ライフサイエンスコーパス: blast phase

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

2 %] had chronic myeloid leukaemia in lymphoid blast phase).

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

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

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

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

7 relapse, and chronic myelogenous leukemia in blast phase.

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

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

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

11 to a form of acute myeloid leukaemia called blast phase.

12 ndency to develop vascular complications and blast phase.

13 ase or chronic myeloid leukaemia in lymphoid blast phase.

14 mia or chronic myeloid leukaemia in lymphoid blast phase.

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

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

17 of chronic myeloid leukaemia in the myeloid blast phase and in the accelerated phase, and Philadelph

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

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

20 8 MPN patients, as well as 71 cases with MPN-blast phase, and correlated these findings with their cl

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

22 plastic related; myeloproliferative neoplasm-blast phase; and AML post-cytotoxic therapy.

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

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

25 ding the chronic phase and primary/secondary blast phase (BP) of myeloid, lymphoid, or mixed phenotyp

26 ition, acquisition of drug resistance during blast phase (BP) progression remains a critical challeng

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

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

29 ), 50% in accelerated phase (AP), and 33% in blast phase (BP).

30 BCR-ABL1 independence, and transformation to blast phase (BP).

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

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

33 Blast phase chronic myeloid leukemia (BP-CML) poses sign

34 s reached by two (50%) of four patients with blast-phase chronic myeloid leukaemia and the median dur

35 Outcomes for patients with blast-phase chronic myeloid leukaemia are poor.

36 induce second chronic phase in patients with blast-phase chronic myeloid leukaemia, representing an a

37 hia chromosome-positive or BCR-ABL1-positive blast-phase chronic myeloid leukaemia, suitable for inte

38 hia chromosome-positive or BCR-ABL1-positive blast-phase chronic myeloid leukaemia, suitable for inte

39 ) with accelerated-phase, and four (5%) with blast-phase chronic myeloid leukaemia.

40 se allogeneic HSCT outcomes in patients with blast-phase chronic myeloid leukaemia.

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

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

43 refractory myeloid chronic myeloid leukaemia-blast phase, chronic myeloid leukaemia-accelerated phase

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

45 mirrored CML incidence, and advanced and/or blast phase CML was characterized by subsequent genomic

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

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

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

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

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

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

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

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

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

55 NA in CML patients who had progressed to the blast phase compared with the chronic phase of the disea

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

57 ber of patients who developed accelerated or blast phase disease decreased dramatically.

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

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

60 e treated (14 with chronic myeloid leukaemia-blast phase, four with chronic myeloid leukaemia-acceler

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

62 s with chronic myeloid leukaemia in lymphoid blast phase had an overall response.

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

64 atological response for accelerated-phase or blast-phase in phase 2).

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

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

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

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

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

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

71 In a cohort of 64 patients in blast phase of a myeloproliferative neoplasm (BP-MPN), w

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

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

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

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

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

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

78 of response was 6.2 months (IQR 3.2-9.3); no blast-phase patients were enrolled in the phase 2 study.

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

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

81 Progression to blast phase still occurs, particularly in socioeconomica

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

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

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

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

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

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

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