ライフサイエンスコーパス: leukemia relapse

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1 uirement for Ras oncogene activity and drive leukemia relapse.

2 induce alloreactive NK cells, which prevent leukemia relapse.

3 bition assays, which have been implicated in leukemia relapse.

4 used both prophylactically or at the time of leukemia relapse.

5 arrow transplantation may be used to prevent leukemia relapse.

6 tic drugs and might eventually contribute to leukemia relapse.

7 ificant increase in toxicity, infections, or leukemia relapse.

8 own to result in increased graft failure and leukemia relapse.

9 hocyte transfusions in an attempt to prevent leukemia relapse.

10 gy to eradicate residual disease and prevent leukemia relapse.

11 nsplant-related mortality and posttransplant leukemia relapse.

12 optive immunotherapy prevents posttransplant leukemia relapse.

13 ificantly different cumulative incidences of leukemia relapse: 83.3%, 34.8%, and 8.6%, respectively (

14 to recognize leukemia could prevent or treat leukemia relapse after allogeneic HSCT (allo-HSCT).

15 oires are associated with protection against leukemia relapse after allogeneic HSCT.

16 upporting that cytomegalovirus (CMV) reduces leukemia relapse after allogeneic stem cell transplantat

17 therapeutic regimens must focus on reducing leukemia relapse and enhancing quality of life, as well

18 Nonetheless, leukemia relapse and infection are major sources of trea

19 therapy as part of their treatment or had a leukemia relapse are at greatest risk for adverse outcom

20 nce of GVHD, the proportion of patients with leukemia relapse at 2 years was 0.17 (CI, 0.00-0.38) and

21 There was little difference in the risk of leukemia relapse between the treatment group (30% at 5 y

22 isequilibrium with KIR2DS1, had no effect on leukemia relapse but was associated with decreased morta

23 stem and progenitor cells and may facilitate leukemia relapse following chemotherapeutic treatment.

24 med to identify risk factors associated with leukemia relapse following myeloablative UCB transplanta

25 We observed similar risks of leukemia relapse in patients with and without acute and

26 Subsequent leukemia relapse in some patients was associated with re

27 ly reduced/defective MMR activity conferring leukemia relapse, likely by down-regulating MLH1 express

28 evidence that GH therapy was associated with leukemia relapse or development of a second malignancy.

29 had received GH and estimated their risk of leukemia relapse or development of a second malignancy.

30 Their risk of leukemia relapse or second malignancy was compared with

31 free survival (P = .02) and a higher rate of leukemia relapse (P = .01) and were an independent predi

32 e of genotyping alone for donor selection or leukemia-relapse prognostication because some KIRs may b

33 sistance, and may help explain the increased leukemia relapse rate in obese children and adults.

34 Leukemia relapse remains the major cause of allogeneic h

35 ion of patients with high-risk acute myeloid leukemia (relapsed, resistant/refractory, or adverse gen

36 In the Acute Lymphoblastic Leukemia-Relapse Study of the Berlin-Frankfurt-Munster G

37 no differences in rates of graft rejection, leukemia relapse, treatment-related mortality, and disea

38 l killer (NK) cells can decrease the risk of leukemia relapse, we initiated a phase 1 dose-escalation

39 27), and incidence of serious infections and leukemia relapse were similar on both treatment arms.

40 Three-year leukemia relapses were 33%, 33%, 29%, 25%, and 21% in th

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