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1 lification of the specific Ig genes from the B-cell tumor.
2 within hours of cloning the Ig genes from a B-cell tumor.
3 f the first reports of CD40L expression in a B-cell tumor.
4 large B cell lymphoma (DLBCL) and additional B cell tumors.
5 iverse and heterogeneous group of high-grade B cell tumors.
6 constitutively active in abl/myc induced pre-B cell tumors.
7 gs the survival of mice with implanted human B-cell tumors.
8 o the poor outcome reported in all MHC II(-) B-cell tumors.
9 efficacy should be examined in patients with B-cell tumors.
10 activity in p37(Ing1b)/p53-null B cells and B-cell tumors.
11 enter B cells and in germinal center-derived B-cell tumors.
12 s is a frequent event in the pathogenesis of B-cell tumors.
14 helps explain oncogene mutations observed in B-cell tumors, and further, that many oncogenes are vuln
15 ession was validated in Ewing sarcoma cells, B-cell tumors, and human keratinocytes where NOTCH dysre
16 novel marker for this lymphoma across mature B-cell tumors, and support the distinction of NMZL as an
17 eric antigen receptors (CAR) specific to the B cell tumor antigen CD19 can successfully eradicate sys
18 stigations of VH gene mutational patterns in B-cell tumors are often performed at an arbitrary time p
21 patients may not have any increased risk for B-cell tumors at all or even to all T-cell types but onl
23 icantly increases CD20 levels in established B-cell tumor cell lines and primary malignant cells.
24 ing NKG2D ligands had increased incidence of B cell tumors, confirming that the inability to clear NK
25 This differential expression of CXCR3 in B-cell tumors contrasts with that of another B-cell-asso
27 in human lymphoma cell lines and in primary B-cell tumors demonstrated a predominant TIMP-1 expressi
28 mice also succumb reproducibly to progenitor B cell tumors, demonstrating that Artemis is a tumor sup
29 g is not constitutive in raf/myc induced pre-B cell tumors, demonstrating that subversion of this com
31 ave now addressed whether Ink4c loss impacts B-cell tumor development in the Emu-Myc transgenic mouse
32 howed that BCL-6 mutations are restricted to B cell tumors displaying GC or post-GC phenotype and car
34 several human B cell cancer lines, and human B cell tumors expressing AID at high levels have genomic
35 growth, were enriched in NMZL across mature B-cell tumors, functionally caused the loss of the phosp
36 y using a safe idiotypic (Id) antigen from a B cell tumor fused to a fragment C (FrC) sequence from t
37 lymphocytic leukemia (CLL) and other related B-cell tumors have been described in the literature and
38 has been found to be mutated in a variety of B cell tumors, here we sought to determine whether p53 a
42 redisposition to T-cell tumors compared with B-cell tumors in A-T patients may be related to a prefer
43 ncertainty concerning the ratio of T-cell to B-cell tumors in A-T, but this could be clarified by the
49 and slows the growth of these "addicted" pre-B-cell tumors in vivo, suggesting a promising therapeuti
52 sarcoma (KS) and is also linked to the rare B-cell tumor known as primary effusion lymphoma (PEL).
56 to spontaneous translocations in other mouse B-cell tumor models, CP B-cell tumor translocations were
57 known as HHV8) is the causative agent of two B cell tumors, multicentric Castleman disease (MCD) and
60 B2 mutant p80HT, which develop predominantly B cell tumors, p52 transgenic mice are not prone to lymp
61 BALB/c mice predominantly develop late stage B cell tumors (plasmacytomas) and less frequently develo
62 ffective in controlling these EBV-associated B-cell tumors.Recently the demonstration that EBV transc
64 otch activation in multiple murine and human B-cell tumors, representing both immature and mature sub
67 (2) such peptides can be used to generate a B-cell tumor-specific vaccine; and (3) a vaccine targeti
71 nal zone lymphoma (NMZL) is a rare, indolent B-cell tumor that is distinguished from splenic marginal
72 als, which may explain the high incidence of B-cell tumors that arise from oncogene translocation int
73 sociated lymphoid tissue (MALT) are indolent B-cell tumors that have a predilection for epithelial si
74 passes a closely related group of aggressive B-cell tumors that includes sporadic, endemic, and human
75 AIDS-PCNSL biopsy samples and in EBV+ human B-cell tumors that spontaneously developed in severe com
76 examined DNA methylation patterns in TCL1-tg B-cell tumors to discover tumor-associated epigenetic ch
77 tions in other mouse B-cell tumor models, CP B-cell tumor translocations were not recurrent and did n
78 n SYK credentials as a therapeutic target in B-cell tumors, we explored the role of PDE4B in these re
82 oplastic transformation, imprints V genes of B-cell tumors with the mutational history of the cell of
84 GN529 was highly active against subcutaneous B-cell tumor xenografts in severe combined immunodeficie
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