ライフサイエンスコーパス: DLBCL

1 DLBCL patients with concurrent other indolent lymphoma h

2 DLBCL, MCL, and disseminated EMZL and FL were primarily

3 Among 105 DLBCL cases analyzed, PD-L1 alterations were identified

4 We evaluated 2124 DLBCL patients treated from 1998 to 2009 with frontline

5 hods: Baseline (18)F-FDG PET/CT scans of 301 DLBCL patients from the REMARC trial (NCT01122472) were

6 Methods: Of 609 DLBCL patients participating in the PET-Guided Therapy o

7 Circulating miRNAs from the serum of 86 DLBCL patients were significantly increased compared wit

8 gers potent cytotoxicity specifically in ABC DLBCL cells.

9 th BCL-2 and MCL-1 inhibitors in killing ABC DLBCL cells.

10 naling as a crucial functional driver of ABC DLBCL and highlight calcineurin inhibition as a novel st

11 rticularly important for the survival of ABC DLBCL.

12 eased NF-kappaB activation contribute to ABC DLBCL survival.

13 e were age >18 years; activated B-cell (ABC) DLBCL profile, HGBCL, NOS, high genetic complexity, 1q21

14 d the aggressive activated B-cell-like (ABC) DLBCL.

15 ABC-DLBCL exhibits plasmablastic features and is characteriz

16 rvival, and that GRK2 knockdown enhances ABC-DLBCL tumor growth in vitro and in vivo.

17 ckade in combinatorial immunotherapy for ABC-DLBCL.

18 e miRNAs were confirmed using RT-qPCR in ABC-DLBCL and GCB-DLBCL cells, respectively.

19 naling pathways that are dysregulated in ABC-DLBCL are, however, not fully understood.

20 tivity is constitutively dysregulated in ABC-DLBCL but not in GCB-DLBCL and BL.

21 2 also controls the expression of MYC in ABC-DLBCL by regulating MYC protein levels.

22 rentiation resulting from Blimp1 loss in ABC-DLBCL lymphomagenesis.

23 vival of ABC-DLBCL in vitro and inhibits ABC-DLBCL growth in xenograft models.

24 cell-type diffuse large B cell lymphoma (ABC-DLBCL) are associated with reduced survival, and that GR

25 cell-like diffuse large B-cell lymphoma (ABC-DLBCL) is an aggressive subtype of lymphoma usually asso

26 d to tumor regression in a CARD11 mutant ABC-DLBCL lymphoma xenograft model.

27 ctive microRNAs (miRNAs) in EBV-negative ABC-DLBCL and GCB-DLBCL cell lines and their EBV-infected co

28 reases the proliferation and survival of ABC-DLBCL in vitro and inhibits ABC-DLBCL growth in xenograf

29 tes to the aberrant molecular program of ABC-DLBCL via its dual ability to modulate both IRF4- and MY

30 therapeutic target for the treatment of ABC-DLBCL.

31 RNAs) between EBV-negative and -positive ABC-DLBCL cells and 12 miRNAs with differential abundances (

32 pes identified MCD/C5 tumors as specific ABC-DLBCLs with unfavorable clinical outcome, activating mut

33 as 10-100 times more potent than Dox against DLBCL cell lines.

34 RNA sequencing of PD-L1-altered DLBCLs revealed upregulation of genes involved in negati

35 The associations of sCD23 with CLL and DLBCL and CXCL13 with DLBCL persisted among cases sample

36 C) B cells, the normal counterpart of FL and DLBCL, and in lymphomagenesis by using conditional GC-di

37 ted with all subtypes and CXCL13 with FL and DLBCL.

38 pment of EP300-specific inhibitors in FL and DLBCL.

39 indings extended evidence for TFA intake and DLBCL risk but not for other NHL subtypes.

40 tion between physical activity (inverse) and DLBCL.

41 with patient-derived xenografts (PDXs), and DLBCL patient serum samples leveraging systems biology a

42 ffect between body mass index (positive) and DLBCL risk, while CXCL13 contributed to the association

43 ar DSS: 93.4%) having the best prognosis and DLBCL (5-year DSS: 52.6%) having the poorest.

44 44 primary immune-privileged site-associated DLBCL (IP-DLBCL) samples originating in the testis or ce

45 ATM deficient background compared to WT-ATM DLBCL cells.

46 ATM(-/-) DLBCL cells have decreased apoptosis in contrast to radi

47 Both DLBCL and its treatments perturb the immune system, yet

48 iguingly, although NFAT is activated in both DLBCL subtypes, long-term calcineurin inhibition with cy

49 factor NFAT is chronically elevated in both DLBCL subtypes.

50 hat identifies 27% of germinal center B-cell DLBCLs (GCB-DLBCLs) as having a double-hit-like expressi

51 human germinal center B and activated B cell-DLBCL cell lines and xenograft models.

52 re highly enriched among non-germinal center DLBCLs and exhibited robust PD-L1 protein expression.

53 f functionally and genetically characterized DLBCL cell line models.

54 s on a panel of 32 genetically characterized DLBCL cell lines.

55 In conclusion, DLBCL patients with concurrent FL predominantly had the

56 adjusting for IPI, patients with concurrent DLBCL and FL had similar event-free survival (EFS) (haza

57 (n = 1153; 87.1%), patients with concurrent DLBCL and follicular lymphoma (FL) (n = 109; 8.2%) had f

58 B) subtype, whereas patients with concurrent DLBCL and other indolent lymphomas (n = 62; 4.7%) had mo

59 Patients with concurrent DLBCL and other indolent lymphomas had similar EFS (HR =

60 luded patients with histologically confirmed DLBCL morphology derived from large prospective trials a

61 CR6 and S100A8 in BLS-type than conventional DLBCL.

62 ta and BCL-2 blockade in genetically defined DLBCLs.

63 ty of copanlisib/venetoclax in BCR-dependent DLBCLs with genetic bases for BCL-2 dysregulation in vit

64 As these were largely BCR-dependent DLBCLs, we hypothesized that combined inhibition of PI3K

65 he highest cytotoxicity in all BCR-dependent DLBCLs.

66 lly underlying MYC dysregulation in DHITsig+ DLBCL, suggesting that gene expression profiling is more

67 followed 1,324 patients with newly diagnosed DLBCL from 2002 to 2015 and treated with immunochemother

68 vely followed cohort of 1324 newly diagnosed DLBCL patients treated with immunochemotherapy, we defin

69 Methods: 145 patients with newly diagnosed DLBCL underwent pre-treatment PET (PET-0) and PET-2 asse

70 In total, 145 patients with newly diagnosed DLBCL underwent pretreatment PET and PET-2 assessment.

71 The classifier described here discriminates DLBCL tumors based on tumor and nontumor composition and

72 tat had no benefit; patients with Myc-driven DLBCL, low CD4, and low DTI had less favorable outcomes.

73 monstrated strong EBV miR expression in EBV+ DLBCL.

74 examine this, a novel in vitro model of EBV+ DLBCL was developed, using the viral strain EBV WIL, whi

75 und in patients with orbital lymphoma: EMZL, DLBCL, FL, and MCL.

76 ion, EZH2 and thymidylate synthase, enhanced DLBCL MHC-I presentation.

77 ble treatments, 48% (95% CI, 28% to 69%) for DLBCL/PMBCL, 63% (95% CI, 25% to 92%) for low-grade lymp

78 i-CD37 therapies will be more beneficial for DLBCL patients without CD37 mutations.

79 riate and associated with potential harm for DLBCL patients.

80 However, previously developed signatures for DLBCL suffer from many major inadequacies such as lack o

81 SIRT3 as an important therapeutic target for DLBCL patients with ATM null phenotype.

82 ncogene addiction and therapeutic target for DLBCLs.

83 tients should not be summarily excluded from DLBCL clinical trials.

84 DNA extracted from DLBCL tumors diagnosed in patients residing in a catchme

85 for both ATR and WEE1 inhibitors in non-GCB DLBCL subtypes that represent an area of unmet clinical

86 subtype with outcomes similar to that of GCB DLBCL patients.

87 s other cases were genetically closer to GCB DLBCL.

88 (HR = 0.84) compared with patients with GCB DLBCL alone.

89 ad non-germinal center B-cell-like (non-GCB) DLBCL, 33% had transformed DLBCL, 60% were refractory, a

90 s (miRNAs) in EBV-negative ABC-DLBCL and GCB-DLBCL cell lines and their EBV-infected counterparts.

91 confirmed using RT-qPCR in ABC-DLBCL and GCB-DLBCL cells, respectively.

92 ely dysregulated in ABC-DLBCL but not in GCB-DLBCL and BL.

93 the biology underlying poor outcomes in GCB-DLBCL.

94 cell-like diffuse large B cell lymphoma (GCB-DLBCL) and Burkitt lymphoma(1,3-6), and the ligand for t

95 GC B cell-diffuse large B cell lymphoma (GCB-DLBCL), and Burkitt lymphoma (BL).

96 RNAs) between EBV-negative and -positive GCB-DLBCL cells.

97 ral other types of cancer in addition to GCB-DLBCL and Burkitt lymphoma, we speculate that GGG might

98 cally distinct subgroup of tumors within GCB-DLBCL characterized by a gene expression signature of HG

99 Here, 20 DHITsig+ GCB-DLBCLs apparently lacking MYC and/or BCL2 rearrangements

100 es 27% of germinal center B-cell DLBCLs (GCB-DLBCLs) as having a double-hit-like expression pattern (

101 signature (DHITsig) that assigned 27% of GCB-DLBCLs to the DHITsig-positive group, with only one half

102 e in situ hybridization was used to identify DLBCLs harboring PD-L1 gene alterations, thereby enablin

103 or high-throughput generation of immunogenic DLBCL spheroids.

104 tumor burden dissemination further improves DLBCL patient risk stratification at staging.

105 nd causes of specific genetic alterations in DLBCL and their role in disease development and progress

106 have identified many genetic alterations in DLBCL, some of which are specific to B cell lymphomas, w

107 f of concept for the repurposing approach in DLBCL, and point to dasatinib as an attractive strategy

108 line and human lymphoma models as well as in DLBCL patients where they appeared to distinguish clinic

109 tabolic response to standard chemotherapy in DLBCL.

110 le of K(+) channel encoding genes emerged in DLBCL accompanied by the over-expression of the fatty ac

111 te the use of TMTV as a predictive factor in DLBCL patients.

112 ced stage disease (i.e., III-IV vs. I-II) in DLBCL patients and higher levels of miR-27a and miR-24 w

113 tic impact of TMTV and prognostic indices in DLBCL patients, aged 60 to 80 years, from the phase 3 RE

114 etic alterations of 9p24.1 are infrequent in DLBCL.

115 ential therapeutic use of PARP inhibitors in DLBCL and T-ALL.

116 However, the pathogenic role of KLHL14 in DLBCL and its molecular function are largely unknown.

117 nstability, and immune evasion mechanisms in DLBCL and provide preclinical proof of concept for inclu

118 bitors of BTK and BCR signaling mediators in DLBCL.

119 d a shift towards an oxidative metabolism in DLBCL.

120 nterrogation of genes recurrently mutated in DLBCL.

121 a favorable outcome and uniquely observed in DLBCL.

122 ion as a potential new therapeutic option in DLBCL.

123 gnificant prognostic value for PFS and OS in DLBCL patients.

124 ot visual analysis, on i-PET predicted OS in DLBCL, although the low number of events limited the sta

125 The negative prognostic impact of MYC-R in DLBCL is largely observed in patients with MYC double hi

126 (single-, double-, and triple-hit status) in DLBCL within the context of the MYC partner gene.

127 assessing this target for the first time in DLBCL.

128 evaluate the best automated MTV workflow in DLBCL; determine whether uptake time, compliance or nonc

129 in combination with other targeted agents in DLBCLs and other forms of iNHL.

130 of deregulated functionally active miRNAs in DLBCLs and could possibly lead to the identification of

131 Interestingly, DLBCL patients with PD-L1 alterations had inferior progr

132 er after the incorporation of rituximab into DLBCL treatments.

133 immune-privileged site-associated DLBCL (IP-DLBCL) samples originating in the testis or central nerv

134 mutations were exclusively identified in IP-DLBCL cases (10/44, 23%) but absent in non-IP-DLBCL case

135 LBCL cases (10/44, 23%) but absent in non-IP-DLBCL cases.

136 nsight into the molecular pathogenesis of IP-DLBCL and indicates that anti-CD37 therapies will be mor

137 ed the effects of SIRT3 depletion and killed DLBCL cells.

138 SIRT3 promotes growth of ATM CRISPR knockout DLBCL xenografts compared to wild-type ATM control xenog

139 Cumulative incidences of late DLBCL and indolent lymphoma relapses were analyzed as co

140 tional type I/II versus type III EBV latency DLBCL cell lines.

141 f these tumors, we studied 31 diffuse LBCLs (DLBCLs), not otherwise specified (NOS); 20 LBCL-IRF4 cas

142 roliferative effect on activated B-cell like DLBCL spheroids and reduced several cytokines and other

143 s subsequently being evaluated in first-line DLBCL in the phase 2 portion of the study.

144 , followed by diffuse large B-cell lymphoma (DLBCL) (15%, n = 118), follicular lymphoma (FL) (11%, n

145 n = 26, 10%), diffuse large B-cell lymphoma (DLBCL) (n = 25, 10%), and mantle cell lymphoma (MCL) (n

146 lterations in diffuse large B cell lymphoma (DLBCL) and follicular lymphoma (FL).

147 n subtypes of diffuse large B-cell lymphoma (DLBCL) and identify a potential therapeutic vulnerabilit

148 analyze human diffuse large B-cell lymphoma (DLBCL) and non-DLBCL pathologic images from three hospit

149 ractory (R/R) diffuse large B-cell lymphoma (DLBCL) are limited, with no standard of care; prognosis

150 es (PET-2) in diffuse large B-cell lymphoma (DLBCL) by applying 2 different methods of interpretation

151 es (PET-2) in diffuse large B-cell lymphoma (DLBCL) by applying two different methods of interpretati

152 B-cell (GCB) diffuse large B-cell lymphoma (DLBCL) cell lines, characterized by high MYC protein exp

153 c analysis of diffuse large B-cell lymphoma (DLBCL) from the British Columbia population-based regist

154 patients with diffuse large B-cell lymphoma (DLBCL) has been the subject of much debate.

155 ng studies of diffuse large B cell lymphoma (DLBCL) have identified hundreds of recurrently altered g

156 advances for diffuse large B-cell lymphoma (DLBCL) have led to an increasing number of survivors.

157 patients with diffuse large B-cell lymphoma (DLBCL) have migrated from a focus on dose-intense and do

158 lity loci for diffuse large B-cell lymphoma (DLBCL) in individuals of European ancestry through a lar

159 Diffuse large B-cell lymphoma (DLBCL) is a heterogeneous disease, commonly described by

160 nt.IMPORTANCE Diffuse large B-cell lymphoma (DLBCL) is a highly aggressive tumor of lymphoid origin w

161 Diffuse large B cell lymphoma (DLBCL) is a highly heterogeneous lymphoid neoplasm with

162 or refractory diffuse large B-cell lymphoma (DLBCL) is an aggressive cancer with a median overall sur

163 pproaches for diffuse large B cell lymphoma (DLBCL) is confounded by its pronounced genetic, phenotyp

164 Diffuse large B-cell lymphoma (DLBCL) may present initially in bone marrow, liver and s

165 TH- BCL2) and diffuse large B-cell lymphoma (DLBCL) morphology through examination of gene expression

166 y or relapsed diffuse large B-cell lymphoma (DLBCL) often associates with the activated B-cell-like (

167 of ultra-risk diffuse large B-cell lymphoma (DLBCL) patients is needed to aid stratification to innov

168 from selected diffuse large B-cell lymphoma (DLBCL) patients, 2 recent whole-exome sequencing studies

169 vival (OS) in diffuse large B-cell lymphoma (DLBCL) patients.

170 patients with diffuse large B-cell lymphoma (DLBCL) present with a concurrent indolent lymphoma at di

171 Diffuse large B-cell lymphoma (DLBCL) presents as a limited-stage disease in 25% to 30%

172 R blockade in diffuse large B-cell lymphoma (DLBCL) remains undefined.

173 Diffuse large B-cell lymphoma (DLBCL) represents the most common adult lymphoma and can

174 A levels with diffuse large B cell lymphoma (DLBCL) risk [n = 98 cases; OR (95% CI) per 1 SD increase

175 deficiency in diffuse large B-cell lymphoma (DLBCL) significantly induce mitochondrial deacetylase si

176 c factors for diffuse large B-cell lymphoma (DLBCL) such as the international prognostic index (IPI)

177 tic factor in diffuse large B-cell lymphoma (DLBCL) whose measurement requires the segmentation of al

178 homa (FL) and diffuse large B-cell lymphoma (DLBCL) within the context of prior knowledge, and highli

179 ll-like (ABC) diffuse large B-cell lymphoma (DLBCL) xenograft model, but this compound suffered from

180 also occur in diffuse large B-cell lymphoma (DLBCL), albeit with a lower incidence.

181 a feature of diffuse large B-cell lymphoma (DLBCL), and the existence of a subgroup with poor progno

182 patients with diffuse large B-cell lymphoma (DLBCL), most relapses occur within the first 2 years of

183 Diffuse large B cell lymphoma (DLBCL), the most common subtype of Non-Hodgkin lymphoma,

184 compounds for diffuse large B cell lymphoma (DLBCL), we screened a library of drugs and other targete

185 ic subtype of diffuse large B cell lymphoma (DLBCL), which relies on B cell receptor (BCR) signaling

186 patients with diffuse large B-cell lymphoma (DLBCL).

187 oma (FL), and diffuse large B-cell lymphoma (DLBCL).

188 patients with diffuse large B-cell lymphoma (DLBCL).

189 re aggressive Diffuse Large B Cell Lymphoma (DLBCL).

190 usly develops diffuse large B-cell lymphoma (DLBCL).

191 ed/refractory diffuse large B-cell lymphoma (DLBCL).

192 iagnosed with diffuse large B-cell lymphoma (DLBCL).

193 cal needs for diffuse large B-cell lymphoma (DLBCL).

194 treatment of diffuse large B-cell lymphoma (DLBCL).

195 tment risk in diffuse large B-cell lymphoma (DLBCL).

196 homa or primary mediastinal B-cell lymphoma (DLBCL/PMBCL; n = 28), low-grade B-cell lymphoma (n = 8),

197 homa (43%) or diffuse large B-cell lymphoma (DLBCL; 32%).

198 patients with diffuse large B-cell lymphoma (DLBCL; n = 61), plasmablastic lymphoma (n = 15), primary

199 d refractory diffuse large B cell lymphomas (DLBCL).

200 herapy (EBRT), whereas high-grade lymphomas (DLBCL and MCL) were treated with chemotherapy in combina

201 ately 10% of diffuse large B-cell lymphomas (DLBCLs) and has been associated with poor prognosis in m

202 for ~80% of diffuse large B cell lymphomas (DLBCLs) and identified novel prognostic subgroups of DLB

203 B-cell (ABC)-diffuse large B-cell lymphomas (DLBCLs) are clinically aggressive and phenotypically com

204 Diffuse large B cell lymphomas (DLBCLs) are genetically heterogeneous and highly prolife

205 itive (EBV+) diffuse large B-cell lymphomas (DLBCLs) express high levels of programmed death ligand 1

206 nstrate that diffuse large B cell lymphomas (DLBCLs) expressing LMO2 protein are functionally deficie

207 e a group of diffuse large B-cell lymphomas (DLBCLs) with inferior outcomes after standard chemoimmun

208 ing in human diffuse large B cell lymphomas (DLBCLs).

209 y-T-BCR-dependent NF-kappaB signaling in MCD DLBCL and suggest that the genetic status of KLHL14 shou

210 al interaction was retained in CREBBP-mutant DLBCL cells and could be pharmacologically targeted with

211 Most double-expressor (BCL2(+) and MYC(+)) DLBCL patients (87.5%; n = 7/8) achieved CR.

212 Overall, patients with Myc+ DLBCL had a significantly lower EFS.

213 iffuse large B-cell lymphoma (DLBCL) and non-DLBCL pathologic images from three hospitals separately

214 ession profiles from newly diagnosed de novo DLBCL patients, yielding 2 biologically distinct subgrou

215 nase inhibitor, was effective against 50% of DLBCL cell lines, as well as against in vivo xenografts.

216 ession of these markers in a large cohort of DLBCL including BLS-type cases and found that expression

217 tilize deep learning models for diagnosis of DLBCL and ultimately other human hematopoietic malignanc

218 e role of immune function in the etiology of DLBCL, the most common lymphoma subtype.

219 Further elaboration of the genetics of DLBCL will not only improve our understanding of disease

220 nderstanding of the genetic heterogeneity of DLBCL deepens, a precision medicine approach should be a

221 s, the incredible molecular heterogeneity of DLBCL is likely to be a major complicating factor.

222 The incidence of DLBCL relapse was similar in patients with DLBCL alone a

223 the evolving diverse molecular landscape of DLBCL will create new opportunities to produce the next

224 as helped to define the genetic landscape of DLBCL.

225 antitumor activity in preclinical models of DLBCL associated with replication stress, but new mechan

226 , the lack of preclinical in vitro models of DLBCL TME hinders optimal therapeutic screening.

227 prevalence, characteristics, and outcome of DLBCL with concurrent indolent lymphoma.

228 th policy measures may support prevention of DLBCL, an aggressive NHL subtype.

229 In patients with DLBCL alone, the rate of DLBCL relapse was similar in the germinal center B-cell-

230 Importantly, screening of DLBCL patient samples identified SIRT3 as a putative the

231 consistently treated and assessed series of DLBCL patients, iPET had good prognostic value interpret

232 consistently treated and assessed series of DLBCL, iPET had good prognostic value interpreted either

233 and identified novel prognostic subgroups of DLBCL.

234 tions identify a unique biological subset of DLBCL in which an endogenous antilymphoma immune respons

235 evealed the existence of genetic subtypes of DLBCL using clustering methodologies.

236 nfirm the existence of molecular subtypes of DLBCL, providing evidence that genomic tests have progno

237 volume (TMTV) negatively impacts survival of DLBCL patients.

238 ny immune-related conditions in survivors of DLBCL compared with other cancer survivors, including si

239 ohort study, we compared 21,690 survivors of DLBCL from the California Cancer Registry (CCR) to survi

240 trate impaired immune health in survivors of DLBCL.

241 RNAs as biomarkers for the classification of DLBCLs or even as targets for personalized targeted trea

242 were selected from U.K. and Dutch studies on DLBCL to provide a balance between scans at 60 and 90 mi

243 rall, 90% of the miRNAs were enriched in PDX DLBCL models and human lymphoma cell lines.

244 Classifier-positive DLBCL patients (de novo) had an ORR of 44%, median progr

245 ilar to BRCA1-deficient cells, LMO2-positive DLBCLs and T cell acute lymphoblastic leukemia (T-ALL) c

246 sis was performed in a cohort of 137 primary DLBCL samples, including 44 primary immune-privileged si

247 We recently characterized primary DLBCL subsets with distinct genetic bases for perturbed

248 MHC-I regulation, and a majority of primary DLBCL tumors displayed genetic alterations in multiple r

249 p B, reflecting similar biology to published DLBCL stratification research.

250 ide monotherapy in patients with de novo R/R DLBCL and transformed lymphoma.

251 Ninety-seven patients with R/R DLBCL, including 12 patients with transformed lymphoma,

252 Among 84 patients with de novo R/R DLBCL, overall response rate (ORR) was 29%, including 11

253 n to enrich for response to avadomide in R/R DLBCL.

254 Recent DLBCL reclassification based on mutational landscapes id

255 ort, in patients with relapsed or refractory DLBCL who had no therapeutic options of potential clinic

256 file in patients with relapsed or refractory DLBCL who received at least two lines of previous chemoi

257 histologically confirmed relapsed/refractory DLBCL after at least 1 prior therapy.

258 etreatment biopsies from relapsed/refractory DLBCL patients receiving avadomide (NCT01421524).

259 ted clinical activity in relapsed/refractory DLBCL patients, independent of COO subtypes.

260 bel study, patients with relapsed/refractory DLBCL who were ineligible for autologous hematopoietic c

261 volumab in patients with relapsed/refractory DLBCL.

262 of increased TFR1 expression with high-risk DLBCL cases.

263 presents a new opportunity against high-risk DLBCL tumors using potency and precision.

264 ined with ECOG PS may identify an ultra-risk DLBCL population.

265 have prognostic significance in non-selected DLBCL patients.

266 es with gene-overexpressed and gene-silenced DLBCL cell lines showed that expression of NANOG and HOX

267 study in the United States of limited-stage DLBCL in the rituximab era, with the best NCTN results i

268 ents having a markedly better prognosis than DLBCL and MCL.

269 survival of 92% and 71%, respectively) than DLBCL and MCL patients (10-year disease-specific surviva

270 Here, we show that DLBCLs are dependent on mitochondrial lysine deacetylase

271 Our comprehensive sequence analysis of the DLBCL miRNA profiles identified sets of deregulated miRN

272 d single-agent activity of venetoclax in the DLBCLs and identified a subset with limited sensitivity

273 n reveals genetic similarities between these DLBCL subtypes and various indolent and extranodal lymph

274 further elucidate genetic susceptibility to DLBCL, we sought to validate two loci at 3q13.33 and 3p2

275 ll-like (non-GCB) DLBCL, 33% had transformed DLBCL, 60% were refractory, and 27% were primary refract

276 ding to the overall content of miRNAs in two DLBCL cell lines and their EBV-converted counterparts.

277 pt that tumor or precursor cells of BLS-type DLBCL are attracted by chemotaxis and home to the bone m

278 any lymphadenopathy (referred to as BLS-type DLBCL), which is aggressive and frequently associated wi

279 with nonbulky (< 10 cm) stage I/II untreated DLBCL received 3 cycles of standard R-CHOP therapy and u

280 t improve outcome in patients with untreated DLBCL.

281 gains of chromosome 7, 11q12.3-q25, whereas DLBCL, NOS was predominantly of germinal center B-cell (

282 773363; MAF = 0.45) was also associated with DLBCL risk (OR = 1.20, P = 2.31 x 10-12).

283 frequency [MAF] = 0.40) was associated with DLBCL risk [odds ratio (OR) = 0.83, P = 3.62 x 10-13].

284 tic effect of copanlisib was associated with DLBCL subtype-specific dysregulated expression of BCL-2

285 tion, and compromised TCA flux compared with DLBCL cells expressing wild type (WT)-ATM.

286 of sCD23 with CLL and DLBCL and CXCL13 with DLBCL persisted among cases sampled > 9 years before dia

287 A total of 574 patients with DLBCL age 18 to 80 years were randomly assigned to induc

288 Compared with patients with DLBCL alone (n = 1153; 87.1%), patients with concurrent

289 f DLBCL relapse was similar in patients with DLBCL alone at diagnosis (6.3% at 5 years), compared wit

290 (OS) (HR = 0.75) compared with patients with DLBCL alone, but nearly identical EFS (HR = 1.00) and OS

291 In patients with DLBCL alone, the rate of DLBCL relapse was similar in th

292 similar outcomes compared with patients with DLBCL alone.

293 d OS (HR = 1.09) compared with patients with DLBCL alone.

294 robustly discriminate low-risk patients with DLBCL from high-risk ones.

295 course, splitting the pool of patients with DLBCL into smaller groups on the basis of molecular char

296 ion rate of 91% for serum from patients with DLBCL versus normal controls.

297 ow overall response rate among patients with DLBCL who are ineligible for auto-HCT or who experienced

298 ully improve long-term care of patients with DLBCL.

299 Patients who relapsed with DLBCL had a worse prognosis than those who relapsed with

300 was inferior for patients who relapsed with DLBCL than for those who relapsed with indolent lymphoma

301 In vivo xenograft DLBCL models confirmed differences in single-agent antit