ライフサイエンスコーパス: chronic myeloid leukaemia

1 erated-phase, and four (5%) with blast-phase chronic myeloid leukaemia.

2 c HSCT outcomes in patients with blast-phase chronic myeloid leukaemia.

3 atinib in previously untreated patients with chronic myeloid leukaemia.

4 newly diagnosed patients with chronic-phase chronic myeloid leukaemia.

5 ations identified using NGS in patients with chronic myeloid leukaemia.

6 ase is elevated in several cancers including chronic myeloid leukaemia.

7 eatment for patients in the chronic phase of chronic myeloid leukaemia.

8 tyrosine kinase inhibitors in patients with chronic myeloid leukaemia.

9 treatment recommendations and frameworks in chronic myeloid leukaemia.

10 ains a treatment challenge for patients with chronic myeloid leukaemia.

11 front-line and subsequent-line strategies in chronic myeloid leukaemia.

12 Positive associations were also observed for chronic myeloid leukaemia (9.57, 4.00 to 17.91, n=122) a

13 nic myeloid leukaemia-blast phase, four with chronic myeloid leukaemia-accelerated phase, and two wit

14 eloid chronic myeloid leukaemia-blast phase, chronic myeloid leukaemia-accelerated phase, or advanced

15 biology and heavily implicated in acute and chronic myeloid leukaemia (AML and CML).

16 ration TKIs would offer 90% of patients with chronic myeloid leukaemia an effective, safe, and afford

17 BCR-ABL1 fusion gene is a driver oncogene in chronic myeloid leukaemia and 30-50% of cases of adult a

18 was demonstrated in acute myeloid leukaemia, chronic myeloid leukaemia and acute lymphoid leukaemia,

19 hosphatase activity of PP2A is suppressed in chronic myeloid leukaemia and other malignancies charact

20 two (50%) of four patients with blast-phase chronic myeloid leukaemia and the median duration of res

21 To revise the current goals of therapy of chronic myeloid leukaemia and to incorporate the influen

22 Further, in blast crisis chronic myeloid leukaemia, and a subset of acute myeloid

23 tment options, side-effects, and outcomes of chronic myeloid leukaemia, and discusses the possibility

24 B- and mantle-cell lymphomas, chronic myeloid leukaemia, and multiple myeloma, however

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

26 New and mature data with TKI therapy in chronic myeloid leukaemia are producing observations tha

27 nation of health utilities for chronic-phase chronic myeloid leukaemia (base case 0.89, range 0-1) an

28 incorporate the influence of the underlying chronic myeloid leukaemia biology on directing therapeut

29 untreated or relapsed or refractory myeloid chronic myeloid leukaemia-blast phase, chronic myeloid l

30 y 8, 2023, 20 patients were treated (14 with chronic myeloid leukaemia-blast phase, four with chronic

31 For this study the well characterised chronic myeloid leukaemia cell line KYO-1 was selected a

32 wo different types of cancer cells (KU812, a chronic myeloid leukaemia cell line; and DU145, a prosta

33 adult patients with acute myeloid leukaemia, chronic myeloid leukaemia, chronic myelomonocytic leukae

34 two decades, leukaemia stem cells (LSCs) in chronic myeloid leukaemia (CML) and acute myeloid leukae

35 Here we use a chimeric mouse model of chronic myeloid leukaemia (CML) and human bone marrow (B

36 Targeted therapies for chronic myeloid leukaemia (CML) are effective, but rarel

37 Chronic myeloid leukaemia (CML) arises after transformat

38 purine synthesis has a cytostatic effect on chronic myeloid leukaemia (CML) cells.

39 In chronic myeloid leukaemia (CML) expression of the chimer

40 The prognosis of chronic myeloid leukaemia (CML) has improved remarkably

41 y diagnosed Philadelphia chromosome-positive chronic myeloid leukaemia (CML) in chronic phase after a

42 ntly activated and functionally required for chronic myeloid leukaemia (CML) in humans and in mouse m

43 Chronic myeloid leukaemia (CML) is a clonal disorder of

44 Chronic myeloid leukaemia (CML) is a myeloproliferative

45 Chronic myeloid leukaemia (CML) is characterized by the

46 Chronic myeloid leukaemia (CML) is driven by the activit

47 Chronic Myeloid Leukaemia (CML) is initiated and maintai

48 Chronic myeloid leukaemia (CML) is quintessential to thi

49 has provided a curative treatment option for chronic myeloid leukaemia (CML) over the past 20-30 year

50 such as imatinib have increased survival of chronic myeloid leukaemia (CML) patients, they fail to e

51 The Philadelphia chromosome in chronic myeloid leukaemia (CML) provided the very first

52 he ABL tyrosine kinase inhibitor imatinib in chronic myeloid leukaemia (CML) serves as a model for mo

53 Chronic myeloid leukaemia (CML), a hematopoietic stem ce

54 hibitors (TKIs), the treatment of choice for chronic myeloid leukaemia (CML), can cause lower gastroi

55 ls (LSC) that persist as residual disease in chronic myeloid leukaemia (CML), developing therapeutic

56 The clonogenic cells of chronic myeloid leukaemia (CML), unlike normal haemopoie

57 TKIs) to eradicate LSC in chronic phase (CP) chronic myeloid leukaemia (CML).

58 topical issues in the clinical management of chronic myeloid leukaemia (CML).

59 b treatment of newly diagnosed chronic-phase chronic myeloid leukaemia compared with imatinib could n

60 Therapeutic advances in chronic myeloid leukaemia continue to circumvent the cha

61 Chronic myeloid leukaemia continues to instruct us in th

62 rosine-kinase inhibitors, most patients with chronic myeloid leukaemia could enjoy a near normal life

63 If these advances reach all patients with chronic myeloid leukaemia, cure might eventually become

64 Dec 31, 2014, we screened 121 patients with chronic myeloid leukaemia for BCR-ABL1 kinase domain mut

65 fordable generic imatinib, all patients with chronic myeloid leukaemia globally should be able to acc

66 The management of chronic myeloid leukaemia has been revolutionized by tar

67 In less than 10 years, the prognosis of chronic myeloid leukaemia has changed from that of a fat

68 inase inhibitors (TKIs) for the treatment of chronic myeloid leukaemia has changed patient outcome an

69 atment-free remission (TFR) in patients with chronic myeloid leukaemia have discontinued tyrosine kin

70 Treatment-free remission in chronic myeloid leukaemia-ie, achievement of a sustained

71 rs improve overall survival in patients with chronic myeloid leukaemia in chronic phase (CML-CP).

72 are available for treatment of patients with chronic myeloid leukaemia in chronic phase (CML-CP).

73 older with Philadelphia chromosome-positive chronic myeloid leukaemia in chronic phase and Eastern C

74 s used as frontline therapy in patients with chronic myeloid leukaemia in chronic phase in relation t

75 BL1 tyrosine kinase inhibitors (TKIs) in the chronic myeloid leukaemia in chronic phase of the diseas

76 Optimal management of patients with chronic myeloid leukaemia in chronic phase with suboptim

77 pen-label, randomised trial in patients with chronic myeloid leukaemia in chronic phase with suboptim

78 e recruited patients (aged >/=18 years) with chronic myeloid leukaemia in first chronic phase who had

79 We recruited patients (aged >=18 years) with chronic myeloid leukaemia in first chronic phase, who ha

80 Five (83%) of six patients with chronic myeloid leukaemia in lymphoid blast phase had an

81 e lymphoblastic leukaemia, and six [10%] had chronic myeloid leukaemia in lymphoid blast phase).

82 Ph-positive acute lymphoblastic leukaemia or chronic myeloid leukaemia in lymphoid blast phase.

83 ients with relapsed or refractory disease or chronic myeloid leukaemia in lymphoid blast phase.

84 not offer good value as frontline therapy in chronic myeloid leukaemia in order to achieve sustained

85 hibitors have changed the natural history of chronic myeloid leukaemia in such a way that patients wi

86 osome-positive myeloid disease-consisting of chronic myeloid leukaemia in the myeloid blast phase and

87 ing activity in patients with advanced phase chronic myeloid leukaemia, including those with multiple

88 Chronic myeloid leukaemia is a haemopoietic stem cell di

89 Chronic myeloid leukaemia is a paradigmatic haematopoiet

90 n this study, we used the p53 negative human chronic myeloid leukaemia K562 cell line.

91 n 44 (70%) of 63 patients with chronic-phase chronic myeloid leukaemia, of which 12 (75%) of 16 patie

92 ents aged 18 years or older with Ph-positive chronic myeloid leukaemia or acute lymphoblastic leukaem

93 ong-read sequencing and standard RNA-Seq for chronic myeloid leukaemia patient samples.

94 Treatment of a T315I chronic myeloid leukaemia patient with axitinib resulted

95 d chronic phase in patients with blast-phase chronic myeloid leukaemia, representing an active salvag

96 For patients with accelerated-phase chronic myeloid leukaemia, six (86%) of seven patients h

97 reatment in the treatment of newly diagnosed chronic myeloid leukaemia suggest that this first-genera

98 me-positive or BCR-ABL1-positive blast-phase chronic myeloid leukaemia, suitable for intensive chemot

99 me-positive or BCR-ABL1-positive blast-phase chronic myeloid leukaemia, suitable for intensive chemot

100 Ponatinib has shown potent activity against chronic myeloid leukaemia that is resistant to available

101 After two decades of use in chronic myeloid leukaemia, the risks and benefits of est

102 ed consecutive patients newly diagnosed with chronic myeloid leukaemia treated with first-line tyrosi

103 six with myelodysplastic syndrome, five with chronic myeloid leukaemia (two with chronic-phase and th

104 hibitor imatinib is used in the treatment of chronic myeloid leukaemia, where it targets the intracel

105 iladelphia chromosome-positive (Ph-positive) chronic myeloid leukaemia who previously received at lea

106 ble safety profile in patients with advanced chronic myeloid leukaemia who previously received multip

107 nts with second-generation-TKI resistance or chronic myeloid leukaemia with 944C->T (Thr315Ile)-mutat

108 ) therapy is feasible for some patients with chronic myeloid leukaemia with deep molecular responses;