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1 asia and, in some animals, mucosa-associated B cell lymphoma.
2 ly repair these off-target lesions can cause B cell lymphoma.
3 B cell function, induces the development of B cell lymphoma.
4 ve malignancy resembling human diffuse large B cell lymphoma.
5 clinically useful end point in diffuse large B-cell lymphoma.
6 ntreated elderly patients with diffuse large B-cell lymphoma.
7 eating patients with high-risk diffuse large B-cell lymphoma.
8 enesis in the c-Myc driven, Emu-Myc model of B-cell lymphoma.
9 Th2 ACT was also curative against B-cell lymphoma.
10 ffects in vivo in mouse models of Myc-driven B-cell lymphoma.
11 urkitt lymphoma and GC-derived diffuse large B-cell lymphoma.
12 cificity and cytotoxicity against A20 murine B-cell lymphoma.
13 ose with aggressive forms like diffuse large B-cell lymphoma.
14 form into germinal center-type diffuse large B-cell lymphoma.
15 l cancers, particularly multiple myeloma and B-cell lymphoma.
16 arge B-cell lymphoma and primary mediastinal B-cell lymphoma.
17 pic HCV strains derived from an HCV-positive B-cell lymphoma.
18 a, Hodgkin lymphoma, and primary mediastinal B-cell lymphoma.
19 mia, plasma cell neoplasms, or diffuse large B-cell lymphoma.
20 ooperate with Bcl2 overexpression to promote B-cell lymphoma.
21 with lymphoproliferative diseases, including B cell lymphomas.
22 evels and causes cell death in EBNA1-induced B cell lymphomas.
23 on and are associated with cancer, including B cell lymphomas.
24 human activated B cells and by several human B cell lymphomas.
25 ns with curative potential for patients with B-cell lymphomas.
26 e BCR expression is conserved in most mature B-cell lymphomas.
27 es using PDL immune-checkpoint inhibitors in B-cell lymphomas.
28 e biology and therapy of human marginal-zone B-cell lymphomas.
29 ently affected by chromosomal alterations in B-cell lymphomas.
30 in radiosensitive malignancies, particularly B-cell lymphomas.
31 ection is associated with increased risk for B-cell lymphomas.
32 ncluding mostly germinal center (GC)-derived B-cell lymphomas.
33 ome of high-risk patients with diffuse large B-cell lymphomas.
34 ntrolling acute infection and EBV-associated B-cell lymphomas.
35 se model strongly predisposed to spontaneous B-cell lymphomas.
42 samples suggested the antiapoptotic mediator B-cell lymphoma 2 (BCL2) as a potential therapeutic targ
43 be largely rescued by ectopic expression of B-cell lymphoma 2 (Bcl2), despite a persisting block at
44 es involved in the control of cell survival (B-cell lymphoma 2 [BCL2]), cell proliferation (hepatocyt
45 d elevated levels of Mcl-1, an antiapoptotic B-cell lymphoma 2 family member, with selective reductio
46 The recently discovered role of the BCL2 (B-cell lymphoma 2 gene) promoter i-motif DNA in modulati
47 inhibitors of B-cell receptor signaling and B-cell lymphoma 2 have opened up new opportunities in th
48 further clarify the role of the proapoptotic B-cell lymphoma 2 homology domain 3 (BH3)-only protein B
50 pression of downstream genes, such as Bcl-2 (B-cell lymphoma 2), c-Myc, MMP7 (matrix metalloproteinas
53 um of pro- and anti-apoptotic members of the B-cell lymphoma-2 (Bcl-2) protein family in the mitochon
54 Inducible nitric oxide synthase (iNOS) and B-cell lymphoma-2-associated X (bax) protein expressions
55 re noncutaneous lymphomas were diffuse large B-cell lymphomas (32.4%), follicular lymphomas (15.3%),
56 urred in 6 of 14 patients with diffuse large B-cell lymphoma (43%; 95% CI, 18 to 71) and 10 of 14 pat
58 (+) T cells were capable of expressing PD-1, B cell lymphoma 6, and CXCR5 during early infection, ind
59 Inhibition of CD45 prevented expression of B-cell lymphoma 6 (Bcl-6), a transcriptional inhibitor t
60 itch of RNA processing, resulting in loss of B-cell lymphoma 6 (Bcl6) expression and increased Ig pro
61 ession of interferon regulatory factor 4 and B-cell lymphoma 6 (BCL6) in human peripheral blood monon
66 atients (18 to 80 years old) with aggressive B-cell lymphomas (80% DLBCL) treated with rituximab and
67 ractions, bromodomains, and the beta-catenin/B-cell lymphoma 9 (BCL9) interaction were used to examin
68 lecule inhibitors selective for beta-catenin/B-cell lymphoma 9 (BCL9) over beta-catenin/cadherin PPIs
70 d efficacy in patients with refractory large B-cell lymphoma after the failure of conventional therap
71 ly, BCL-W was overexpressed in diffuse large B cell lymphoma and correlated with decreased patient su
73 , 29% of activated B-cell type diffuse large B-cell lymphoma and 90% of Waldenstrom macroglobulinemia
74 icular lymphoma and aggressive diffuse large B-cell lymphoma and are associated with H3K27me3 hyperac
76 estigated the effects of HDACi in Myc-driven B-cell lymphoma and five other hematopoietic malignancie
78 aB subunit c-Rel, is frequently amplified in B-cell lymphoma and functions as a tumour-promoting tran
81 radiotherapy in patients with diffuse large B-cell lymphoma and primary mediastinal B-cell lymphoma.
82 raffin-embedded tissues derived from primary B-cell lymphomas and 1 cell line to detect and character
83 binutuzumab, or ofatumumab) for treatment of B-cell lymphomas and chronic lymphocytic leukemia (CLL).
84 effects of BCR ablation on MYC-driven mouse B-cell lymphomas and compare them with observations in h
86 reveal that BCL-W profoundly contributes to B cell lymphoma, and its expression could serve as a bio
87 lec) that is highly expressed on B-cells and B cell lymphomas, and is a validated target for antibody
89 gnature in the ABC subgroup of diffuse large B-cell lymphoma, and one of the most frequent mutations
90 , I review the history of targeting BCL-2 in B-cell lymphomas, and I discuss recent data on venetocla
95 ll receptor (BCR) signaling in diffuse large B-cell lymphoma as a model system to establish a computa
98 LF(-/-) p53(-/-) mice develop aggressive pro-B cell lymphomas bearing complex chromosomal translocati
99 n older patients with advanced diffuse large B-cell lymphoma, but further comparative studies are nee
100 n older patients with advanced diffuse large B-cell lymphoma, but further comparative studies are nee
101 cooperates with BCL6 in a mouse model of GC B-cell lymphoma, but not with the development of multipl
102 acute and chronic lymphocytic leukaemia and B-cell lymphomas, but feasibility, toxicity, and respons
105 its the proliferation of human diffuse large B cell lymphoma cells that depend upon aberrant CARD11 s
106 that the expression of wild-type Galpha13 in B-cell lymphoma cells with mutant GNA13 has limited impa
113 We carried out a proteomic analysis of a B cell lymphoma-derived cell line, BJAB, that requires U
114 ed by mutations in JAK2, CALR, or MPL In the B-cell lymphomas, detection of characteristic rearrangem
115 , Bcl-w loss profoundly delayed MYC-mediated B cell lymphoma development due to increased MYC-induced
117 B-cell activation seemed to play a role in B-cell lymphoma development at early stages across diffe
118 nated two prediagnostic blood samples before B-cell lymphoma diagnosis, along with 170 matched cancer
119 hat are frequently observed in diffuse large B cell lymphoma (DLBCL) and that disrupt ID-mediated aut
120 d EZH2 cooperate to accelerate diffuse large B cell lymphoma (DLBCL) development and combinatorial ta
121 plastic cells in patients with diffuse large B cell lymphoma (DLBCL) directly correlated with activat
123 onally developed therapies for diffuse large B cell lymphoma (DLBCL) requires rapid assimilation of n
124 d B cell-like (ABC) subtype of diffuse large B cell lymphoma (DLBCL), engages the CARD11-MALT1-BCL10
128 ve genetic characterization of diffuse large B cell lymphomas (DLBCL), including large-scale exome ca
129 lymphoma (FL) (23% [n = 20]), diffuse large B-cell lymphoma (DLBCL) (10% [n = 9]), mantle cell lymph
131 ients with relapsed/refractory diffuse large B-cell lymphoma (DLBCL) achieve prolonged disease-free s
132 TORC pathway is upregulated in diffuse large B-cell lymphoma (DLBCL) and can be targeted with the mTO
133 hogenesis and heterogeneity of diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL) has
134 zed incidence ratios (SIRs) of diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL) wer
135 mphomas (DELs) are subtypes of diffuse large B-cell lymphoma (DLBCL) associated with poor outcomes af
136 ockdown showed that almost all diffuse large B-cell lymphoma (DLBCL) cell lines are addicted to the e
141 eral outlook for patients with diffuse large B-cell lymphoma (DLBCL) in first remission is important
143 ard treatment of patients with diffuse large B-cell lymphoma (DLBCL) is rituximab in combination with
150 , transformation to aggressive diffuse large B-cell lymphoma (DLBCL) reduces median survival to only
152 nd germinal center B-cell-like diffuse large B-cell lymphoma (DLBCL) represent the 2 major molecular
153 ressive activated B cell (ABC) diffuse large B-cell lymphoma (DLBCL) subtype from the better prognosi
155 Patients with newly diagnosed diffuse large B-cell lymphoma (DLBCL) underwent both FLT and FDG PET/C
156 or patients with limited-stage diffuse large B-cell lymphoma (DLBCL) was shown in the Southwest Oncol
157 sion in human Burkitt (BL) and diffuse large B-cell lymphoma (DLBCL) xenografts blocked tumor growth,
158 euroblastoma, medulloblastoma, diffuse large B-cell lymphoma (DLBCL), and EOC microarray gene express
159 itt lymphoma, Hodgkin disease, diffuse large B-cell lymphoma (DLBCL), and posttransplant lymphoprolif
160 nd BCL2 genetic alterations in diffuse large B-cell lymphoma (DLBCL), apart from translocations, has
183 licular lymphoma (FL; n = 29), diffuse large B-cell lymphoma (DLBCL; n = 34), DLBCL arising from chro
184 the subgroup of patients with diffuse large B-cell lymphoma (DLBCL; n=9), and three occurred in thos
186 nd will reclassify a subset of diffuse large B-cell lymphomas (DLBCLs) and HGBLs with features interm
188 double- and triple-hit (DH/TH) diffuse large B-cell lymphomas (DLBCLs) feature activation of Hsp90 st
189 eceptor (BCR) signal-dependent diffuse large B-cell lymphomas (DLBCLs) inhibits cellular proliferatio
190 lase L1 (UCH-L1) is induced in diffuse large B-cell lymphomas (DLBCLs), and that levels of this molec
191 orted that early-stage gastric diffuse large B-cell lymphomas (DLBCLs), including DLBCLs with mucosa-
196 ht with relapsed or refractory diffuse large B-cell lymphoma (due to progressive disease in four pati
198 an cooperate with human CD4 T cells to cause B cell lymphomas even when a major viral transforming pr
201 son-mediated gain-of-function alterations in B-cell lymphoma-extra large (Bcl-xL), Mdm4, and two TP53
202 olated transmembrane domains of Bax, Bcl-xL (B-cell lymphoma-extra large), and Bcl-2 can mediate inte
203 xygenase-1, inducible nitric oxide synthase, B-cell lymphoma-extra large, and protein expression of t
204 additional patients (two with diffuse large B-cell lymphoma, four with indolent lymphomas) had evide
205 alyses comparing senescent and non-senescent B-cell lymphomas from Emu-Myc transgenic mice revealed s
209 cogenes, cellular-myelocytomatosis (MYC) and B-cell lymphoma gene-2 (BCL2), in diffuse large B-cell l
210 pression pattern of CD22 on B cells and most B cell lymphomas has made CD22 a therapeutic target for
211 inhibitors in the treatment of diffuse large B-cell lymphoma has not been defined; we suggest that JA
212 hich occur in <10% of cases of diffuse large B-cell lymphoma, have been referred to as double-hit lym
214 s, including Burkitt lymphoma, diffuse large B-cell lymphoma, Hodgkin lymphoma, and primary mediastin
215 hronic hepatitis C virus (HCV) infection and B-cell lymphoma, however, the mechanisms by which HCV ca
216 inib has demonstrated high response rates in B-cell lymphomas; however, a growing number of ibrutinib
217 be a crucial part of the pathophysiology of B-cell lymphomas; however, several early attempts to tar
218 urvival time for patients with diffuse large B-cell lymphoma, illustrate the behavior of our methodol
219 cking CD37 developed germinal center-derived B cell lymphoma in lymph nodes and spleens with a higher
220 owed that an LMP1-deleted EBV mutant induces B cell lymphomas in a newly developed cord blood-humaniz
222 n controlling the progression of early-stage B cell lymphomas in humans, we found higher expression o
224 y essential for the ability of EBV to induce B cell lymphomas in the cord blood-humanized mouse model
227 aling pathways is a hallmark of a variety of B-cell lymphomas, including classical Hodgkin lymphoma (
228 mutated gene in germinal center (GC)-derived B-cell lymphomas, including nearly a quarter of Burkitt
231 that KLHL6, which is recurrently mutated in B cell lymphomas, is an off-target of the normal somatic
232 generated and characterized a panel of large B-cell lymphoma (LBCL) patient-derived xenograft (PDX) m
233 d Epstein-Barr virus-positive (EBV(+)) large B-cell lymphomas (LBCLs) in young patients without immun
234 icular lymphomas (PTLs) are extranodal large B-cell lymphomas (LBCLs) with inferior responses to curr
236 ins, with the founding member of the family (B-cell lymphoma/leukemia-2) discovered via its involveme
237 or end-stage renal disease, type 2 diabetes, B-cell lymphoma, lichen planus, Sjogren's syndrome, porp
238 use a targeted short-hairpin RNA screen in a B-cell lymphoma line to identify the BRCT-domain protein
241 nd in their human counterparts: IGK-CCND3 in B-cell lymphoma, MPB-BRAF in glioma, and COL3A1-PDGFB in
242 ents with follicular lymphoma, diffuse large B-cell lymphoma, mycosis fungoides, and peripheral T-cel
243 amples, including FL (n = 20), diffuse large B-cell lymphoma (n = 10), classical Hodgkin lymphoma (n
244 cross NHL subtypes and 55% for diffuse large B-cell lymphoma (n = 11); median response duration was 4
245 (follicular lymphoma, n = 10; diffuse large B-cell lymphoma, n = 11; other B-cell lymphomas, n = 10;
246 diffuse large B-cell lymphoma, n = 11; other B-cell lymphomas, n = 10; mycosis fungoides, n = 13; per
247 lymphoma, Burkitt's lymphoma, diffuse large B-cell lymphomas, nasopharyngeal carcinoma (NPC), and ly
250 CTL019) to treat patients with diffuse large B-cell lymphoma or follicular lymphoma that had relapsed
252 e large B-cell lymphoma, primary mediastinal B-cell lymphoma, or transformed follicular lymphoma who
253 an indolent subtype to an aggressive form of B cell lymphoma over time (Richter s syndrome) and show
255 DS nor risk stratification of diffuse large B-cell lymphoma patients is affected by the choice of PE
258 significantly associated with diffuse large B cell lymphoma (pooled HR per SD: 1.47; 95% CI: 1.06, 2
259 2-3 or stage 3-4 CD20-positive diffuse large B-cell lymphoma, previously untreated, and not eligible
260 stleman's disease, as well as a rare form of B cell lymphoma (primary effusion lymphoma) primarily ob
261 we enrolled 111 patients with diffuse large B-cell lymphoma, primary mediastinal B-cell lymphoma, or
262 patients with newly diagnosed diffuse large B-cell lymphoma remains suboptimal in the rituximab era.
263 essment of IT-901 for the treatment of human B-cell lymphoma revealed antitumor properties in vitro a
264 ous NHL histologies, including diffuse large B-cell lymphoma, Richter's transformation, mantle cell l
265 homas, the association between diffuse large B-cell lymphoma risk and slope was restricted to CXCL13.
267 elapsed/refractory primary mediastinal large B-cell lymphoma (rrPMBCL) are limited, and prognosis is
269 tivated B cell-like subtype of diffuse large B cell lymphoma somehow perturb ID-mediated autoinhibiti
270 ARD11 variants associated with diffuse large B cell lymphoma spontaneously induce Lin(Ub)n-Bcl10 prod
272 study, patients with relapsed or refractory B-cell lymphoma, T-cell lymphoma, and multiple myeloma r
273 ory of lymphoma, separate from diffuse large B-cell lymphoma, termed high-grade B-cell lymphoma with
274 e outcome of ACT against a mouse non-Hodgkin B cell lymphoma that expresses OVA as a model neoantigen
276 mpaired in approximately 6% of diffuse large B-cell lymphomas that carry inactivating genetic alterat
277 Given that p73 is lost or silenced in human B-cell lymphomas, the Mdm2(Tg);p73(+/-) mouse serves as
278 ranslocations associated with GC and post-GC B-cell lymphomas, the role of downstream AID-associated
279 et al used an immunocompetent mouse model of B-cell lymphoma to discover an interesting new way in wh
281 Current diagnostic tests for diffuse large B-cell lymphoma use the updated WHO criteria based on bi
282 and eight of 20 patients with diffuse large B-cell lymphoma vs one of 15 patients with follicular ly
285 ective study in patients with advanced-stage B-cell lymphoma, we investigated the prognostic and pred
286 eviously untreated DLBCL or other aggressive B-cell lymphoma were 60 to 80 years old, had CR or PR af
287 Overall, 126 patients with diffuse large B-cell lymphoma were included (56 female and 70 male; me
288 Patients with any stage of diffuse large B-cell lymphoma were treated with six cycles of R-CHOP-1
289 tory NHL, who included 14 with diffuse large B-cell lymphoma, were enrolled; 42 received treatment in
290 homa (NMZL) is a rare form of indolent small B-cell lymphoma which has only been clearly identified i
291 immunotherapy in patients with diffuse large B-cell lymphoma who are not candidates for transplantati
292 6 months, 86% of patients with diffuse large B-cell lymphoma who had a response (95% CI, 33 to 98) an
293 center study, patients with refractory large B-cell lymphoma who received CAR T-cell therapy with axi
294 ents with Hodgkin lymphoma and diffuse large B-cell lymphoma will relapse, requiring additional thera
296 f adult Burkitt lymphoma (BL) and high-grade B-cell lymphoma with BL gene signature (adult-molecularl
297 diatric-type follicular lymphoma (PTFL) is a B-cell lymphoma with distinctive clinicopathological fea
298 use large B-cell lymphoma, termed high-grade B-cell lymphoma with translocations involving myc and bc
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