        After remission induction, patients were randomized to one of
83 nd short-term oral JAK inhibitors during the remission induction phase.
84 ia of 0.01% or more at the end of the 6-week remission induction phase.
85                                          The remission induction rate supports further development of
86                                          The remission induction rate was 40% in Flt3/ITD-positive pa
87                                          The remission induction rate was similar in the non-DS-Frenc
88         Preliminary results indicated a high remission induction rate with the human CD52 antibody, C
89 h normal karyotype, FLT3/ITD mutations, high remission induction rates, and improved survival (partic
90                                          For remission induction, recent randomized trial data sugges
91                                          The remission induction regimen consisted of oral prednisone
92 tively maintain remission after a "standard" remission induction regimen for patients with antineutro
93 py) were treated with rituximab as part of a remission induction regimen.
94 erapy when oral etoposide is used as part of remission induction regimens for relapsed or refractory
95                                              Remission-induction regimens were RTX at 375 mg/m(2) x 4
96 gether with the increasing clinical drive to remission induction, requires that further therapeutic t
97                          However, benefit of remission induction strategy (RIST) before alloHCT has n
98                                              Remission induction, survival, and event-free survival r
99 had a higher CR rate and fewer deaths during remission induction than did those receiving placebo (P
100 atment for 2 years: 2 doses of 1 gm each for remission induction, then 1 gm every 6 months (total of
101 re likely to die during the first 8 weeks of remission induction therapy (hazard ratio = 7.26; 95% co
102 rates (n = 629) were collected at the end of remission induction therapy and at 3 intervals thereafte
103 nants of the early cytoreductive response to remission induction therapy and subsequent clinical outc
104 e who had peripheral blood MRD at the end of remission induction therapy but only 13.3% +/- 9.1% for
105 eukaemia and 0.01% or more MRD at the end of remission induction therapy could benefit from augmented
106  monoclonal antibody, has proven efficacy in remission induction therapy for AAV, and two trials with
107                      Rituximab was effective remission induction therapy for refractory ANCA-associat
108 cal decision-making concerning the choice of remission induction therapy for this subset of patients
109 levels of MRD (0.001%-< 0.01%) at the end of remission induction therapy have prognostic significance
110 nitoring residual T-LL cells in blood during remission induction therapy identified patients with slo
111                             After 45 days of remission induction therapy on Eastern Cooperative Oncol
112 ony-stimulating factor (G-CSF) following ALL remission induction therapy prompted us to examine this
113 and of these, 111 were randomized to receive remission induction therapy with all-trans retinoic acid
114 gh-risk presenting features (85.7%) received remission induction therapy with dexamethasone, vincrist
115 e: one, rate of complete response (CR) after remission induction therapy with methotrexate, temozolom
116                   Patients received standard remission induction therapy, and responding patients wer
117 l trials evaluating mycophenolate mofetil as remission induction therapy, gusperimus, belimumab and c
118  daunomycin, cytarabine, and etoposide (DAV) remission induction therapy.
119 , prednisone, and asparaginase were used for remission induction therapy.
120 vated minimal residual disease at the end of remission induction therapy.
121  mouse model of acute myeloid leukemia (AML) remission induction therapy.
122  negative for minimal residual disease after remission induction therapy.
123  poorer leukemia cell clearance on day 19 of remission induction therapy.
124 on comparative analysis following successful remission-induction therapy (AUC > 0.9, 100% sensitivity
125 ), beginning one day after the completion of remission-induction therapy and continuing until the neu
126                                   Three-drug remission-induction therapy combined with MRD-based risk
127    All patients received the same intensive, remission-induction therapy followed by 120 weeks of ris
128 glucocorticoids have been the cornerstone of remission-induction therapy for severe antineutrophil cy
129                                   Failure of remission-induction therapy is a rare but highly adverse
130 Minimal residual disease (MRD) at the end of remission-induction therapy predicts relapse in acute ly
131             The addition of PLEX to standard remission-induction therapy showed no benefit in our coh
132 ed thirty-three patients were registered for remission-induction therapy with VAD or VAD plus the che
133 ny extramedullary site after 4 to 6 weeks of remission-induction therapy, in 1041 of 44,017 patients
134 mal residual disease during or at the end of remission induction; they were less likely to have the t
135       Minimal residual disease levels during remission induction treatment have important prognostic
136 sk cytogenetic features, or poor response to remission induction treatment), and for the estimated 2%
137                     FLAG-Ida is an effective remission induction treatment, with a high complete remi
138 ormed at diagnosis and in CR after intensive remission induction treatment.
139  disease (MRD) results obtained on day 19 of remission induction treatment.
140 al disease (MRD) levels on days 19 and 46 of remission induction treatment.
141  the level of minimal residual disease after remission-induction treatment.
142 y satisfactory means to evaluate efficacy of remission-induction treatments in AAV with severe renal
143   This 12-month double-blind study attempted remission induction using standard therapy with or witho
144                                              Remission induction utilized non-cross-resistant regimen
145 nts with and without detectable leukaemia at remission induction was 32.5% (10.6) and 7.5% (4.0), res
146                                  The rate of remission induction was 60.5%, with a 48% rate of subseq
147 ce of lymphoblasts (even 1%-4%) on day 15 of remission induction was associated with a poor prognosis
148 mal residual disease (<=0.01%) at the end of remission induction were enrolled into Ma-Spore (MS) ALL
149 esidual disease (> or = 1%) after 6 weeks of remission induction were significantly associated with p
150 at initial diagnosis was selected for during remission induction with glucocorticoids and contributed
151                                              Remission induction with infliximab plus MTX provided a
152 V and renal involvement respond similarly to remission induction with RTX plus glucocorticoids or CYC
153 nal and/or biologic immunosuppressants after remission-induction with anti-B cell antibodies.
154     Remission, relapse, ESKD and death after remission-induction with CYC or RTX, with or without the

 
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