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1 gy to eradicate residual disease and prevent leukemia relapse.
2 nsplant-related mortality and posttransplant leukemia relapse.
3 optive immunotherapy prevents posttransplant leukemia relapse.
4  induce alloreactive NK cells, which prevent leukemia relapse.
5 m cells (LSC) that drive chemoresistance and leukemia relapse.
6 bition assays, which have been implicated in leukemia relapse.
7 used both prophylactically or at the time of leukemia relapse.
8 nsitivity to ASNase can increase the risk of leukemia relapse.
9 arrow transplantation may be used to prevent leukemia relapse.
10 tic drugs and might eventually contribute to leukemia relapse.
11 rapeutic armamentarium against acute myeloid leukemia relapse.
12 ificant increase in toxicity, infections, or leukemia relapse.
13 own to result in increased graft failure and leukemia relapse.
14 hocyte transfusions in an attempt to prevent leukemia relapse.
15 , CAR silencing was observed coincident with leukemia relapse.
16 s of GVHD-related morbidity, infections, and leukemia relapse.
17 uirement for Ras oncogene activity and drive leukemia relapse.
18 ificantly different cumulative incidences of leukemia relapse: 83.3%, 34.8%, and 8.6%, respectively (
19                                     However, leukemia relapse accounts for nearly half of deaths.
20 to recognize leukemia could prevent or treat leukemia relapse after allogeneic HSCT (allo-HSCT).
21 oires are associated with protection against leukemia relapse after allogeneic HSCT.
22 upporting that cytomegalovirus (CMV) reduces leukemia relapse after allogeneic stem cell transplantat
23 of T cells in the host drastically increased leukemia relapse after dasatinib or cytotoxic chemothera
24 competent mouse model of chronic lymphocytic leukemia, relapse after initial treatment response frequ
25  therapeutic regimens must focus on reducing leukemia relapse and enhancing quality of life, as well
26                                 Nonetheless, leukemia relapse and infection are major sources of trea
27  therapy as part of their treatment or had a leukemia relapse are at greatest risk for adverse outcom
28 nce of GVHD, the proportion of patients with leukemia relapse at 2 years was 0.17 (CI, 0.00-0.38) and
29   There was little difference in the risk of leukemia relapse between the treatment group (30% at 5 y
30 isequilibrium with KIR2DS1, had no effect on leukemia relapse but was associated with decreased morta
31 stem and progenitor cells and may facilitate leukemia relapse following chemotherapeutic treatment.
32 med to identify risk factors associated with leukemia relapse following myeloablative UCB transplanta
33                 We observed similar risks of leukemia relapse in patients with and without acute and
34                                   Subsequent leukemia relapse in some patients was associated with re
35                                              Leukemia relapse is a major cause of death after allogen
36 ly reduced/defective MMR activity conferring leukemia relapse, likely by down-regulating MLH1 express
37                                              Leukemia relapse on central nervous system, despite rare
38 evidence that GH therapy was associated with leukemia relapse or development of a second malignancy.
39  had received GH and estimated their risk of leukemia relapse or development of a second malignancy.
40                                Their risk of leukemia relapse or second malignancy was compared with
41 free survival (P = .02) and a higher rate of leukemia relapse (P = .01) and were an independent predi
42 e of genotyping alone for donor selection or leukemia-relapse prognostication because some KIRs may b
43 sistance, and may help explain the increased leukemia relapse rate in obese children and adults.
44                                              Leukemia relapse remains the major cause of allogeneic h
45 tly the standard curative treatment of acute leukemia, relapse remains unacceptably high.
46 ion of patients with high-risk acute myeloid leukemia (relapsed, resistant/refractory, or adverse gen
47                   In the Acute Lymphoblastic Leukemia-Relapse Study of the Berlin-Frankfurt-Munster G
48  no differences in rates of graft rejection, leukemia relapse, treatment-related mortality, and disea
49 l killer (NK) cells can decrease the risk of leukemia relapse, we initiated a phase 1 dose-escalation
50 27), and incidence of serious infections and leukemia relapse were similar on both treatment arms.
51                                   Three-year leukemia relapses were 33%, 33%, 29%, 25%, and 21% in th