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1 ng smouldering multiple myeloma and solitary plasmacytoma.
2 ) and CD45-reconstituted (CD45+) J558L mu m3 plasmacytoma.
3 glycoprotein), was recently isolated from a plasmacytoma.
4 ies to subsets of human multiple myeloma and plasmacytoma.
5 in human endemic Burkitt lymphoma and mouse plasmacytoma.
6 igh-grade angiogenesis was present in 64% of plasmacytomas.
7 sing an Emicro-v-abl oncogene solely develop plasmacytomas.
8 d and significantly suppressed the growth of plasmacytomas.
9 d the function of this enhancer in mammalian plasmacytomas.
10 ecursor clones into Igh alpha/c-myc-positive plasmacytomas.
11 o reflect the general genomic instability of plasmacytomas.
12 l translocations in t(12;15)-positive BALB/c plasmacytomas.
13 ry cytogenetic aberrations in primary BALB/c plasmacytomas.
14 ulated into BALB/c mice to produce growth of plasmacytomas.
15 nal A-type particle long terminal repeats in plasmacytomas.
16 , 4 cases of hairy cell leukemia (HCL) and 3 plasmacytomas.
17 ging System stage III, high tumor burden, or plasmacytomas.
18 pathway to confer IL6 independence on murine plasmacytomas.
19 s, and macrophages not seen with plasmacytic plasmacytomas.
20 features of transgenic and pristane-induced plasmacytomas.
21 cation that deregulates Myc in certain mouse plasmacytomas.
22 vation of Myc in the great majority of mouse plasmacytomas.
23 ve mutant or a structural homolog, protected plasmacytomas against IL6 withdrawal-induced apoptosis a
24 s affecting c-myc occur in almost all murine plasmacytoma and human Burkitt's lymphoma tumors and are
25 ned if angiogenesis is increased in solitary plasmacytoma and if it can help identify patients likely
30 adioimmunotherapy (RIT) in the management of plasmacytomas and multiple myeloma has undergone only li
31 dominantly develop late stage B cell tumors (plasmacytomas) and less frequently develop earlier B-lin
32 tterns held up in murine xenograft models of plasmacytoma, and disseminated bone marrow predominant d
35 tin superfamily of adhesion molecules, Pang (plasmacytoma-associated neuronal glycoprotein), was rece
39 r studies reveal: (a) antibodies secreted by plasmacytomas bind to different antigens in a manner sim
41 lasms (PCNs, comprising multiple myeloma and plasmacytoma), but little is known about risk factors in
42 raise suspicion about associated lymphoma or plasmacytoma, but negative PET results do not exclude th
43 was observed in one of the IL-6-independent plasmacytomas, but not in others, making an autocrine me
44 kground of C increased the incidence of GALT plasmacytomas by a factor of 2.5 in first-generation bac
45 st cell-derived Ang-1 promotes the growth of plasmacytomas by stimulating neovascularization and prov
46 eristic of Burkitt lymphomas (BL) and murine plasmacytomas, c-myc genes become juxtaposed to immunogl
49 activated endogenous mb-1 transcription in a plasmacytoma cell line, but could not when the promoter
50 ning the B29 octamer motif is expressed in a plasmacytoma cell line, while the wild-type mb-1 promote
53 unterpart in inducing growth arrest of mouse plasmacytoma cell lines and preventing ras-induced trans
54 cells accelerate tumor growth by established plasmacytoma cell lines and that neutralization of Ang-1
55 but not Ang-2 and that 2 established murine plasmacytoma cell lines express high levels of VEGF-A bu
56 f cell death in IL-6-starved T1165 and T1198 plasmacytoma cell lines is apoptosis, and that it can be
57 spond to this approach, we examined 3 murine plasmacytoma cell lines, 2 (MPC-11 and S107) expressing
62 tion that p28/CLF, unlike IL-27, sustains B9 plasmacytoma cell proliferation prompted us to investiga
63 e is evolutionarily conserved and exhibits a plasmacytoma cell-specific DNase I-hypersensitive site i
65 EBF1 and RUNX1 in terminally differentiated plasmacytoma cells activated multiple early B cell-speci
66 ve NF-kappaB activation, similarly protected plasmacytoma cells against IL6 withdrawal-induced apopto
67 gize with E47 inhibited enhancer activity in plasmacytoma cells and could not activate transcription
68 t XBP-1(S) binds to the promoter of ERdj3 in plasmacytoma cells and in LPS-stimulated primary splenic
69 romoter activity was up-regulated by BSAP in plasmacytoma cells and T cells in a dose-dependent manne
70 survival factors for malignant lymphoma and plasmacytoma cells derived from transgenic Emu-Myc mice
74 s Ang-1, and recombinant Ang-1 together with plasmacytoma cells promotes extracellular matrix neovasc
75 d, major histocompatibility complex-negative plasmacytoma cells to maturing mouse dendritic cells (DC
76 tor expression in both fibroblasts and mouse plasmacytoma cells, and Mzf1 knockdown increased Mtor ex
77 ression of a number of genes in AID-silenced plasmacytoma cells, and upregulation of CD200 was shown
78 dogenous early B-cell-specific mb-1 genes in plasmacytoma cells, but only when the promoter is hypome
79 Lysine 170 was acetylated in pre-B cells and plasmacytoma cells, but TSA treatment did not stimulate
80 istent inactivation of TGF-beta receptors in plasmacytoma cells, demonstrating for the first time tha
82 h received chambers containing untransfected plasmacytoma cells, secreted primarily IL-2 and IL-4, wi
83 matrix components shows that mast cells and plasmacytoma cells, together, promote marked neovascular
91 nd 3' RR elements in MPC11, which like other plasmacytomas contains a reciprocal translocation betwee
92 ted that the iMyc(Emu) transgene accelerates plasmacytoma development by collaborating with tumor sus
94 ns (oil granulomata) during pristane-induced plasmacytoma development in susceptible BALB/cAn mice.
96 at small interfering RNA silencing of AID in plasmacytoma dramatically increased its susceptibility t
98 control and survival rates of extramedullary plasmacytoma (EMP) with respect to various treatment app
99 lasmacytoma (SBP; n = 35) and extramedullary plasmacytoma (EMP; n = 29) through multiparameter flow c
100 ll neoplasms resembling human extramedullary plasmacytoma (EP) as well as follicular and diffuse larg
101 y reduces kiss1 and serotonin-related genes (plasmacytoma expressed transcript 1 and solute carrier f
102 at the light chain level with at least three plasmacytomas expressing both kappa and lambda light cha
104 gene expression profiles of newly identified plasmacytomas from NFS.V(+) congenic mice with plasmacyt
105 emic Burkitt lymphoma-like translocations in plasmacytomas from uracil N-glycosylase and activation-i
107 f monoclonal immunoglobulin (Ig) produced by plasmacytomas have found no universally common binding p
110 ified, is a tumor rejection antigen for J558 plasmacytoma in mice with an unperturbed T-cell repertoi
115 ping (SKY) to evaluate 10 established BALB/c plasmacytomas in which the T(12;15) had been previously
116 ded by the Pctm locus, in which mouse B-cell plasmacytomas induced by pristane are associated with he
119 he genetic susceptibility of BALB/c mice for plasmacytoma induction and that p16(INK4a) is a strong c
122 lambdaLIZ N5 mice in the terminal stage of a plasmacytoma induction experiment, 213-280 days after th
126 ptibility of BALB/c mice to pristane-induced plasmacytomas is a complex genetic trait involving multi
127 step in the malignant progression of murine plasmacytomas is the transition from dependence on IL-6
128 tumor immunity, we generated IL-35-producing plasmacytoma J558 and B16 melanoma cells and observed th
129 ited into B7-1-transfected class II-negative plasmacytoma J558, and the virus-infected central nervou
132 ne mustard) to mice bearing a large MOPC-315 plasmacytoma led to a rapid up-regulation of B7-1 (CD80)
134 nds to the OBF-1/BOB-1/OCA-B promoter in the plasmacytoma line and in primary B cells not only during
136 RNA was used to decrease XBP-1 expression in plasmacytoma lines, ERdj3 transcripts were concomitantly
137 nic acid, a very-long-chain FFA, in a murine plasmacytoma model displayed a reduction in tumor burden
138 odels: human MM injected subcutaneously (the plasmacytoma model) and luciferase-expressing human MM i
139 r, despite some evidence obtained from mouse plasmacytoma models, it is still unclear whether Id-spec
140 es significant antitumor activity in a human plasmacytoma mouse model, associated with down-regulatio
144 lymphoma (n = 7), Burkitts lymphoma (n = 6), plasmacytoma (n = 5), and mucosa-associated lymphoid tis
146 location in all of these tumors and in three plasmacytomas newly identified secondary cytogenetic cha
148 rrow disease (OMD) in patients with solitary plasmacytoma of bone and assess its value in predicting
149 1, 9732, and 9734 were assigned for solitary plasmacytoma of bone, plasma cell myeloma, and extraosse
152 lated to immunoblastic lymphomas, less so to plasmacytomas of Fasl mutant and SJL mice, and least to
154 asmacytomas from NFS.V(+) congenic mice with plasmacytomas of IL6 transgenic, Fasl mutant, and SJL-be
157 tumors arose in peripheral lymphoid organs (plasmacytomas) or within the bone marrow and often led t
158 re-, and mature B-cell lines, but not in two plasmacytomas; Pax-5b was shown to be present at low lev
159 er (10 to 20 microg/mL) profoundly inhibited plasmacytoma (PCT) development initiated by three 0.2- o
160 lammation- and interleukin 6-dependent mouse plasmacytoma (PCT), is the premier model of cancer-assoc
162 -activating translocations characteristic of plasmacytomas (PCT), little is known about genetic facto
163 itical oncogenic event in the development of plasmacytomas (PCTs) although it is not sufficient for t
170 to confirm a suspected diagnosis of solitary plasmacytoma, provided that whole-body MRI is unable to
171 obulinemia, chronic lymphocytic leukemia, or plasmacytoma (relative risk of progression, 25.0, 2.4, 8
175 mphoid tissues, raising the possibility that plasmacytoma resistance genes may inhibit tumor developm
177 cations in normal and immunized mice of both plasmacytoma resistant and susceptible lineages in the a
181 Patients with high-grade angiogenesis in the plasmacytoma sample were more likely to progress to myel
183 BM evaluation of patients with solitary bone plasmacytoma (SBP; n = 35) and extramedullary plasmacyto
187 most cases of mantle cell lymphoma, HCL, and plasmacytoma show high levels of pRB in contrast to foll
189 by the most prevalent tumors, plasmablastic plasmacytomas, showed them to be most closely related to
191 r 1B and Chr 4C7-D2, are suspected to harbor plasmacytoma susceptibility loci; Pctr1 and Pctr2 on Chr
192 ound to be increased approximately 3-fold in plasmacytoma-susceptible BALB/c and C.D2-Idh1-Pep3 mice,
193 s were detected in as many as 73% (32/44) of plasmacytoma-susceptible BALB/cAn mice 30 days after an
195 range, 3.1-6.7) and 1 patient with a pleural plasmacytoma (SUVmax, 7.2); the remaining 3 patients had
198 558L HI, an interleukin 5-transfected murine plasmacytoma that is infiltrated by numerous degranulati
199 15) found in a subset (approximately 20%) of plasmacytomas that develop "spontaneously" in the gut-as
201 However, the kappaB binding complex in the plasmacytomas that were examined lacked c-Rel and instea
202 We have thus examined the ability of murine plasmacytoma to produce disseminated growth similar to t
203 Diffusion chambers injected with X63.Ag-653 plasmacytoma transfectants that constitutively produce r
204 sceptible to inflammation-induced peritoneal plasmacytomas (tumor incidence, 100%; mean tumor onset,
205 ells (IC(50) < 100 nM), inhibits xenografted plasmacytoma tumors in mice, and is synergistically cyto
208 ntibodies secreted by silicone-induced mouse plasmacytomas using a broader panel of antigens includin
210 TASc-expressed long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) was triggere
211 ion of miR-1204 through p53 interaction with plasmacytoma variant translocation 1, and miR-1204 induc
212 reported association between variants in the plasmacytoma variant translocation gene (PVT1) and ESRD
214 of the oncogenic long noncoding RNA (lncRNA) Plasmacytoma Variant Translocation-1 (PVT-1), which is a
217 at typically occur in pristane-induced mouse plasmacytomas were detected in secondary lymphoid tissue
218 ch as Burkitt's lymphoma and t(12;15) BALB/c plasmacytomas, where most breakpoints are found near the
219 osphorylated in a subset of IL-6-independent plasmacytomas, whereas other IL-6-independent lines show
221 n binding properties, but instead, groups of plasmacytomas with specific antigen-binding activities t
222 tro in the absence of IL6 and form abdominal plasmacytomas with visceral involvement when injected in
223 diffuse large B-cell lymphomas, and CD138(+) plasmacytomas, with an overall incidence of 68% by 21 mo
224 silencing of B lymphocyte-specific genes in plasmacytoma x T lymphoma hybrids can be prevented by pr
225 his transcription factor on the phenotype of plasmacytoma x T lymphoma hybrids established a critical