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1 innate immunity to virally induced acute pro-B cell leukemia.
2 ed by the t(1;19) translocation in human pre-B cell leukemia.
3 nd correlate these networks with subtypes of B cell leukemia.
4 nized anti-CD22 mAb having been used against B cell leukemia.
5 re-BCR) signaling, spontaneously develop pre-B cell leukemia.
6 therapy for relapsed or refractory pediatric B cell leukemia.
7 s well as in a subset of patients with acute B-cell leukemia.
8 gens have been studied for the management of B-cell leukemia.
9 x and mEg5 contributes to the development of B-cell leukemia.
10 oncogene product, v-Abl, and also causes pre-B-cell leukemia.
11 manner in a Nalm-6 xenograft rodent model of B-cell leukemia.
12 ients with lymphoma than in those with acute B-cell leukemia.
13 of miR-125b in mice can promote myeloid and B-cell leukemia.
14 mplying a role in the pathogenesis of mature B-cell leukemia.
15 favorable outcome in patients with precursor B-cell leukemia.
16 with peripheral blood eosinophila and T- or B-cell leukemias.
17 of the IL-2R in T-cell leukemias and p75 in B-cell leukemias.
18 the most frequent genetic alteration in AKXD B-cell leukemias.
19 plicated in the development of childhood pre-B-cell leukemias.
20 not been detected in patients with human pre-B-cell leukemias.
21 patients with autoimmune diseases or various B-cell leukemias.
22 ibition as a potential therapeutic target in B-cell leukemias.
24 ld down-regulated in MCL; in addition to the B-cell leukemia 2 (BCL2) system other apoptotic pathways
25 duced expression of the proapoptotic protein B-cell leukemia 2 homology 3 (BH3) interacting domain de
27 ia-1 (Mcl-1), an antiapoptotic member of the B-cell leukemia-2 family, is an important participant in
31 on of NR4A1 and NR4A3 in chronic lymphocytic B-cell leukemia (71%), in follicular lymphoma (FL, 70%),
32 y HIT receptors in xenograft mouse models of B cell leukemia and acute myeloid leukemia, targeting CD
33 9 have led to remarkable clinical results in B cell leukemia and lymphoma but eliminate all B lineage
37 eficiency strongly suppressed Emu-Myc-driven B cell leukemia and the antiapoptotic effects of Emu-BCL
38 Clinical trials in patients with advanced B cell leukemias and lymphomas treated with CD19-specifi
39 vailability of life-extending treatments for B cell leukemias and lymphomas, many of these cancers re
43 n younger than 6 years of age with precursor B-cell leukemia and no adverse genetic features had a 10
47 ed from the bone marrow of patients with pre-B-cell leukemias and these findings should facilitate th
52 monstrated that miR-125b induces myeloid and B-cell leukemia by inhibiting interferon regulatory fact
56 pment, and is expressed in a number of human B cell leukemia cell lines, primary human chronic myeloi
57 HC II expression restrained growth of murine B-cell leukemia cell lines in vitro and in vivo, indepen
60 cts of RAR and RXR rexinoids in human T- and B-cell leukemia cells and demonstrated that RXR rexinoid
63 across all subgroups of B-cell lymphomas and B-cell leukemias, establishing CD22 as a valuable immuno
70 otein (PBXIP1/HPIP) is a co-repressor of pre-B-cell leukemia homeobox 1 (PBX1) and is also known to r
76 in LIC progression and maintenance in T- and B-cell leukemias, (iii) novel epigenetic and age-related
77 degradation of ZFP574 suppressed Myc-driven B cell leukemia in mice, but normal B cells were largely
79 ase in childhood megakaryocyte-erythroid and B-cell leukemia in Down syndrome implicates trisomy 21 (
81 were frequent in patients with other mature B-cell leukemias in which CD20 surface expression is inc
82 gnancies, but are consistently absent in pre-B cell leukemias induced by the chimeric oncoprotein E2a
85 the product of a proto-oncogene in acute pre-B-cell leukemia, is a global regulator of embryonic deve
87 s (IFNs)-alpha/beta and -gamma, whereas, pro-B-cell leukemia lines derived from Emu-ret mice are mark
89 such as TNFR-associated factors 2 and 5 and B cell leukemia/lymphoma 10, were readily decreased upon
90 Myeloid cell leukemia sequence 1 (MCL-1) and B cell leukemia/lymphoma 2 (BCL-2) are anti-apoptotic pr
92 4, expression of the anti-apoptotic molecule B cell leukemia/lymphoma 2 (Bcl-2), and enhanced IL-2 pr
95 gher percentage of CD44(v.low) cells express B cell leukemia/lymphoma 2, interleukin-7 receptor, and
96 we show that the transcriptional coregulator B cell leukemia/lymphoma 3 (Bcl3) limits granulopoiesis
99 e Kruppel-like transcription factor 6 (KLF6)-B cell leukemia/lymphoma 6 (BCL6) signaling axis as a no
103 deletions and mutations in Bcl11b (encoding B cell leukemia/lymphoma-11B) and identify the presence
104 ependence of CG2-expressing leukemias on the B cell leukemia/lymphoma-2 (BCL-2) family of antiapoptot
105 nd truncating temperature-induced changes in B cell leukemia/lymphoma-2 associated X protein alpha an
106 t key repressors of the plasmacytic program, B cell leukemia/lymphoma-6 and paired box gene 5, are re
111 ed cyclin D1 expression and progression of a B-cell leukemia/lymphoma 1 tumor in mice by preferential
113 sis, we report that the transcription factor B-cell leukemia/lymphoma 11A (BCL11A) is highly expresse
115 labrutinib, zanubrutinib, or ibrutinib) or a B-cell leukemia/lymphoma 2 (BCL2) inhibitor (venetoclax)
116 hese tumors are genetically characterized by B-cell leukemia/lymphoma 2 (BCL2) translocation and muta
118 ns, including an enrichment in antiapoptotic B-cell leukemia/lymphoma 2 family protein expression, in
120 factor profile, with elevated expression of B-cell leukemia/lymphoma 6 (Bcl-6), CXC chemokine recept
121 trast, inhibitory cyclin G2, p27/Cdkn1b, and B-cell leukemia/lymphoma 6 (Bcl6) were sharply down-modu
122 body-dependent cellular cytotoxicity against B-cell leukemia/lymphoma cell lines and primary chronic
123 odel consisting of highly disseminated human B-cell leukemia/lymphoma was developed by i.v. inoculati
127 ), endothelial nitric oxide synthase (eNOS), B-cell leukemia/lymphoma-2 (Bcl-2), and inducible nitric
128 ceptor-associated factor-1 (TRAF-1), TRAF-2, B-cell leukemia/lymphoma-2 (Bcl-2), Bcl-x, A1, and cellu
129 ciated with colorectal cancer formation (eg, B-cell leukemia/lymphoma-2 [Bcl2]) and 1.8% (18/906) wit
130 liminary efficacy of venetoclax, a selective B-cell leukemia/lymphoma-2 inhibitor, together with low-
135 transduced T cells efficiently lysed primary B-cell leukemia, mantle cell lymphoma, and multiple myel
138 ip in B cell diseases, especially in chronic B cell leukemia, needs to be considered further in regar
140 ificantly more common in patients with other B-cell leukemias, occurring in five (50%) of 10 patients
142 ecreased, and neurotensin was unexpressed in B cell leukemia patient's cells, as compared with health
143 ) chromosomal translocation of pediatric pre-B cell leukemia produces chimeric oncoprotein E2a-Pbx1,
146 ll activating factor, BAFF) developed CD5(+) B-cell leukemia resembling human chronic lymphocytic leu
150 w here the generation of autologous anti-pre-B-cell leukemia-specific cytolytic T-cell lines from the
151 ed iNKT cell cytotoxicity against T-cell and B-cell leukemia targets in vitro and iNKT-cell-mediated
152 x1, E2a-Pbx1, is an oncoprotein in human pre-B cell leukemia that strongly suppresses differentiation
154 he transcriptional activation of IL10 by pre-B cell leukemia transcription factor-1b and another Hox
156 eletion of CDH-implicated genes encoding pre-B cell leukemia transcription factors (Pbx) led to letha
158 otropic viral insertion site (MEIS), and pre-B-cell leukemia transcription factor 1 (PBX) may regulat
159 nhibitors showed that the homeoproteins, pre B-cell leukemia transcription factor 1 (PBX1) and PBX-re
160 CDKIs, we observed a cellular gene, the pre-B-cell leukemia transcription factor 1 (Pbx1) gene, down
161 out mice for one of the candidate genes, pre-B-cell leukemia transcription factor 1 (Pbx1), and ident
162 -binding protein 4) homeobox genes PBX1 (pre-B-cell leukemia transcription factor 1) and MEIS1 (myelo
164 without altering the genomic DNA and induces B-cell leukemia via genetic deletion of the gene encodin
165 a dramatic increase in the frequency of pro-B cell leukemia was observed in mice with combined heter
166 ng a humanized model of treatment refractory B cell leukemia, we find that infiltration of leukemia c
167 most importantly primary Bcr-Abl-transformed B-cell leukemias were completely eradicated by the alloa
168 T cells from patients with acute or chronic B cell leukemia, which were also metabolically exhausted
169 c B-cell lymphoma and, upon transplantation, B-cell leukemia with leukemic infiltrates in liver and l
170 therapy, whereas patients who have precursor B-cell leukemia without other adverse features appear to
172 -AHPC-mediated cleavage of the antiapoptotic B-cell leukemia XL (Bcl-XL) protein to a proapoptotic 18
173 NF-kappaB-dependent antiapoptotic proteins, B-cell leukemia XL (Bcl-XL), Bcl-2, X-linked inhibitor o