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1 istration rescue anergic Env(+) (non-edited) precursor B cells.
2 the expression of naked IgL on a surface of precursor B cells.
3 e, replenishment must involve replication of precursor B cells.
4 ication artifacts and are unique to leukemic precursor B cells.
5 D86, but not CD80, on follicular, MZ, and MZ precursor B cells.
6 e bnAb induction by activating bnAb germline precursor B cells.
7 ice despite a significant loss of H3K9me2 in precursor B cells.
8 d recombination of Iglambda gene segments in precursor B cells.
9 n from B220+CD43+ progenitor B to B220+CD43- precursor B cells.
10 y and correlate with poor prognosis in human precursor B cell acute lymphoblastic leukemia (B-ALL).
11 Ikaros (IKZF1) is a hallmark of BCR-ABL1(+) precursor B cell acute lymphoblastic leukemia (pre-B ALL
14 IKAROS function indicates poor prognosis in precursor B-cell acute lymphoblastic leukemia (B-ALL).
15 To test the suitability of targeting CD22 on precursor B-cell acute lymphoblastic leukemia (BCP-ALL),
17 d on xenografts from pediatric patients with precursor B-cell acute lymphoblastic leukemia (pre-B ALL
20 the clonal evolution of a form of childhood precursor-B cell acute lymphoblastic leukemia that is ch
21 ecently been established from a patient with precursor-B-cell acute lymphoblastic leukemia (ALL), whi
22 and TCF3-PBX1 (E2A-PBX1)-frequently found in precursor-B-cell acute lymphoblastic leukemia (preB-ALL)
25 rmed genomic profiling of 1725 patients with precursor B-cell ALL and detailed genomic analysis of 15
27 r patients with PGR in the large subgroup of precursor B-cell ALL, dexamethasone especially reduced t
28 ined that LOH of 6q was demonstrated both in precursor-B cell ALLs (15 of 93; 16%) and in T cell ALLs
30 caused no change in the cell cycle status of precursor B cells and only modest changes in cycling pro
31 up-regulation of CD86(high) expression on MZ precursor B cells and trafficking of MZ precursor B cell
33 lete loss of marginal zone and marginal zone precursor B cells, and 'preferential' population expansi
34 on of plasmacytoid dendritic cells (DCs), MZ precursor B cells, and CD4 T cells in the spleens of BXD
35 ular mimicry in Graves' disease, where early precursor B cells are expanded by Y. enterocolitica pori
36 ified impaired Ig locus contraction in adult precursor B cells as a likely mechanism by which ID2-med
37 ferentiation into germinal center and memory precursor B cells as well as preplasmablasts that rapidl
39 ings expand the range of NF-kappaB action in precursor B cells beyond Igkappa to include the control
40 ntified on splenic marginal zone (MZ) and MZ precursor B cells, but not on the bulk of newly formed B
41 arily to B lymphocytes and can be induced in precursor B cells by stimulation with bacterial lipopoly
42 n IFN receptor-intact BXD2 mouse spleens, MZ precursor B cells clustered at the T cell-B cell border.
44 49F) and IL-7Ralpha(-/-) mice had comparable precursor B cell defects, indicating that signaling from
46 ed in a blockage of the progenitor B-cell-to-precursor B-cell development in bone marrow (BM) and B-c
49 dependent on sufficient levels of IL-7 than precursor B cell differentiation because the number of B
50 The transcription factor E2A can promote precursor B cell expansion, promote G(1) cell cycle prog
51 se renin-expressing progenitors enriches the precursor B-cell gene programme and constrains lymphocyt
53 rturbs B-cell development, as evidenced by B-precursor/B-cell hyperplasia, and corrupts the regulatio
54 69 and CD86 observed in RBP(+) marginal zone precursor B cells in the spleens of BXD2 mice compared w
56 LBL (T-LBL) and six (8%) of 73 patients with precursor B-cell LBL (pB-LBL) suffered from relapse.
57 uption of the NF-kappaB signaling pathway in precursor B cells led to the loss of inducible Oct-2 DNA
58 Children younger than 6 years of age with precursor B-cell leukemia and no adverse genetic feature
59 with chemotherapy, whereas patients who have precursor B-cell leukemia without other adverse features
62 nt patient with Epstein-Barr virus-negative, precursor B cell lymphoblastic lymphoma diagnosed 6 mont
67 er(fl/fl)/Emicro-myc mice were of very early precursor B-cell origin, a stage of B-cell development p
69 serve to distinguish between the presumed MZ precursor B cell population in the spleen and other IgD-
70 ontrol the progenitor B cell (pro-B cell) to precursor B cell (pre-B cell) transition have not been w
71 ates with GC sensitivity in a panel of human precursor B-cell (pre-B) acute lymphoblastic leukemia (A
75 e critical for maintaining quiescence before precursor B cell receptor (pre-BCR) expression and for r
76 truncated/V(H)-less mouse H chain Dmu forms precursor B cell receptors with the surrogate L chain co
77 expression of Blimp-1 in Abelson-transformed precursor B cells repressed endogenous c-Myc and caused
78 ms behind are still unknown, we studied five precursor B cell subsets (ProB, PreBI, PreBII large, Pre
80 bs are important vaccine leads because their precursor B cells targeted by an engineered priming immu
81 approximately 10 times fewer virus-specific precursor B cells than normal spleen cells, had no signi
82 n MZ precursor B cells and trafficking of MZ precursor B cells to the T cell-B cell border to provide
83 gH) locus and a block in the progenitor-B-to-precursor-B-cell transition, which was partially rescued
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