ライフサイエンスコーパス: lymphoma

1 agent with promising activity in non-Hodgkin lymphoma.

2 ountries, for the treatment of leukaemia and lymphoma.

3 the most common subtypes of cutaneous T-cell lymphoma.

4 patients with relapsed or refractory Hodgkin lymphoma.

5 hoid expansion and subsequent development of lymphoma.

6 apsed and/or refractory diffuse large B cell lymphoma.

7 ents with relapsed or refractory mantle-cell lymphoma.

8 ntensive chemotherapy in adults with Burkitt lymphoma.

9 -interactome in cells derived from Burkitt's lymphoma.

10 , follicular lymphoma, and peripheral T-cell lymphoma.

11 rrent or refractory non-CNS solid tumours or lymphoma.

12 ients with de novo R/R DLBCL and transformed lymphoma.

13 the early diagnosis of primary vitreoretinal lymphoma.

14 ative syndrome with marked predisposition to lymphoma.

15 inal center B cells and diffuse large B cell lymphoma.

16 3 follicular lymphoma, and one marginal zone lymphoma.

17 nts with CD30-positive anaplastic large cell lymphoma.

18 pproximately 20% of patients with follicular lymphoma.

19 nifestations of the disease and diagnosis of lymphoma.

20 ation of cancer, including aggressive B-cell lymphoma.

21 T/CT images in patients with lung cancer and lymphoma.

22 nd shows activating mutations in subtypes of lymphoma.

23 ients with relapsed or refractory follicular lymphoma.

24 , anaplastic lymphoma kinase-negative T-cell lymphoma.

25 additional much needed treatment option for lymphoma.

26 hile dysregulated MALT1 activity can lead to lymphoma.

27 rimary patient-derived anaplastic large cell lymphomas.

28 rs) with relapsed or refractory large B-cell lymphomas.

29 ch is relevant for inflammatory diseases and lymphomas.

30 improved responses against their autologous lymphomas.

31 g the association of HPgV viremia with adult lymphomas.

32 nfected B lymphocytes and in post-transplant lymphomas.

33 mplications of a MB cell-of-origin for these lymphomas.

34 an association of HPgV viremia with risk of lymphomas.

35 of B-cell disorders including leukemias and lymphomas.

36 future treatment option for cutaneous T-cell lymphomas.

37 ult tissues and its overexpression in B-cell lymphomas.

38 hat the transcription factor B-cell leukemia/lymphoma 11A (BCL11A) is highly expressed in triple-nega

39 qPET relates residual lymphoma (18)F-FDG uptake to physiologic liver uptake, c

40 rexpression of the prosurvival factor B cell lymphoma 2 (BCL-2) as a distinguishing feature of CD4+ T

41 oninfected bystander cells.IMPORTANCE B cell lymphoma 2 (Bcl-2) family proteins play important roles

42 The B-cell lymphoma 2 (BCL-2) inhibitor venetoclax has an emerging

43 The Bcl-2 (B cell lymphoma 2)-related protein Nr-13 plays a major role in

44 hways, especially apoptosis inhibitor B-cell lymphoma 2.

45 ude venetoclax, the oral inhibitor of B-cell lymphoma-2, and inhibitors of kinases in the B-cell rece

46 and TP53 expression succumbed to pro-B cell lymphoma(3).

47 led and treated; 19 had diffuse large B-cell lymphoma, 53 follicular lymphoma, and one marginal zone

48 The B-cell lymphoma 9 (BCL9) oncogene functions as a transcriptiona

49 n activated B cell-type diffuse large B cell lymphoma (ABC-DLBCL) are associated with reduced surviva

50 Hu19-CD828Z T cells had clinical anti-lymphoma activity similar to that of T cells expressing

51 Lymphomas afflict all age groups of people, with certain

52 athologically confirmed diffuse large B-cell lymphoma, an Eastern Cooperative Oncology Group performa

53 ntric Castleman disease, or primary effusion lymphoma and 8 HIV-uninfected men receiving HIV preexpos

54 oma (DLBCL) represents the most common adult lymphoma and can be divided into 2 major molecular subty

55 ical overlap with primary mediastinal B-cell lymphoma and conferred excellent prognosis.

56 n-Hodgkin's lymphomas, including mantle cell lymphoma and diffuse large B-cell lymphoma, and supports

57 nesis and increased resistance to Myc-driven lymphoma and Eml4-Alk-driven lung cancer.

58 cers, including B lymphocyte-derived Burkitt lymphoma and immunocompromise-associated lymphoprolifera

59 diagnosis, in 1 patient to lymphoplasmacytic lymphoma and in 2 patients to multiple myeloma.

60 ody-based agents targeting CD22 or CD20 on B lymphoma and leukemia cells exhibit clinical efficacy fo

61 is a routine tool for staging patients with lymphoma and lung cancer.

62 pendent B-cell neoplasms such as non-Hodgkin lymphoma and multiple myeloma.

63 s, Epstein-Barr virus (EBV) causes Burkitt's lymphoma and nasopharyngeal carcinoma.

64 The aim of treatment of diffuse large B-cell lymphoma and peripheral T-cell lymphoma is potential cur

65 linicians treating patients with non-Hodgkin lymphoma and stresses the need for cardiac monitoring du

66 rade, high-risk, mature B-cell non-Hodgkin's lymphoma and was associated with a higher incidence of h

67 the genetic architecture of mammary tumours, lymphomas and sarcomas induced by high ((56)Fe-ions) or

68 tive, relapsed or refractory solid tumour or lymphoma, and a Lansky Play/Karnofsky Performance status

69 st-line treatment for aggressive non-Hodgkin lymphoma, and doxorubicin and cyclophosphamide are both

70 ndolent lymphoma, primary mediastinal B-cell lymphoma, and follicular lymphoma grade 3B.

71 diffuse large B-cell lymphoma, 53 follicular lymphoma, and one marginal zone lymphoma.

72 of diffuse large B-cell lymphoma, follicular lymphoma, and peripheral T-cell lymphoma.

73 l to the management of patients with Hodgkin lymphoma, and PET-adapted strategies have facilitated ma

74 ell malignancies like CLL, small lymphocytic lymphoma, and so forth.

75 antle cell lymphoma and diffuse large B-cell lymphoma, and supports constitutive expression of CYCLIN

76 heimer's disease, Parkinson's disease, brain lymphomas, and other ailments.

77 In high-grade B-cell lymphoma, angiogenesis correlates with poor prognosis, b

78 nds on the tissue compartment from which the lymphomas are derived.

79 mic architecture of carcinomas, sarcomas and lymphomas arising in the same animals are significantly

80 as a target for the treatment of subsets of lymphomas as well as autoimmune diseases, and there is a

81 mise-associated lymphoproliferative diseases/lymphomas as well as epithelial cell-derived nasopharyng

82 ional Working Group criteria for non-Hodgkin lymphoma, assessed by an independent radiology committee

83 Delta3A caused B cell lymphomas at rates similar to their induction by WT EBV

84 ell-of-origin and alter interactions between lymphoma B-cells and other cells within the microenviron

85 B-cell non-Hodgkin lymphomas (B-NHL) represent the most common type of hema

86 Members of the B-cell lymphoma (BCL-2) protein family regulate mitochondrial o

87 Residual mNK cells in spleens of MYC(ON) T-lymphoma-bearing mice exhibit perturbations in the termi

88 ssion of a BL/B-AL included in Non-Hodgkin's Lymphoma-Berlin-Frankfurt-Munster studies between 1986 a

89 ast implant-associated anaplastic large cell lymphoma (BI-ALCL) remain elusive.

90 ast implant-associated anaplastic large-cell lymphoma (BIA-ALCL) is a CD30-positive, anaplastic lymph

91 citabine treatment of latency I EBV+ Burkitt lymphoma (BL) sensitized cells to lysis by EBV-specific

92 rge B cell lymphoma (GCB-DLBCL), and Burkitt lymphoma (BL).

93 ast implant-associated anaplastic large cell lymphoma (breast implant ALCL) is an uncommon T cell lym

94 amide ((18)F-ISO-1) to image solid tumors in lymphoma, breast cancer, and head and neck cancer has be

95 rPan Viewer on publicly available follicular lymphoma, breast cancer, and multiple myeloma data.

96 19-CAR-ML NK cells controlled lymphoma burden in vivo and improved survival in human x

97 ng B-cell development are hijacked in B-cell lymphoma by genetic alterations that directly or indirec

98 for cancer in patients with lung cancer and lymphoma by using a convolutional neural network is feas

99 Casitas B-lineage lymphoma (c-Cbl) is a recently identified ubiquitin liga

100 step toward automated PET/CT assessment for lymphoma.(C) RSNA, 2020.

101 was formed between anti-CD20 antibodies and lymphoma cancer cell receptors.

102 The performance of the immunosensor for lymphoma cancer cells in clinical blood samples is consi

103 and tested for the impedimetric detection of lymphoma cancer cells, a blood cancer biomarker.

104 The risk of misdiagnosis as more aggressive lymphomas, causing patient overtreatment, needs also to

105 Loss of FBXW7 inhibited diffuse large B-cell lymphoma cell growth and further sensitized cells to OxP

106 nd reinforce PRMT5's relevance for promoting lymphoma cell growth and survival.

107 For effective lymphoma cell killing in vivo, we further functionalized

108 or cholesterol depleting therapy, we treated lymphoma cell lines known to be sensitive to the reducti

109 All compounds were further tested on six lymphoma cell lines, and eight showed potent growth inhi

110 ed in germinal centre B cells, the Burkitt's lymphoma cell of origin, providing a molecular link betw

111 edicted targets of these miRNAs, and reduced lymphoma cell survival.

112 with HDL NPs in cholesterol uptake-addicted lymphoma cells abolishes GPX4, resulting in cancer cell

113 EZH2 mutant human lymphoma cells also require multiple divisions before H3

114 nal silencing of tumor-suppressing miRNAs in lymphoma cells and reinforce PRMT5's relevance for promo

115 esistance to CX-5461 in previously sensitive lymphoma cells confers collateral resistance to the topo

116 Recent data suggest that lymphoma cells dependent upon lipoprotein-mediated chole

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

118 We also discuss how oncogenic alterations in lymphoma cells may affect the cellular composition of th

119 A few lymphoma cells were sufficient to activate the angiogeni

120 within transplanted fully malignant Emu-Myc lymphoma cells, we significantly extended transplant rec

121 es a metabolic crisis and selective death of lymphoma cells.

122 -grade B cell lymphoma (diffuse large B cell lymphoma) cells.

123 ade is highly effective in classical Hodgkin lymphomas (cHLs), which exhibit frequent copy-number gai

124 imary cancer diagnosis, including leukaemia, lymphoma, CNS tumours, neuroblastoma, Wilms tumour, soft

125 s and enhanced their cytotoxic activity in a lymphoma coculture system.

126 ion in 7 postmenopausal female patients with lymphoma compared to healthy controls using electrochemi

127 at increased risk of Hodgkin and non-Hodgkin lymphoma compared with HIV-negative individuals.

128 patients with relapsed or refractory Hodgkin lymphoma, consistent with experience in adult patients.

129 mphomas constituted 99% (n = 258) and T-cell lymphomas constituted 1% (n = 2).

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

131 lin D3 is overexpressed in ~50% of Burkitt's lymphoma correlating with a mutation of Thr-283.

132 f spontaneous liver tumorigenesis and B-cell lymphoma development at old age.

133 conferring selective advantage during B-cell lymphoma development.

134 that induce the development of leukaemia and lymphoma did not transform Ifitm3(-/-) B cells.

135 ficiently bind B cells and high-grade B cell lymphoma (diffuse large B cell lymphoma) cells.

136 CL2, BCL6, or both (double-hit or triple-hit lymphoma), diffuse large B-cell lymphoma transformed fro

137 patients with NLPHL who had received Hodgkin lymphoma-directed first-line treatment in randomized GHS

138 ty-four patients (with pathologically proven lymphoma disease) underwent staging (18)F-FDG PET/CT sca

139 oma (FL) (n = 26, 10%), diffuse large B-cell lymphoma (DLBCL) (n = 25, 10%), and mantle cell lymphoma

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

141 lapsed/refractory (R/R) diffuse large B-cell lymphoma (DLBCL) are limited, with no standard of care;

142 nscriptomic analysis of diffuse large B-cell lymphoma (DLBCL) from the British Columbia population-ba

143 herapeutic advances for diffuse large B-cell lymphoma (DLBCL) have led to an increasing number of sur

144 susceptibility loci for diffuse large B-cell lymphoma (DLBCL) in individuals of European ancestry thr

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

146 Diffuse large B-cell lymphoma (DLBCL) may present initially in bone marrow, l

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

148 f total TFA levels with diffuse large B cell lymphoma (DLBCL) risk [n = 98 cases; OR (95% CI) per 1 S

149 that ATM deficiency in diffuse large B-cell lymphoma (DLBCL) significantly induce mitochondrial deac

150 cular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL) within the context of prior knowledge,

151 vated B-cell-like (ABC) diffuse large B-cell lymphoma (DLBCL) xenograft model, but this compound suff

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

153 ts newly diagnosed with diffuse large B-cell lymphoma (DLBCL).

154 nmet clinical needs for diffuse large B-cell lymphoma (DLBCL).

155 et for the treatment of diffuse large B-cell lymphoma (DLBCL).

156 ecurrent and refractory diffuse large B cell lymphomas (DLBCL).

157 Anti-lymphoma efficacy of the APDC nanotherapeutics was evalu

158 r imbalance and splenic marginal zone B-cell lymphoma-emerged in combination with gene dose reduction

159 ubtypes were extranodal marginal zone B-cell lymphoma (EMZL) (n = 177, 68%), follicular lymphoma (FL)

160 Primary cutaneous lymphomas encompass a wide spectrum of rare lymphoprolif

161 daptation of NK cells to the fatty-acid rich lymphoma environment.

162 (EBV) is a human herpesvirus that can cause lymphomas, epithelial cancers, and other diseases, most

163 l lymphoma (EMZL) (n = 177, 68%), follicular lymphoma (FL) (n = 26, 10%), diffuse large B-cell lympho

164 tly published studies centered on follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL)

165 A minority of patients with follicular lymphoma (FL) undergo histological transformation (HT).

166 the origin of malignancy, namely follicular lymphoma (FL), GC B cell-diffuse large B cell lymphoma (

167 ET in the assessment of diffuse large B-cell lymphoma, follicular lymphoma, and peripheral T-cell lym

168 nts with relapsed and refractory mantle cell lymphoma following prior failed Bruton's tyrosine kinase

169 Combined RNA-seq and ChIP-seq analysis of lymphomas from Lck-Dlx5;Lck-MyrAkt mice demonstrated tha

170 Duodenal involvement in adenocarcinoma, lymphoma, gastrointestinal stromal tumours, Crohn's dise

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

172 roved survival of most patients with Hodgkin lymphoma globally is a triumph of the complementary appr

173 mediastinal B-cell lymphoma, and follicular lymphoma grade 3B.

174 ls without eliminating A20-luciferase B-cell lymphoma graft-versus-leukemia (GVL).

175 was higher in the AML/MDS group than in the lymphoma group (P <= 0.05) or the multiple myeloma group

176 ors in the combined patient group and in the lymphoma group, and neutrophil engraftment (p = 0.008) i

177 -positive relapsed or refractory non-Hodgkin lymphoma, had an Eastern Cooperative Oncology Group perf

178 the treatment of multiple myeloma and B-cell lymphomas has made the ubiquitin pathway an important em

179 While some of the immune cells present in lymphoma have effector function, the immune system is un

180 Other B cell lymphomas have acquired an oncogenic mutation in the mye

181 However, subsequent investigations in lymphomas have uncovered a significant heterogeneity of

182 l diseases, including some peripheral T-cell lymphomas, hemophagocytic lymphohistiocytosis, and chron

183 RF4 cases; and 12 cases of high-grade B-cell lymphoma (HGBCL), NOS in patients <=25 years using an in

184 ical subgroups included diffuse large B-cell lymphoma, high-grade B-cell lymphoma with rearrangements

185 oL) after diagnosis and treatment of Hodgkin lymphoma (HL) are still unknown because large longitudin

186 A unique feature of Hodgkin lymphoma (HL) is the presence of CD4+ T cells that surro

187 al/iatrogenic) are known to increase Hodgkin lymphoma (HL) risk, but the effects of allergic immune d

188 In first-line treatment of Hodgkin lymphoma (HL), Deauville scores 1-3 define complete meta

189 YC/IGH chromosome translocation in Burkitt's lymphoma, homozygous Mnt deletion greatly reduced lympho

190 The optimal strategy for this highly curable lymphoma, however, remains a topic of intense discussion

191 Hepatosplenic T-cell lymphoma (HSTCL) is a rare T-cell neoplasm that most com

192 ic interventions for treating EBV-associated lymphomas.IMPORTANCE Epstein-Barr virus (EBV), as the fi

193 w the mechanisms of T cell control of B cell lymphoma in gammaHV-infected mice overlap with those nec

194 nt oncogenic herpesvirus that induces T-cell lymphoma in infected chickens.

195 percent (two of 25) of examinations failed (lymphoma in one patient and technical failure in one pat

196 n for relapsed aggressive B-cell non-Hodgkin lymphoma in part on the basis of durable remission rates

197 recommendations for the treatment of Burkitt lymphoma in patients with HIV on the basis of retrospect

198 xis of monocytes in a syngeneic mouse T-cell lymphoma in skin.

199 eved complete separation between uveitis and lymphoma in the aqueous data set.

200 ed therapies to effectively treat MYC-driven lymphomas in the future.

201 oma, homozygous Mnt deletion greatly reduced lymphoma incidence by enhancing apoptosis and markedly d

202 expressed in aggressive B-cell non-Hodgkin's lymphomas, including mantle cell lymphoma and diffuse la

203 nts with relapsed or refractory large B-cell lymphomas, including those with diverse histological sub

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

205 relapsed or refractory diffuse large B-cell lymphoma ineligible for autologous stem-cell transplanta

206 Lymphoma-intrinsic MYC arrests NK maturation by transcri

207 Cutaneous T-cell lymphoma is a form of non-Hodgkin lymphoma that manifest

208 For example, classical Hodgkin lymphoma is characterized by an inflammatory environment

209 large B-cell lymphoma and peripheral T-cell lymphoma is potential cure, during which PET is mainly u

210 Lymphoma is the most common type of canine hematological

211 pheral blood involvement by cutaneous T-cell lymphoma is typically assessed by flow cytometry and pla

212 ng Tfh cells for the treatment of GC-derived lymphomas is discussed.

213 We discovered anaplastic lymphoma kinase (ALK) as a candidate thinness gene.

214 s of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) blocked D2R desensitization in neu

215 35) translocation which fuses the Anaplastic Lymphoma Kinase (ALK) gene with the Nucleophosmin (NPM)

216 Anaplastic lymphoma kinase (Alk) is a receptor tyrosine kinase of t

217 ined that the Midkine-a receptor, anaplastic lymphoma kinase, is upstream of the HLH regulatory prote

218 ma (BIA-ALCL) is a CD30-positive, anaplastic lymphoma kinase-negative T-cell lymphoma.

219 Pediatric large B-cell lymphomas (LBCLs) share morphological and phenotypic fea

220 er category of the disease-peripheral T-cell lymphoma-let alone any of the specific subtypes, except

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

222 a wide range of tumor cell types, including lymphoma, lung, glioblastoma, breast cancer, and several

223 GC B cell lymphomas maintain their GC transcriptional signatures a

224 phoma (DLBCL) (n = 25, 10%), and mantle cell lymphoma (MCL) (n = 17, 7%).

225 , open-label, phase III European Mantle Cell Lymphoma (MCL) Elderly trial (ClinicalTrials.gov identif

226 Mantle cell lymphoma (MCL) is a mature B-cell neoplasm initially dri

227 Mantle cell lymphoma (MCL) is an uncommon B-cell non-Hodgkin lymphom

228 B lymphoma Mo-MLV insertion region 1 (BMI1) has been repor

229 f IL-1 and IL-6 in a xenotransplanted B-cell lymphoma model without affecting CD19-specific CAR T-cel

230 ond malignancy during follow-up (non-Hodgkin lymphoma, n = 13; leukemia, n = 6; solid tumor, n = 25;

231 of self-reported TFA intake with non-Hodgkin lymphoma (NHL) risk.

232 homa (MCL) is an uncommon B-cell non-Hodgkin lymphoma (NHL) that is incurable with standard therapies

233 Patients with non-Hodgkin lymphoma (NHL) who are treated with rituximab may develo

234 his proof-of-concept study, 11 patients with lymphoma of the CNS (8 primary and 3 secondary involveme

235 histologically verified primary or secondary lymphoma of the lacrimal gland were included.

236 We treated 20 patients with B-cell lymphoma on a phase I, first-in-human clinical trial of

237 The dependency of lymphomas on MNT for survival suggests that drugs inhibi

238 ractory CD19-positive cancers (non-Hodgkin's lymphoma or chronic lymphocytic leukemia [CLL]).

239 uptake in the leukemia/MDS group than in the lymphoma or multiple myeloma group.

240 urinary, gynecological, head and neck, lung, lymphoma, or melanoma cancers were eligible.

241 urs mostly in adults secondary to infection, lymphoma, or rheumatic disease.

242 ouse, we identified 31 447 breast cancer and lymphoma patients (age >=18 years) who were treated with

243 rthermore, 19-CAR-ML NK cells generated from lymphoma patients exhibited improved responses against t

244 Because some treated lymphoma patients experience relapse and die, targeting

245 have the potential to improve the outcome of lymphoma patients.

246 ciated with lower median overall survival in lymphoma patients.

247 ANCE One hundred percent of primary effusion lymphoma (PEL) cases are associated with Kaposi sarcoma-

248 nt for Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and multicentric Castleman disease (MCD)

249 ent of Kaposi's sarcoma and primary effusion lymphoma (PEL).

250 f Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL).

251 ion and similarities with primary extranodal lymphomas (PENLs).

252 lead to a striking extranodal immunoblastic lymphoma phenotype that mimics the human disease.

253 -cell lymphoma transformed from any indolent lymphoma, primary mediastinal B-cell lymphoma, and folli

254 ypersprouting morphology was orchestrated by lymphoma-provided VEGFC and lymphotoxin (LT).

255 In relapsed/refractory Hodgkin lymphoma (R/R HL), immunotherapies such as the anti-prog

256 of consecutive patients with lung cancer or lymphoma referred to a single center from August 2011 to

257 POCH-R therapy is effective in adult Burkitt lymphoma regardless of age or HIV status and was well to

258 However, control of lymphoma remained intact in the absence of CD4 T cells.

259 ting common antigens for Vdelta1 and Vdelta2 lymphomas respectively.

260 matin conformation in a diffuse large B-cell lymphoma sample; and (4) the systematic identification o

261 mours were melanoma (eight patients, 17.8%), lymphoma (seven patients, 15.6%), and prostate carcinoma

262 cell subsets from 86 patients without T-cell lymphoma showed polytypic TRBC1 staining, except for fiv

263 lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL).

264 with high-risk, mature B-cell non-Hodgkin's lymphoma (stage III with an elevated lactate dehydrogena

265 ithin phase 3 trials of the German Low-Grade Lymphoma Study Group, were comparatively analyzed.

266 blood transplantations and adjusted for age, lymphoma subtype, and disease status, survival was lower

267 The most frequent lymphoma subtypes were extranodal marginal zone B-cell l

268 In multiple lymphoma subtypes, malignant B cells hijack AgR signalin

269 kemia (T-ALL) and T-cell acute lymphoblastic lymphoma (T-LBL) are aggressive hematological malignanci

270 ative mucositis (p = 0.769), more often with lymphoma than MM (p = 0.009).

271 ous T-cell lymphoma is a form of non-Hodgkin lymphoma that manifests initially in the skin and dissem

272 ch as acute leukemia or diffuse large B-cell lymphoma that require rapid interventions.

273 d transplantation for Hodgkin or non-Hodgkin lymphoma, the data support haploidentical related donor

274 ike the malignant cells in classical Hodgkin lymphoma, the disease-defining lymphocyte-predominant ce

275 only observed across various types of T-cell lymphomas, the extent of deregulation is significantly h

276 ted cancer, and CLL/SLL forms of non-Hodgkin lymphomas; these cancers were associated with HLA class

277 ological cancer cell lines, including B-cell lymphomas, to the potent pan-NMT inhibitor PCLX-001.

278 r triple-hit lymphoma), diffuse large B-cell lymphoma transformed from any indolent lymphoma, primary

279 e with rituximab in patients with follicular lymphoma treated in the CALGB 50401 (Alliance; NCT002382

280 PET-Guided Therapy of Aggressive Non-Hodgkin Lymphomas trial, iPET scans of 596 patients originally e

281 cterize viable, necrotic and apoptotic human lymphoma U937 cells.

282 assessment of BMI in patients diagnosed with lymphoma using (18)F-FDG PET/CT.

283 retreated relapsed or refractory non-Hodgkin lymphoma warrants further investigation as a chemotherap

284 ith relapsed or refractory classical Hodgkin lymphoma was a post-hoc decision.

285 ed, prospective clinical trial in large cell lymphoma, we conducted serial fluorodeoxyglucose positro

286 nvironment promotes tumour growth in Hodgkin lymphoma, we hypothesised that activating immunity might

287 In this Review of HIV-associated Burkitt lymphoma, we summarise expert opinion and provide genera

288 usly untreated patients with classic Hodgkin lymphoma were eligible for study enrolment if they were

289 otal, 1695 patients with mature T-cell or NK lymphomas were enrolled between Oct 12, 2006 and Feb 28,

290 ncy (leukaemia, myelodysplastic syndrome, or lymphoma), were between 16 and 70 years of age, eligible

291 (breast implant ALCL) is an uncommon T cell lymphoma, which is associated with textured surface brea

292 relapsed or refractory diffuse large B-cell lymphoma who are ineligible for autologous stem-cell tra

293 ins undiagnosed in patients with non-Hodgkin lymphoma who received first-line R-CHOP or CHOP.

294 wly diagnosed, untreated mature T-cell or NK lymphomas (WHO 2001 or 2008 classifications) from 74 cen

295 istologically confirmed diffuse large B-cell lymphoma, who relapsed or had refractory disease after p

296 T represents a novel diagnostic tool for CNS lymphoma with potential implications for theranostic app

297 ent treated with obinutuzumab for follicular lymphoma with protracted COVID-19 and viremia.

298 use large B-cell lymphoma, high-grade B-cell lymphoma with rearrangements of MYC and either BCL2, BCL

299 experience relapse and die, targeting B-cell lymphomas with a NMT inhibitor potentially provides an a

300 ne environments associated with major B-cell lymphomas with an emphasis on the immune escape pathways

301 The Delta3A virus caused lymphomas with delayed onset compared to the onset of th

302 in vivo on a panel of three patient-derived lymphoma xenografts derived from two patients with R/R B