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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.
13  noncoding region of the bcl-6 gene, in both B-cell tumors and in normal germinal center B cells.
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
19                Follicular lymphoma (FL) is a B-cell tumor arising in germinal centers and retaining f
20          Oncogenes are often dysregulated in B cell tumors as a result of a reciprocal translocation
21 patients may not have any increased risk for B-cell tumors at all or even to all T-cell types but onl
22 lonal translocations, nearly all analyzed CP B-cell tumors carried clonal translocations.
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
26                                        Among B-cell tumors, deletion of 7q and NOTCH2 mutations are a
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
30             We also profiled the microRNA of B-cell tumors derived from diffuse large B-cell lymphoma
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
33                                  A subset of B-cell tumors exhibits recurrent translocations of Bcl-3
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
39 lling the malignant growth of this incurable B cell tumor in patients.
40  and rapid targeting to lymphoid tissues and B cell tumors in mice.
41  J(H) probe was consistent with a monoclonal B-cell tumor in 13 cases.
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
44    BLV infection is strongly associated with B-cell tumors in cattle.
45          In this study, we characterized the B-cell tumors in MSH6-deficient mice and describe their
46 ll lines in vitro as well as in EBV-positive B-cell tumors in SCID mice.
47 n site 3 (Evi3), has been implicated in most B-cell tumors in the AKXD-27 strain.
48 uency of T-cell tumors compared with that of B-cell tumors in these patients.
49 and slows the growth of these "addicted" pre-B-cell tumors in vivo, suggesting a promising therapeuti
50 whereas single-transgenic Myc mice developed B cell tumors infrequently (4 of 43, 9.3%).
51      Chronic lymphocytic leukemia (CLL) is a B-cell tumor involving small lymphocytes that generally
52  sarcoma (KS) and is also linked to the rare B-cell tumor known as primary effusion lymphoma (PEL).
53 nally active in the latently infected murine B-cell tumor line S11.
54 ssion also has been seen in many established B cell tumor lines.
55 se data indicate that TC-PTP is required for B-cell tumor maintenance.
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
58 or immune modulation as well as treatment of B cell tumors of GC origin.
59                 Multiple myeloma is a clonal B-cell tumor of slowly proliferating plasma cells within
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
63                          Fourteen of sixteen B cell tumors removed from spleens of five such hu-SPL-S
64 otch activation in multiple murine and human B-cell tumors, representing both immature and mature sub
65  is a partner in recurrent translocations in B cell tumors, resulting in deregulated expression.
66                        Human germinal center B cell tumors retain the ability of their nontransformed
67  (2) such peptides can be used to generate a B-cell tumor-specific vaccine; and (3) a vaccine targeti
68 -catalyzed DNA-dependent p53 acetylation and B-cell tumor suppression.
69 sion of human carcinomas, e.g. diffuse large B cell tumors, T cell lymphomas, etc.
70 beverage type and were slightly stronger for B-cell tumors than for T-cell tumors.
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
79 s lymphoma, and, by extension, for the other B cell tumors with which EBV is associated.
80                    An unusual group of human B-cell tumors with cellular features of chronic lymphocy
81 here exists a wide spectrum of IgM-secreting B-cell tumors with different clinical behavior.
82 oplastic transformation, imprints V genes of B-cell tumors with the mutational history of the cell of
83         Knock-in mice developed IgM-positive B-cell tumors, with most being typical of eBL by histolo
84 GN529 was highly active against subcutaneous B-cell tumor xenografts in severe combined immunodeficie

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