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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

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