ライフサイエンスコーパス: B-cell lymphoma

1 re enhanced by anti-PD-1 in a mouse model of B cell lymphoma.

2 that when deregulated leads to emergence of B cell lymphoma.

3 rituximab, which is a standard treatment for B cell lymphoma.

4 zed derivatives as a novel treatment against B cell lymphoma.

5 ith relapsed and/or refractory diffuse large B cell lymphoma.

6 in germinal center B cells and diffuse large B cell lymphoma.

7 issemination of cancer, including aggressive B-cell lymphoma.

8 tumorigenesis in the Emu-Myc mouse model of B-cell lymphoma.

9 is, lymphoproliferative disease, and/or EBV+ B-cell lymphoma.

10 cal Hodgkin lymphoma and primary mediastinal B-cell lymphoma.

11 ing in follicular lymphoma and diffuse large B-cell lymphoma.

12 f the MEF2 family and MEF2B's involvement in B-cell lymphoma.

13 tory (rel/ref) chemorefractory diffuse large B-cell lymphoma.

14 n patients with relapsed or refractory large B-cell lymphoma.

15 ents with previously untreated diffuse large B-cell lymphoma.

16 ute lymphoblastic leukemia and diffuse large B-cell lymphoma.

17 imab in relapsed or refractory diffuse large B-cell lymphoma.

18 CHOP) as frontline therapy for diffuse large B-cell lymphoma.

19 and antitumour activity in a mouse model of B-cell lymphoma.

20 c stem cell transplantation in diffuse large B-cell lymphoma.

21 eing studied as novel therapeutic target for B-cell lymphoma.

22 xhibit many mutations found in diffuse large B-cell lymphoma.

23 that are associated with cancers, including B cell lymphomas.

24 er 95% of all adults and are associated with B cell lymphomas.

25 o be also used in rearranged Ig loci of MALT B cell lymphomas.

26 s the development of autoimmune diseases and B cell lymphomas.

27 associated with epithelial-cell cancers and B cell lymphomas.

28 uration and the cell of origin (COO) of most B cell lymphomas.

29 posed as a diagnostic marker for non-Hodgkin B-cell lymphomas.

30 f MALT1 is associated with highly aggressive B-cell lymphomas.

31 nical models of humoral immune responses and B-cell lymphomas.

32 unmet need in the treatment of MCL and other B-cell lymphomas.

33 vity have delayed development of MYC-induced B-cell lymphomas.

34 therapy that frequently cures Diffuse Large B-Cell Lymphomas.

35 new approaches to disable drug resistance in B-cell lymphomas.

36 =18 years) with relapsed or refractory large B-cell lymphomas.

37 and pathologically distinct subtype of large B-cell lymphomas.

38 n in adult tissues and its overexpression in B-cell lymphomas.

39 the PI3K/AKT/mTOR pathway and glycolysis in B-cell lymphomas.

40 n patients with relapsed or refractory large B-cell lymphomas.

41 0.68) and for melanoma (0.83), diffuse large B-cell lymphoma (0.89), and follicular lymphoma (0.65).

42 ied overexpression of the prosurvival factor B cell lymphoma 2 (BCL-2) as a distinguishing feature of

43 is in noninfected bystander cells.IMPORTANCE B cell lymphoma 2 (Bcl-2) family proteins play important

44 lymphoid malignancies with the FDA-approved B cell lymphoma 2 (BCL-2) inhibitor venetoclax, but resi

45 proteins homologous protein expression, and B cell lymphoma 2 phosphorylation, thereby exacerbating

46 The Bcl-2 (B cell lymphoma 2)-related protein Nr-13 plays a major r

47 The proapoptotic protein B-cell lymphoma 2 (BCL-2) associated X protein (Bax) was

48 rly, inhibition of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) has been shown to induce cell

49 The B-cell lymphoma 2 (BCL-2) inhibitor venetoclax has an em

50 B-cell lymphoma 2 (BCL-2) overexpression is implicated i

51 athway is regulated mainly by members of the B-cell lymphoma 2 (BCL-2) protein family.

52 B-cell lymphoma 2 (Bcl-2) protein is the founding member

53 tivation of PI3K signaling not only prevents B-cell lymphoma 2 (BCL2)-Associated X (Bax)- and BCL2 An

54 rst step toward a new class of antiapoptotic B-cell lymphoma 2 family protein degraders.

55 n tyrosine kinase inhibitor ibrutinib or the B-cell lymphoma 2 inhibitor venetoclax in combination wi

56 B-cell lymphoma 2 is significantly upregulated by TFEB a

57 gulators BCL2-associated X protein (BAX) and B-cell lymphoma 2 toward an antiapoptotic profile.

58 have emerged, including venetoclax to target B-cell lymphoma 2, midostaurin and gilteritinib to targe

59 and the expression of antiapoptotic protein B-cell lymphoma 2, which were reversed by small-molecule

60 ing pathways, especially apoptosis inhibitor B-cell lymphoma 2.

61 The FOXO3a (forkhead box O3a)-BNIP3 (B-cell lymphoma 2/adenovirus E1B 19kDa interacting prote

62 p-regulated modulator of apoptosis (PUMA), a B-cell lymphoma-2 (Bcl-2) homology domain 3 (BH3)-only B

63 L) include venetoclax, the oral inhibitor of B-cell lymphoma-2, and inhibitors of kinases in the B-ce

64 h cNHEJ and TP53 expression succumbed to pro-B cell lymphoma(3).

65 e enrolled and treated; 19 had diffuse large B-cell lymphoma, 53 follicular lymphoma, and one margina

66 cipitates with the transcriptional repressor B cell lymphoma 6 (Bcl-6) in CD4 T cells.

67 domain of the oncogenic transcription factor B cell lymphoma 6 (BCL6) and leads to the proteasomal de

68 The transcriptional corepressor B-cell lymphoma 6 (BCL6) is a member of the Broad-comple

69 aft-versus-host disease (cGVHD) by targeting B-cell lymphoma 6 (BCL6), a transcriptional regulator of

70 The B-cell lymphoma 9 (BCL9) oncogene functions as a transcr

71 ntle cell lymphoma, and 30% in diffuse large B-cell lymphoma; 93% of responses occurred at first asse

72 receptor CXCR5, which is frequently found on B-cell lymphoma-a single dose led to improved control of

73 evels in activated B cell-type diffuse large B cell lymphoma (ABC-DLBCL) are associated with reduced

74 Activated B-cell-like diffuse large B-cell lymphoma (ABC-DLBCL) is an aggressive subtype of

75 e and gastric biopsy confirmed diffuse large-B-cell lymphoma, activated B cell type, with posterior r

76 with pathologically confirmed diffuse large B-cell lymphoma, an Eastern Cooperative Oncology Group p

77 ral human malignancies such as diffuse large B cell lymphoma and chronic lymphocytic leukemia.

78 titutive NF-kappaB activity in diffuse large B cell lymphoma and other lymphoid cancers.

79 Epstein-Barr virus (EBV) causes B cell lymphomas and transforms B cells in vitro The EBV

80 0 patients with HIV-associated diffuse large B-cell lymphoma and 19 patients with symptomatic interle

81 81 patients with diffuse large B-cell lymphoma and 41 patients with follicular lymphoma

82 81 patients with diffuse large B-cell lymphoma and 42 with follicular lymphoma were rec

83 rticipants, excluding those with non-Hodgkin B-cell lymphoma and chronic lymphocytic leukaemia.

84 l patients, excluding those with non-Hodgkin B-cell lymphoma and chronic lymphocytic leukaemia.

85 rticipants, excluding those with non-Hodgkin B-cell lymphoma and chronic lymphocytic leukaemia; and e

86 biological overlap with primary mediastinal B-cell lymphoma and conferred excellent prognosis.

87 for patients with early stage diffuse large B-cell lymphoma and follicular lymphoma suggests better

88 ts with relapsed or refractory diffuse large B-cell lymphoma and follicular lymphoma.

89 ts with relapsed or refractory diffuse large B-cell lymphoma and follicular lymphoma.

90 The aim of treatment of diffuse large B-cell lymphoma and peripheral T-cell lymphoma is potent

91 Application of our tool on diffuse large B-cell lymphoma and prostate cancer demonstrated how syn

92 central nervous system (CNS) involvement of B-cell lymphoma and provides high sensitivity but modera

93 further evaluation at first relapse in large B-cell lymphomas and as a treatment for other relapsed o

94 at PRDM15 fuels the metabolic requirement of B-cell lymphomas and validate it as an attractive and pr

95 commonly mutated in germinal-center-derived B cell lymphomas, and their inactivation is thought to c

96 , 16 (36%) of 45 patients with diffuse large B-cell lymphoma, and 13 (65%) of 20 patients with Richte

97 m any indolent lymphoma, primary mediastinal B-cell lymphoma, and follicular lymphoma grade 3B.

98 del11q), follicular lymphoma, diffuse large B-cell lymphoma, and Richter's transformation.

99 uding mantle cell lymphoma and diffuse large B-cell lymphoma, and supports constitutive expression of

100 In high-grade B-cell lymphoma, angiogenesis correlates with poor progn

101 g follicular lymphoma and most diffuse large B-cell lymphomas, anti-PD-1 therapy has been less effect

102 otomab, a CD37 antibody for the treatment of B-cell lymphomas, are being highlighted.

103 anti-PD1 agents in patients with aggressive B cell lymphoma as well as in preclinical models of othe

104 Delta3A caused B cell lymphomas at rates similar to their induction by

105 B-cell lymphoma (BCL) is the most common hematologic mal

106 on is an important mechanism contributing to B-cell lymphoma (BCL).

107 Members of the B-cell lymphoma (BCL-2) protein family regulate mitochon

108 se large B-cell lymphoma patients and Eu-myc B-cell lymphoma-bearing mice displayed reduced interfero

109 tantially reduced the risks of diffuse large B-cell lymphoma, Burkitt lymphoma, and primary CNS lymph

110 H1-4, respectively) are highly recurrent in B cell lymphomas, but the pathogenic relevance of these

111 ssing T cells are an effective treatment for B-cell lymphoma, but often cause neurologic toxicity.

112 ur during B-cell development are hijacked in B-cell lymphoma by genetic alterations that directly or

113 logically distinct subtypes of diffuse large B-cell lymphoma can be identified using gene-expression

114 Loss of FBXW7 inhibited diffuse large B-cell lymphoma cell growth and further sensitized cells

115 as well as different types of diffuse large B cell lymphoma cells.

116 riptome analysis during KSHV reactivation in B-cell lymphoma cells and determined RTA-binding sites o

117 Re-expression of individual miRNAs in B-cell lymphoma cells down-regulated expression of PRMT5

118 ute lymphoblastic leukemia and diffuse large B-cell lymphoma cells to anti-CD19 CAR T cells.

119 nd high-grade B cell lymphoma (diffuse large B cell lymphoma) cells.

120 Hodgkin lymphoma (HL) is a B cell lymphoma characterized by few malignant cells and

121 Mantle cell lymphoma (MCL) is a B-cell lymphoma characterized by cyclin D1 expression.

122 ted their protumorigenic function in primary B cell lymphoma cocultures.

123 R 16.7-24.3) for the untreated diffuse large B-cell lymphoma cohort treated at the polatuzumab vedoti

124 In the diffuse large B-cell lymphoma cohort, grade 3-5 adverse events occurre

125 led to significantly improved regression of B-cell lymphoma compared with treatment utilizing anti-C

126 Non-Hodgkin B-cell lymphomas constituted 99% (n = 258) and T-cell ly

127 Burkitt lymphoma is an aggressive B-cell lymphoma curable with dose-intensive chemotherapy

128 In vivo xenograft studies using a human B-cell lymphoma demonstrated that treatment with hnCD16-

129 risk of spontaneous liver tumorigenesis and B-cell lymphoma development at old age.

130 hanism conferring selective advantage during B-cell lymphoma development.

131 also efficiently bind B cells and high-grade B cell lymphoma (diffuse large B cell lymphoma) cells.

132 common genetic alterations in diffuse large B cell lymphoma (DLBCL) and follicular lymphoma (FL).

133 Sequencing studies of diffuse large B cell lymphoma (DLBCL) have identified hundreds of recu

134 Diffuse large B cell lymphoma (DLBCL) is a highly heterogeneous lympho

135 cision medicine approaches for diffuse large B cell lymphoma (DLBCL) is confounded by its pronounced

136 ation of total TFA levels with diffuse large B cell lymphoma (DLBCL) risk [n = 98 cases; OR (95% CI)

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

138 To repurpose compounds for diffuse large B cell lymphoma (DLBCL), we screened a library of drugs

139 utant (MCD) genetic subtype of diffuse large B cell lymphoma (DLBCL), which relies on B cell receptor

140 th that of the more aggressive Diffuse Large B Cell Lymphoma (DLBCL).

141 ainst recurrent and refractory diffuse large B cell lymphomas (DLBCL).

142 pe (57%, n = 452), followed by diffuse large B-cell lymphoma (DLBCL) (15%, n = 118), follicular lymph

143 r lymphoma (FL) (n = 26, 10%), diffuse large B-cell lymphoma (DLBCL) (n = 25, 10%), and mantle cell l

144 NFAT) signaling in subtypes of diffuse large B-cell lymphoma (DLBCL) and identify a potential therape

145 We analyze human diffuse large B-cell lymphoma (DLBCL) and non-DLBCL pathologic images

146 for relapsed/refractory (R/R) diffuse large B-cell lymphoma (DLBCL) are limited, with no standard of

147 rapy after 2 cycles (PET-2) in diffuse large B-cell lymphoma (DLBCL) by applying 2 different methods

148 py after two cycles (PET-2) in diffuse large B-cell lymphoma (DLBCL) by applying two different method

149 n-germinal center B-cell (GCB) diffuse large B-cell lymphoma (DLBCL) cell lines, characterized by hig

150 and transcriptomic analysis of diffuse large B-cell lymphoma (DLBCL) from the British Columbia popula

151 ent decisions in patients with diffuse large B-cell lymphoma (DLBCL) has been the subject of much deb

152 Therapeutic advances for diffuse large B-cell lymphoma (DLBCL) have led to an increasing number

153 efine R-CHOP for patients with diffuse large B-cell lymphoma (DLBCL) have migrated from a focus on do

154 t four susceptibility loci for diffuse large B-cell lymphoma (DLBCL) in individuals of European ances

155 Diffuse large B-cell lymphoma (DLBCL) is a heterogeneous disease, comm

156 targeted treatment.IMPORTANCE Diffuse large B-cell lymphoma (DLBCL) is a highly aggressive tumor of

157 Relapsed or refractory diffuse large B-cell lymphoma (DLBCL) is an aggressive cancer with a m

158 Diffuse large B-cell lymphoma (DLBCL) may present initially in bone ma

159 gements (HGBL-DH/TH- BCL2) and diffuse large B-cell lymphoma (DLBCL) morphology through examination o

160 Refractory or relapsed diffuse large B-cell lymphoma (DLBCL) often associates with the activa

161 y identification of ultra-risk diffuse large B-cell lymphoma (DLBCL) patients is needed to aid strati

162 in tumor samples from selected diffuse large B-cell lymphoma (DLBCL) patients, 2 recent whole-exome s

163 ) and overall survival (OS) in diffuse large B-cell lymphoma (DLBCL) patients.

164 Some patients with diffuse large B-cell lymphoma (DLBCL) present with a concurrent indole

165 Diffuse large B-cell lymphoma (DLBCL) presents as a limited-stage dise

166 r, the role of BCR blockade in diffuse large B-cell lymphoma (DLBCL) remains undefined.

167 Diffuse large B-cell lymphoma (DLBCL) represents the most common adult

168 We show that ATM deficiency in diffuse large B-cell lymphoma (DLBCL) significantly induce mitochondri

169 linical prognostic factors for diffuse large B-cell lymphoma (DLBCL) such as the international progno

170 ies, is a prognostic factor in diffuse large B-cell lymphoma (DLBCL) whose measurement requires the s

171 n follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL) within the context of prior know

172 an activated B-cell-like (ABC) diffuse large B-cell lymphoma (DLBCL) xenograft model, but this compou

173 ous in cHL, they also occur in diffuse large B-cell lymphoma (DLBCL), albeit with a lower incidence.

174 heterogeneity is a feature of diffuse large B-cell lymphoma (DLBCL), and the existence of a subgroup

175 In patients with diffuse large B-cell lymphoma (DLBCL), most relapses occur within the

176 dard of care for patients with diffuse large B-cell lymphoma (DLBCL).

177 follicular lymphoma (FL), and diffuse large B-cell lymphoma (DLBCL).

178 rior survival in patients with diffuse large B-cell lymphoma (DLBCL).

179 el that spontaneously develops diffuse large B-cell lymphoma (DLBCL).

180 patients newly diagnosed with diffuse large B-cell lymphoma (DLBCL).

181 stent unmet clinical needs for diffuse large B-cell lymphoma (DLBCL).

182 ic target for the treatment of diffuse large B-cell lymphoma (DLBCL).

183 marker of pretreatment risk in diffuse large B-cell lymphoma (DLBCL).

184 large B-cell lymphoma or primary mediastinal B-cell lymphoma (DLBCL/PMBCL; n = 28), low-grade B-cell

185 h follicular lymphoma (43%) or diffuse large B-cell lymphoma (DLBCL; 32%).

186 In 86 evaluable patients with diffuse large B-cell lymphoma (DLBCL; n = 61), plasmablastic lymphoma

187 providing a sc-COO for ~80% of diffuse large B cell lymphomas (DLBCLs) and identified novel prognosti

188 Here we demonstrate that diffuse large B cell lymphomas (DLBCLs) expressing LMO2 protein are fu

189 genome-wide screening in human diffuse large B cell lymphomas (DLBCLs).

190 occurs in approximately 10% of diffuse large B-cell lymphomas (DLBCLs) and has been associated with p

191 Activated B-cell (ABC)-diffuse large B-cell lymphomas (DLBCLs) are clinically aggressive and

192 ein-Barr virus-positive (EBV+) diffuse large B-cell lymphomas (DLBCLs) express high levels of program

193 GBL-DH/THs) include a group of diffuse large B-cell lymphomas (DLBCLs) with inferior outcomes after s

194 In diffuse large B-cell lymphoma, early assessment of treatment response

195 s-gender imbalance and splenic marginal zone B-cell lymphoma-emerged in combination with gene dose re

196 phoma subtypes were extranodal marginal zone B-cell lymphoma (EMZL) (n = 177, 68%), follicular lympho

197 Extranodal marginal zone B-cell lymphoma (EMZL) was the most frequent subtype (57

198 B-cell lymphoma extra large (BCL-X(L)) is a well-validat

199 ression levels of the anti-apoptotic protein B-cell lymphoma-extra large (BCL-xL).

200 -FDG) PET in the assessment of diffuse large B-cell lymphoma, follicular lymphoma, and peripheral T-c

201 nts with non-Hodgkin lymphoma (diffuse large B-cell lymphoma, follicular lymphoma, mantle cell lympho

202 d by screening mAbs elicited against a human B cell lymphoma for their direct antiproliferative effec

203 article, the aetiology of the single case of B cell lymphoma found in the Mountain gorilla was incorr

204 The most aggressive B cell lymphomas frequently manifest extranodal distribu

205 ly relapsed/refractory, adult, diffuse large B-cell lymphoma from a US health payer perspective over

206 in germinal-centre B cell-like diffuse large B cell lymphoma (GCB-DLBCL) and Burkitt lymphoma(1,3-6),

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

208 2 models without eliminating A20-luciferase B-cell lymphoma graft-versus-leukemia (GVL).

209 G defines a biologically coherent high-grade B-cell lymphoma group with distinct molecular features a

210 Unexpectedly, this system is subverted in B cell lymphomas harboring translocations that produce B

211 on for the treatment of multiple myeloma and B-cell lymphomas has made the ubiquitin pathway an impor

212 hway, which has progrowth functions in other B cell lymphomas, has not been fully explored in PEL.

213 Other B cell lymphomas have acquired an oncogenic mutation in

214 cell acute lymphoblastic leukaemia (ALL) or B cell lymphomas have revolutionized anticancer therapy,

215 LBCL-IRF4 cases; and 12 cases of high-grade B-cell lymphoma (HGBCL), NOS in patients <=25 years usin

216 istological subgroups included diffuse large B-cell lymphoma, high-grade B-cell lymphoma with rearran

217 cular features partly resembled that of MALT B cell lymphoma Ig genes, suggestive of a mechanism in w

218 This antibody inhibits the growth of B cell lymphoma in a xenograft model as effectively as r

219 ata show the mechanisms of T cell control of B cell lymphoma in gammaHV-infected mice overlap with th

220 rapy in relapsed or refractory diffuse large B-cell lymphoma in adults, high rates of durable respons

221 mation of chromosomal instable, pauci-clonal B-cell lymphoma in aging mice.

222 trated that loss of CD37 induces spontaneous B-cell lymphoma in Cd37-knockout mice and correlates wit

223 pressing B cells and showed efficacy against B-cell lymphomas in a single-center, phase 2a study.

224 ses protected against EBNA1-expressing T and B cell lymphomas, including lymphoproliferations that em

225 n patients with relapsed or refractory large B-cell lymphomas, including those with diverse histologi

226 e here identify secondary mutations in mouse B cell lymphomas induced by LMP1, to predict and identif

227 Here, we analyzed Myc-driven B-cell lymphoma-induced angiogenesis in mice.

228 ts with relapsed or refractory diffuse large B-cell lymphoma ineligible for autologous stem-cell tran

229 umor tissue samples from subjects with large B cell lymphoma infected with HHV-6B, (iii) lymphoblasto

230 lymphomas (MZLs) are indolent nonfollicular B-cell lymphomas (INFLs) and have heterogeneous clinical

231 sulo et al to include indolent nonfollicular B-cell lymphomas (INFLs).

232 ot endogenously expressed in the majority of B cell lymphomas, it is highly expressed in acute myeloi

233 erapy approved for relapsed/refractory large B-cell lymphoma (LBCL) on the basis of the single-arm ph

234 s targeting CD19 have high efficacy in large B cell lymphomas (LBCLs), but long-term remissions are o

235 Pediatric large B-cell lymphomas (LBCLs) share morphological and phenoty

236 requently mutated in germinal center-derived B-cell lymphomas like KMT2D or CREBBP An exception is GN

237 In human T-cells and B-cell lymphoma lines, MLT-231 potently and selectively

238 GC B cell lymphomas maintain their GC transcriptional signa

239 lease of IL-1 and IL-6 in a xenotransplanted B-cell lymphoma model without affecting CD19-specific CA

240 ll lymphoma (DLBCL/PMBCL; n = 28), low-grade B-cell lymphoma (n = 8), or chronic lymphocytic leukemia

241 ; amyloid polyneuropathy (N=20); intraneural B-cell lymphoma (N=20) or adult-onset polyglucosan body

242 olution of pathogen-specific B cells to MALT B cell lymphoma occurs.

243 this report, we describe the generation of a B cell lymphoma on the C57BL/6 background, which is driv

244 We treated 20 patients with B-cell lymphoma on a phase I, first-in-human clinical tr

245 ancies of the following types: diffuse large B-cell lymphoma or primary mediastinal B-cell lymphoma (

246 clonal SE mutations are clonally expanded in B cell lymphomas, our studies also offer the potential f

247 NK cells from both diffuse large B-cell lymphoma patients and Eu-myc B-cell lymphoma-bear

248 Compared with HIV-associated diffuse large B-cell lymphoma, PEL was associated with significant hyp

249 Cure rates for primary mediastinal large B-cell lymphoma (PMBCL) have improved with the integrati

250 Primary mediastinal large B-cell lymphoma (PMBL) cells depend on the constitutive

251 Primary mediastinal B-cell lymphoma (PMBL) is a rare but aggressive non-Hodg

252 Primary mediastinal large B-cell lymphoma (PMBL) represents a clinically and patho

253 Primary mediastinal large B-cell lymphomas (PMBLs) are aggressive tumors that typi

254 over, our findings reveal that expression of B-cell lymphoma protein 6 (BCL6), which is critical for

255 hat resemble Epstein-Barr virus (EBV)-driven B-cell lymphomas rather than HCC tumors.

256 patients with newly diagnosed diffuse large B-cell lymphoma received the polatuzumab vedotin recomme

257 the key predictors of risk for diffuse large B-cell lymphoma (recent CD4 count <50 cells per muL vs >

258 actor c-Rel to human autoimmune diseases and B cell lymphomas, respectively.

259 psed or refractory primary mediastinal large B-cell lymphoma (rrPMBCL) have a poor prognosis, and the

260 nt chromatin conformation in a diffuse large B-cell lymphoma sample; and (4) the systematic identific

261 al activity in newly diagnosed diffuse large B-cell lymphoma seems promising and encouraged a phase 3

262 ll therapy in people with HIV and aggressive B-cell lymphoma showed the feasibility of CAR T-cell the

263 imary effusion lymphoma, and a diffuse large B-cell lymphoma subgroup.

264 CD30 is expressed on a variety of B-cell lymphomas, such as Hodgkin lymphoma, primary effu

265 ) plays an important role in pathogenesis of B-cell lymphomas, suggesting that inhibition of BTK is u

266 Mantle cell lymphoma (MCL) is an aggressive B cell lymphoma that is largely chemoresistant.

267 She had a history of diffuse large B-cell lymphoma that had been diagnosed and treated 7 ye

268 Patients with diffuse large B-cell lymphoma that is refractory to primary and second

269 cers such as acute leukemia or diffuse large B-cell lymphoma that require rapid interventions.

270 ymphomas are a heterogeneous group of T- and B-cell lymphomas that present in the skin with no eviden

271 l products for both ALL and certain types of B cell lymphoma - the first approved gene therapies in t

272 ight (18%) of 45 patients with diffuse large B-cell lymphoma to 19 (53%) of 36 patients with chronic

273 the first large-scale study in diffuse large B-cell lymphoma to use real-time molecular characterisat

274 f hematological cancer cell lines, including B-cell lymphomas, to the potent pan-NMT inhibitor PCLX-0

275 e-hit or triple-hit lymphoma), diffuse large B-cell lymphoma transformed from any indolent lymphoma,

276 08 assessable patients with refractory large B-cell lymphoma treated with axicabtagene ciloleucel ach

277 tion of CSR can cause self-reactive BCRs and B cell lymphomas; understanding the timing and location

278 We found that NK cells in aggressive B-cell lymphoma underwent substantial transcriptional re

279 haracterize FBXW7 as a prosurvival factor in B-cell lymphoma via degradation of the chromatin modifie

280 Applying CIRI to patients with diffuse large B cell lymphoma, we demonstrate improved outcome predict

281 -dependent triple-negative breast cancer and B cell lymphoma, we show that beyond the well-characteri

282 ions in DLBCL, some of which are specific to B cell lymphomas, whereas others can also be observed in

283 mutated in PMBL compared with diffuse large B-cell lymphoma, whereas only a limited number of genes

284 mplication of APDS is malignancy (especially B-cell lymphomas), which greatly worsens the prognosis.

285 ncristine, and prednisone) for diffuse large B-cell lymphoma, which have not been associated with muc

286 ion in a 65-year-old male with diffuse large B cell lymphoma who failed initial CAR T cell treatment;

287 ts with relapsed or refractory diffuse large B-cell lymphoma who are ineligible for autologous stem-c

288 ts with relapsed or refractory diffuse large B-cell lymphoma who were ineligible for autologous stem-

289 ts with relapsed or refractory diffuse large B-cell lymphoma who were ineligible for or had disease p

290 with histologically confirmed diffuse large B-cell lymphoma, who relapsed or had refractory disease

291 an HIV provirus in a case of AIDS-associated B-cell lymphoma with an HIV provirus in the same part of

292 patients with newly diagnosed diffuse large B-cell lymphoma with an International Prognostic Index (

293 aldenstrom macroglobulinaemia is an indolent B-cell lymphoma with clearly defined criteria for diagno

294 ed diffuse large B-cell lymphoma, high-grade B-cell lymphoma with rearrangements of MYC and either BC

295 ated, histologically confirmed diffuse large B-cell lymphoma with sufficient diagnostic material from

296 tients experience relapse and die, targeting B-cell lymphomas with a NMT inhibitor potentially provid

297 he immune environments associated with major B-cell lymphomas with an emphasis on the immune escape p

298 the DHITsig was shared with the majority of B-cell lymphomas with high-grade morphology tested.

299 High-grade B-cell lymphomas with MYC and BCL2 and/or BCL6 rearrange

300 rnative splicing of the apoptotic regulator, B-cell lymphoma X (Bcl-x) transcripts: a finding observe