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1 ses with variant cytology (ie, anaplastic or blastic), 6 (28.6%) had p53 mutations as compared with o
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
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
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
19 ronic phase (CP), accelerated phase (AP), or blastic phase (BP) were injected into preirradiated NOD/
22 es (MDS), or chronic myelogenous leukemia in blastic phase (CML-BP) were initially randomly assigned
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
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
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.
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
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
51 D4-dependent oncogenic regulatory network in blastic plasmacytoid dendritic cell neoplasm (BPDCN) and
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
59 delphia-positive chronic myeloid leukemia in blastic transformation for treatment with the ABL tyrosi
61 wn about the molecular mechanisms leading to blastic transformation of CML and propose some novel the
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
70 including 50 cases of MCL (40 typical and 10 blastic variants), 21 follicular lymphomas, 20 diffuse l
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