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1 ed by the t(1;19) translocation in human pre-B cell leukemia.
2 nized anti-CD22 mAb having been used against B cell leukemia.
3 re-BCR) signaling, spontaneously develop pre-B cell leukemia.
4 innate immunity to virally induced acute pro-B cell leukemia.
5 gens have been studied for the management of B-cell leukemia.
6 manner in a Nalm-6 xenograft rodent model of B-cell leukemia.
7 x and mEg5 contributes to the development of B-cell leukemia.
8 oncogene product, v-Abl, and also causes pre-B-cell leukemia.
9 ients with lymphoma than in those with acute B-cell leukemia.
10  of miR-125b in mice can promote myeloid and B-cell leukemia.
11 mplying a role in the pathogenesis of mature B-cell leukemia.
12 favorable outcome in patients with precursor B-cell leukemia.
13 s well as in a subset of patients with acute B-cell leukemia.
14  with peripheral blood eosinophila and T- or B-cell leukemias.
15  of the IL-2R in T-cell leukemias and p75 in B-cell leukemias.
16 the most frequent genetic alteration in AKXD B-cell leukemias.
17 plicated in the development of childhood pre-B-cell leukemias.
18 not been detected in patients with human pre-B-cell leukemias.
19 ibition as a potential therapeutic target in B-cell leukemias.
20  they up-regulated the antiapoptotic protein B-cell leukemia 2 (Bcl-2) by 10-fold.
21 ld down-regulated in MCL; in addition to the B-cell leukemia 2 (BCL2) system other apoptotic pathways
22 duced expression of the proapoptotic protein B-cell leukemia 2 homology 3 (BH3) interacting domain de
23 leukemia sequence-1 (MCL1), an antiapoptotic B cell leukemia-2 family member.
24 ia-1 (Mcl-1), an antiapoptotic member of the B-cell leukemia-2 family, is an important participant in
25 enotype (35%) or a lethal, short-latency pre-B-cell leukemia (20%).
26                                              B cell leukemia 3 (Bcl-3) is an essential negative regul
27             Lipopolysaccharide (LPS)-induced B cell leukemia 3 (Bcl3) expression was strongly impaire
28 on of NR4A1 and NR4A3 in chronic lymphocytic B-cell leukemia (71%), in follicular lymphoma (FL, 70%),
29 ly for multiple myeloma, but also for mature B cell leukemia and lymphoma.
30    Clinical trials in patients with advanced B cell leukemias and lymphomas treated with CD19-specifi
31 impressive results in treating patients with B cell leukemias and lymphomas.
32 inical concepts to target the BCR pathway in B-cell leukemia and lymphoma.
33 n younger than 6 years of age with precursor B-cell leukemia and no adverse genetic features had a 10
34 for the epigenetic changes that occur in pre-B-cell leukemia and other B-cell-related diseases.
35 ed from the bone marrow of patients with pre-B-cell leukemias and these findings should facilitate th
36              We report the identification of B cell leukemia (Bcl)-3 as an essential negative regulat
37 nd modulated by virus-encoded anti-apoptotic B cell leukemia (BCL)2-like suppressors.
38         We report here the identification of B-cell leukemia (Bcl)-3 as a modulator of innate immune
39 monstrated that miR-125b induces myeloid and B-cell leukemia by inhibiting interferon regulatory fact
40  model for an inducible and reversible acute B-cell leukemia caused by p210 BCR/ABL.
41                  In this study, we show that B cell leukemia causes T cells to become activated and h
42           Earlier work with the DT40 chicken B cell leukemia cell line showed that Syk was required t
43 pment, and is expressed in a number of human B cell leukemia cell lines, primary human chronic myeloi
44 ute promyelocytic leukemia (APL) and chronic B-cell leukemia cell lines, respectively.
45                                     In human B cell leukemia cells, binding of wild-type PAX5 to a re
46 cts of RAR and RXR rexinoids in human T- and B-cell leukemia cells and demonstrated that RXR rexinoid
47                                       In pre B cell leukemias containing the t(1;19) chromosome trans
48 AX5-ETV6 as a potent oncoprotein that drives B-cell leukemia development.
49                                          Pre-B cell leukemia homeobox 1 (Pbx1)-d is a dominant-negati
50                                          Pre-B-cell leukemia homeobox (PBX) and myeloid ecotropic vir
51                                          Pre-B-cell leukemia homeobox (PBX) transcription factors are
52                                          Pre-B-cell leukemia homeobox (Pbx)-regulating protein-1 (Pre
53 otein (PBXIP1/HPIP) is a co-repressor of pre-B-cell leukemia homeobox 1 (PBX1) and is also known to r
54 id ecotropic viral integration 1 (Meis1)/pre-B-cell leukemia homeobox 3 (Pbx3) genes.
55                                          Pre-B-cell leukemia homeobox interacting protein 1 or human
56 oteins competitively heterodimerize with pre-B-cell leukemia homeobox-1 (Pbx1).
57 us modified binding of the proadipogenic pre-B-cell leukemia homeobox-1/homeobox 9 complex.
58       The v-Cbl oncogene induces myeloid and B-cell leukemia; however, the mechanism by which transfo
59 s in vitro, while inducing predominantly pre-B cell leukemias in vivo.
60 ase in childhood megakaryocyte-erythroid and B-cell leukemia in Down syndrome implicates trisomy 21 (
61                Activated ABL oncogenes cause B-cell leukemias in mice and chronic myelogenous leukemi
62  were frequent in patients with other mature B-cell leukemias in which CD20 surface expression is inc
63 gnancies, but are consistently absent in pre-B cell leukemias induced by the chimeric oncoprotein E2a
64                                        Thus, B cell leukemia-induced inhibition of T cell Akt/mTORC1
65 the product of a proto-oncogene in acute pre-B-cell leukemia, is a global regulator of embryonic deve
66 2B1-D1 and the parental 12B1 line, but not a B-cell leukemia line, A20.
67 s (IFNs)-alpha/beta and -gamma, whereas, pro-B-cell leukemia lines derived from Emu-ret mice are mark
68 inhibitor, synergized to induce apoptosis in B cell leukemia, lymphoma, and multiple myeloma.
69  such as TNFR-associated factors 2 and 5 and B cell leukemia/lymphoma 10, were readily decreased upon
70 Myeloid cell leukemia sequence 1 (MCL-1) and B cell leukemia/lymphoma 2 (BCL-2) are anti-apoptotic pr
71 4, expression of the anti-apoptotic molecule B cell leukemia/lymphoma 2 (Bcl-2), and enhanced IL-2 pr
72 eukemia 1 (Mcl1) but not other antiapoptotic B cell leukemia/lymphoma 2 (Bcl2) family members.
73                                Antiapoptotic B cell leukemia/lymphoma 2 (BCL2) family proteins are ex
74 gher percentage of CD44(v.low) cells express B cell leukemia/lymphoma 2, interleukin-7 receptor, and
75 we show that the transcriptional coregulator B cell leukemia/lymphoma 3 (Bcl3) limits granulopoiesis
76 e Kruppel-like transcription factor 6 (KLF6)-B cell leukemia/lymphoma 6 (BCL6) signaling axis as a no
77                         Here, we report that B cell leukemia/lymphoma 6 (BCL6), a transcriptional rep
78 at potentiates transcriptional repression by B cell leukemia/lymphoma 6 (BCL6).
79 rus, which encodes v-Abl/p160, induces a pre-B cell leukemia/lymphoma in mice.
80  deletions and mutations in Bcl11b (encoding B cell leukemia/lymphoma-11B) and identify the presence
81 nd truncating temperature-induced changes in B cell leukemia/lymphoma-2 associated X protein alpha an
82 t key repressors of the plasmacytic program, B cell leukemia/lymphoma-6 and paired box gene 5, are re
83                               Using a murine B-cell leukemia/lymphoma (BCL1) model, we showed the dev
84                    Upregulation of cyclin D1/B-cell leukemia/lymphoma 1 (CCND1/BCL1) is present in mo
85 ed cyclin D1 expression and progression of a B-cell leukemia/lymphoma 1 tumor in mice by preferential
86 ion and utilizes the adaptor molecule BCL10 (B-cell leukemia/lymphoma 10).
87                            In apoptosis, the B-cell leukemia/lymphoma 2 (Bcl-2) family members Bcl-2-
88 hese tumors are genetically characterized by B-cell leukemia/lymphoma 2 (BCL2) translocation and muta
89 and tensin homolog, TGFbeta receptor II, and B-cell leukemia/lymphoma 2 -associated X protein.
90  parallel decrease in anti-apoptotic protein B-cell leukemia/lymphoma 2 levels.
91  factor profile, with elevated expression of B-cell leukemia/lymphoma 6 (Bcl-6), CXC chemokine recept
92 trast, inhibitory cyclin G2, p27/Cdkn1b, and B-cell leukemia/lymphoma 6 (Bcl6) were sharply down-modu
93 body-dependent cellular cytotoxicity against B-cell leukemia/lymphoma cell lines and primary chronic
94 odel consisting of highly disseminated human B-cell leukemia/lymphoma was developed by i.v. inoculati
95                       Using a mouse model of B-cell leukemia/lymphoma, we find that differences in tr
96                                          The B-cell leukemia/lymphoma-2 (BCL-2) family of proteins go
97                                      Purpose B-cell leukemia/lymphoma-2 (BCL-2) overexpression is com
98 ), endothelial nitric oxide synthase (eNOS), B-cell leukemia/lymphoma-2 (Bcl-2), and inducible nitric
99 ceptor-associated factor-1 (TRAF-1), TRAF-2, B-cell leukemia/lymphoma-2 (Bcl-2), Bcl-x, A1, and cellu
100 ciated with colorectal cancer formation (eg, B-cell leukemia/lymphoma-2 [Bcl2]) and 1.8% (18/906) wit
101       Moreover, EGCG suppressed the proteins B-cell leukemia/lymphoma-2 protein (Bcl-2), X-linked inh
102 ular assay for the study of therapy of human B-cell leukemia/lymphoma.
103            Transgenic mice that over-express B cell leukemia/lymphomas (Bcl)-2 in myeloid cells under
104                              Thus, precursor B-cell leukemias maintain evolution at the IgH locus at
105 transduced T cells efficiently lysed primary B-cell leukemia, mantle cell lymphoma, and multiple myel
106 ip in B cell diseases, especially in chronic B cell leukemia, needs to be considered further in regar
107       Hairy cell leukemia (HCL) is a chronic B-cell leukemia noted for an indolent course that ultima
108 ificantly more common in patients with other B-cell leukemias, occurring in five (50%) of 10 patients
109 ecreased, and neurotensin was unexpressed in B cell leukemia patient's cells, as compared with health
110 ) chromosomal translocation of pediatric pre-B cell leukemia produces chimeric oncoprotein E2a-Pbx1,
111  genome-scale shRNA screen for modulators of B-cell leukemia progression in vivo.
112 myelocytic leukemia zinc finger protein, and B-cell leukemia protein 6.
113 ll activating factor, BAFF) developed CD5(+) B-cell leukemia resembling human chronic lymphocytic leu
114 d leukemia, and the t(12;21)(p13;q22) in pre-B-cell leukemia, respectively.
115                 We show that loss of Phf6 in B-cell leukemia results in systematic changes in gene ex
116                               These anti-pre-B-cell leukemia-specific CTL lysed both unstimulated and
117 w here the generation of autologous anti-pre-B-cell leukemia-specific cytolytic T-cell lines from the
118 ed iNKT cell cytotoxicity against T-cell and B-cell leukemia targets in vitro and iNKT-cell-mediated
119 x1, E2a-Pbx1, is an oncoprotein in human pre-B cell leukemia that strongly suppresses differentiation
120 he transcriptional activation of IL10 by pre-B cell leukemia transcription factor-1b and another Hox
121 eletion of CDH-implicated genes encoding pre-B cell leukemia transcription factors (Pbx) led to letha
122                                          Pre-B cell leukemia transcription factors (PBXs) act as cofa
123 otropic viral insertion site (MEIS), and pre-B-cell leukemia transcription factor 1 (PBX) may regulat
124 nhibitors showed that the homeoproteins, pre B-cell leukemia transcription factor 1 (PBX1) and PBX-re
125  CDKIs, we observed a cellular gene, the pre-B-cell leukemia transcription factor 1 (Pbx1) gene, down
126 out mice for one of the candidate genes, pre-B-cell leukemia transcription factor 1 (Pbx1), and ident
127 ind to DNA or a key HOX-binding partner, pre-B-cell leukemia transcription factor-1 (PBX1).
128 without altering the genomic DNA and induces B-cell leukemia via genetic deletion of the gene encodin
129  a dramatic increase in the frequency of pro-B cell leukemia was observed in mice with combined heter
130 ng a humanized model of treatment refractory B cell leukemia, we find that infiltration of leukemia c
131 most importantly primary Bcr-Abl-transformed B-cell leukemias were completely eradicated by the alloa
132  T cells from patients with acute or chronic B cell leukemia, which were also metabolically exhausted
133 c B-cell lymphoma and, upon transplantation, B-cell leukemia with leukemic infiltrates in liver and l
134 therapy, whereas patients who have precursor B-cell leukemia without other adverse features appear to
135 -AHPC-mediated cleavage of the antiapoptotic B-cell leukemia XL (Bcl-XL) protein to a proapoptotic 18
136  NF-kappaB-dependent antiapoptotic proteins, B-cell leukemia XL (Bcl-XL), Bcl-2, X-linked inhibitor o

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