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1 ses with variant cytology (ie, anaplastic or blastic), 6 (28.6%) had p53 mutations as compared with o
2 astic large lymphocytes, some of which had a blastic appearance or resembled virocytes.
3     Survival was compared for both lytic and blastic bone metastases and for patients with high and l
4 en compared to the more highly proliferative blastic cases or cell lines (mean arbitrary units: 58 ve
5 activation markedly accelerated leukemia and blastic crisis onset in Tec-p210bcr/abl transgenic mice
6              The patient with extramedullary blastic disease achieved complete response.
7  1 had a complete response in extramedullary blastic disease).
8  phase in 5 patients, accelerated in 15, and blastic in 8 (7 medullary, 1 extramedullary); median tim
9 ive p53 construct developed leukocytosis and blastic infiltration of lymph nodes, spleen, and liver w
10 eloid disorders, then the emergence of acute blastic leukemias; and treating malignant and nonmaligna
11 on primarily by mononuclear cells (including blastic lymphocytes), and increased crypt cell apoptosis
12 essed at variable levels in both typical and blastic MCLs.
13 mo2 and gata1 promoters exhibit an immature, blastic morphology and express only erythroid and myeloi
14  chromosome imbalances were observed in both blastic natural killer and cutaneous natural killer-like
15 vestigate comprehensively genomic changes in blastic natural killer and extranodal natural killer-lik
16  the RB1 gene at 13q14.2 was detected in one blastic natural killer cell lymphoma with 13q loss using
17 continuous infusion to 19 adults with CML in blastic or accelerated phase.
18 plete cytogenetic response in 8) and 43% for blastic phase (3 of 7 patients).
19 ronic phase (CP), accelerated phase (AP), or blastic phase (BP) were injected into preirradiated NOD/
20           In AML, accelerated phase (AP) and blastic phase (BP)-CML, basal TA was 10- to 50-fold high
21 se (CP), 175 accelerated phase (AP), and 246 blastic phase (BP).
22 es (MDS), or chronic myelogenous leukemia in blastic phase (CML-BP) were initially randomly assigned
23 es (MDS), or chronic myelogenous leukemia in blastic phase (CML-BP).
24 me (MDS; n = 8), chronic myeloid leukemia in blastic phase (CMLBP; n = 11), and acute lymphocytic leu
25 s leukemia (CML) in chronic, accelerated, or blastic phase and in 8 patients with myelofibrosis (MF)
26 tion of patients with CML in accelerated and blastic phase but not in chronic phase CML patients and
27 subclassified as either accelerated phase or blastic phase disease.
28            Progression to the accelerated or blastic phase of CML occurred in 5 patients who were rec
29  leukemic progenitors in the accelerated and blastic phase of CML.
30                      Of 33 patients with the blastic phase of disease, 13 had a hematologic response
31 herapy (resistance/loss of response, n = 33; blastic phase on TKI therapy, n = 6; intolerance/toxicit
32     No patients progressed to accelerated or blastic phase or developed clonal chromosomal abnormalit
33 ith CML (93% chronic, 5% accelerated, and 2% blastic phase) corresponding to an annual incidence of 0
34 c phase, 17 in accelerated phase, and six in blastic phase).
35  phase, 41% in accelerated phase, and 34% in blastic phase).
36  months, 3% had progressed to accelerated or blastic phase.
37  no patient has progressed to accelerated or blastic phase.
38 hase, 83% for accelerated phase, and 43% for blastic phase.
39 ed by transformation into an accelerated and blastic phase.
40 ich inevitably terminates in a rapidly fatal blastic phase.
41 ted-phase (33.3%; 95% CI, 19.7% to 46.9%) or blastic-phase (16.7%; 95% CI, 1.9% to 31.9%) relapse.
42  SCT still remains an option for accelerated/blastic-phase and selected chronic-phase CML.
43 nly the chronic but also the accelerated and blastic phases of chronic myelogenous leukemia.
44 les from 184 (148 chronic and 36 accelerated/blastic phases) CML patients and found the levels to be
45 ients with CML (19 of them in accelerated or blastic phases) treated with dasatinib after treatment f
46 are made for patients in the accelerated and blastic phases, and for allogeneic stem cell transplanta
47 k of efficacy, progression to accelerated or blastic phases, or death at any time.
48 C(+) subset of DCs; the relationship between blastic plasmacytoid DC neoplasia cells and healthy DCs;
49 neoplasms, including a series of 45 cases of blastic plasmacytoid dendritic cell (BPDC) neoplasms and
50                                              Blastic plasmacytoid dendritic cell (PDC) neoplasm (BPDC
51 D4-dependent oncogenic regulatory network in blastic plasmacytoid dendritic cell neoplasm (BPDCN) and
52                                Patients with blastic plasmacytoid dendritic cell neoplasm (BPDCN) hav
53                                              Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is
54                                              Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is
55  Frankel et al describe a novel treatment of blastic plasmacytoid dendritic cell neoplasm (BPDCN) usi
56 spective study of treatment of patients with blastic plasmacytoid dendritic cell neoplasm (BPDCN), an
57               Cells in the colonies are very blastic, showing no cytoplasmic differentiation, and exp
58                                       Sudden blastic transformation (SBT) has been reported in 0.5% t
59 delphia-positive chronic myeloid leukemia in blastic transformation for treatment with the ABL tyrosi
60                                              Blastic transformation of chronic myelogenous leukemia (
61 wn about the molecular mechanisms leading to blastic transformation of CML and propose some novel the
62             Median survival from the date of blastic transformation was 5 months.
63  present follow-up, the survival and time to blastic transformation were similar.
64 tase 2A (PP2A) activity is important for CML blastic transformation.
65 Disease evolution does not generally involve blastic transformation.
66  natural killer (NK)-cell origin, CD4+ CD56+ blastic tumors (BTs) of skin have recently been proposed
67  15 of 50 cases of MCL: 7 of 10 (70%) in the blastic variant and 8 of 40 (20%) in the typical MCL (70
68 nhanced cell death, which was synergistic in blastic variant MCL cell lines.
69                        Paradoxically, in the blastic variant of MCL, 8 of 10 (80%) cases showed expre
70 including 50 cases of MCL (40 typical and 10 blastic variants), 21 follicular lymphomas, 20 diffuse l
71 o patients had nodular, and two patients had blastic variants.

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