ライフサイエンスコーパス: blast phase

1 and transformation to a treatment-refractory blast phase).

2 apse and/or malignant progression to a fatal blast phase.

3 vely detected in JAK2V617F(-) cases with MPN-blast phase.

4 phase (CP), 9 in accelerated phase, and 8 in blast phase.

5 phase (CP), 6 in accelerated phase, and 6 in blast phase.

6 relapse, and chronic myelogenous leukemia in blast phase.

7 e, they had a high rate of transformation to blast phase.

8 ary mutation in some cases of CML during the blast phase.

9 ogenous leukemia (CML) in the accelerated or blast phase.

10 onic (42 cases), accelerated (17 cases), and blast phases (32 cases).

11 versible outcomes, such as transformation to blast phase and death.

12 s of chronic myelogenous leukemia during the blast phase and in therapy-related myelodysplasia and ac

13 onic phase, 4 in accelerated phase, and 2 in blast phase) and 1 had Philadelphia-positive acute lymph

14 8 MPN patients, as well as 71 cases with MPN-blast phase, and correlated these findings with their cl

15 on-treatment transformations to accelerated/blast phase, and fewer CML-related deaths with bosutinib

16 with Ph(+) ALL, or accelerated phase (AP) or blast phase (BP) CML achieve a major cytogenetic respons

17 enous leukemia (CML) to accelerated (AP) and blast phase (BP) is because of secondary molecular event

18 CP), 10 in accelerated phase (AP), and 13 in blast phase (BP).

19 (CP), 1 in accelerated phase (AP), and 4 in blast phase (BP).

20 ), 50% in accelerated phase (AP), and 33% in blast phase (BP).

21 , n = 34; accelerated phase [AP], n = 9; and blast phase [BP], n = 4) who underwent HSCT and had BCR-

22 or mutated BCR/ABL kinase, as is typical of blast phase cells and very primitive chronic phase CML c

23 h-risk myelodysplastic syndrome (MDS), and 1 blast-phase chronic myeloid leukemia (CML).(1) Clofarabi

24 nce of resistant subclones and experience in blast-phase chronic myeloid leukemia and acute promyeloc

25 bodies in mice transplanted with chronic and blast phase CML cells resulted in therapeutic effects me

26 of imatinib mesylate to treat 75 patients in blast-phase CML (median age, 53 years; 65 with nonlympho

27 Transformation to accelerated-/ blast-phase CML on study occurred in 2.3% with dasatinib

28 Of 22 patients with accelerated-phase or blast-phase CML or Ph-positive ALL, 36% had a major hema

29 Among 62 patients with blast-phase CML, 31% had a major hematologic response an

30 ith other drugs to improve the prognosis for blast-phase CML.

31 ary mutation in some cases of CML during the blast phase (CML-BC), in the rapid induction of an acute

32 Chronic myeloid leukemia blast phase (CML-BP) cells commonly express the multidru

33 somal instability and disease progression to blast phase (CML-BP).

34 f eight with chronic myelogenous leukemia in blast phase (CML-BP).

35 n = 29), and to lymphoid (n = 15) or myeloid blast phase disease (n = 12).

36 aemia (two with chronic-phase and three with blast-phase disease), one with chronic myelomonocytic le

37 fective palliation for CML in accelerated or blast phases, even for heavily pretreated patients.

38 Fifteen genes in the panel distinguished blast phase from chronic phase disease, and 12 genes dis

39 CML had not progressed to the accelerated or blast phases in an estimated 89 percent of patients, and

40 Myeloproliferative neoplasm blast phase is associated with a dismal prognosis.

41 ly aggressive chronic myeloid leukemia (CML)-blast phase-like disease in mice compared with less mali

42 nts with chronic myelogenous leukemia during blast phase, myelodysplastic syndrome, or acute myelogen

43 On-treatment transformation to accelerated/blast phase occurred in 5 patients.

44 Transformation to accelerated/blast phase occurred in 5% and 7% of patients in the das

45 On-treatment transformation to accelerated/blast phase occurred in four patients (2%) on bosutinib

46 patients), AML in relapse (29 patients), and blast phase of chronic myeloid leukemia (CML-BP; 10 pati

47 One 64-year-old man with lymphoid blast phase of CML had a morphologic and cytogenetic CR

48 the mutation facilitates progression to the blast phases of myeloproliferative disorders.

49 re were fewer progressions to accelerated or blast phase on treatment, including clonal evolution, in

50 durable responses; however, most responding blast phase patients relapse despite continued therapy.

51 t committed CML progenitors from chronic and blast phase patients.

52 h BCR-ABL(-) myeloproliferative neoplasms in blast phase receiving induction chemotherapy (55%), low-

53 sorder (MPD) in mice, but progression to CML blast phase requires additional mutations.

54 gene signatures of chronic, accelerated, and blast phases suggest that the progression of chronic pha

55 o hematologic failure, accelerated phase, or blast phase was also significantly different (3% vs 17%,

56 lower rates of transformation to accelerated/blast phase were reported compared with patients with BC

57 out treatment, most patients progress to the blast phase when additional oncogenic mutations result i

58 ndency for transformation into leukemia (MPN-blast phase), which is hypothesized to be accompanied by

59 with imatinib in chronic phase, 23 developed blast phase, which was of sudden onset (ie, occurring in

60 P was a necessary step in the progression to blast phase, with leukemic transformation being exceedin