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1 2-dependent myeloproliferative neoplasms and B cell acute lymphoblastic leukemia.
2 response in a phase 1 trial for treatment of B cell acute lymphoblastic leukemia.
3 sociated with nearly one-fourth of pediatric B cell acute lymphoblastic leukemia.
4 syndrome as well as in t(12;21) in childhood B cell acute lymphoblastic leukemia.
5 y the t(1;19) translocation in pediatric pre-B cell acute lymphoblastic leukemia.
6 lymphoid blast crisis or abolish established B-cell acute lymphoblastic leukemia.
7 X5-PML chimeric protein in two patients with B-cell acute lymphoblastic leukemia.
8 ) chromosomal translocation of childhood pre-B-cell acute lymphoblastic leukemia.
9 st frequent translocation found in pediatric B-cell acute lymphoblastic leukemias.
10 iagnoses included 28 non-Hodgkin lymphoma, 4 B-cell acute lymphoblastic leukemia, 1 Hodgkin disease,
11 defined CD4+:CD8+ composition to adults with B cell acute lymphoblastic leukemia after lymphodepletio
13 fficacy in patients with relapsed/refractory B-cell acute lymphoblastic leukemia (ALL) and chronic ly
15 translocation t(6;12)(q23;13) in a childhood B-cell acute lymphoblastic leukemia (ALL) cell line fuse
17 cell death in normal pre-B cells and in pre-B-cell acute lymphoblastic leukemia (ALL) driven by BCR-
18 ronic lymphocytic leukemia (CLL) or relapsed B-cell acute lymphoblastic leukemia (ALL) we have enroll
19 en established from a patient with precursor-B-cell acute lymphoblastic leukemia (ALL), which exhibit
21 monocytic leukemia, myelodysplasic syndrome, B-cell acute lymphoblastic leukemia, and acute myelogeno
22 to impaired B cell development, followed by B cell acute lymphoblastic leukemia at 100% incidence an
23 eukemia (CML) in chronic phase but not Ph(+) B cell acute lymphoblastic leukemia (B-ALL) and CML blas
25 ment of myeloproliferative neoplasms (MPNs), B cell acute lymphoblastic leukemia (B-ALL) with rearran
26 syndrome confers a 20-fold increased risk of B cell acute lymphoblastic leukemia (B-ALL), and polysom
27 nt effects in relapsed and/or refractory pre-B cell acute lymphoblastic leukemia (B-ALL), but antigen
32 signaling, including the high-risk subset of B cell acute lymphoblastic leukemias (B-ALLs) with CRLF2
34 includes chronic myeloid leukemia (CML) and B-cell acute lymphoblastic leukemia (B-ALL) and is induc
36 ority of treatment failures in patients with B-cell acute lymphoblastic leukemia (B-ALL) receiving al
38 acute lymphoblastic leukemia (T-ALL) and (3) B-cell acute lymphoblastic leukemia (B-ALL) samples, (c)
40 ic strategies, particularly in diseases like B-cell acute lymphoblastic leukemia (B-ALL), where few t
51 We investigated DNA methylomes of pediatric B-cell acute lymphoblastic leukemias (B-ALLs) using whol
52 eration of secondary genetic events in human B-cell acute lymphoblastic leukemias (B-ALLs), illustrat
53 e a significant effect on the development of B-cell acute lymphoblastic leukemia (BALL) induced by BC
54 e suitability of targeting CD22 on precursor B-cell acute lymphoblastic leukemia (BCP-ALL), lymphobla
56 d blood cancers and primary, patient-derived B-cell acute lymphoblastic leukemia blasts compared with
57 se of patients suffering from T-cell and pre-B-cell acute lymphoblastic leukemia by increasing steroi
58 R-125b is also up-regulated in patients with B-cell acute lymphoblastic leukemia carrying the t(11;14
59 he t(17;19) chromosomal translocation in pro-B-cell acute lymphoblastic leukemia, incorporates the tr
60 usion protein in t(17;19)-positive human pro-B cell acute lymphoblastic leukemias is believed to prom
61 lar results were obtained in human precursor B-cell acute lymphoblastic leukemia lines when Notch act
62 marrow commonly occurs in T-ALL and relapsed B-cell acute lymphoblastic leukemia patients, and is ass
67 rafts from pediatric patients with precursor B-cell acute lymphoblastic leukemia (pre-B ALL) in NSG m
68 BX1 (E2A-PBX1)-frequently found in precursor-B-cell acute lymphoblastic leukemia (preB-ALL), we devel
71 l evolution of a form of childhood precursor-B cell acute lymphoblastic leukemia that is characterize
72 me-positive chronic myelogenous leukemia and B cell acute lymphoblastic leukemia through the inhibiti
73 tive acute lymphoblastic leukemia and mature B-cell acute lymphoblastic leukemia using biologically t
74 1-induced CML-like MPN and the appearance of B-cell acute lymphoblastic leukemia, whereas complete de
75 patients with acute myelogenous leukemia and B-cell acute lymphoblastic leukemia whose tumors harbor
76 and effector function of human NK cells in a B-cell acute lymphoblastic leukemia xenotransplants mode
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