ライフサイエンスコーパス: lymphoma

1 ts aged 70 years or younger with primary CNS lymphoma.

2 L) is the most common subtype of non-Hodgkin lymphoma.

3 tial part of the management of patients with lymphoma.

4 diffuse large B-cell lymphoma and follicular lymphoma.

5 apeutic option for advanced-stage follicular lymphoma.

6 cell lymphoma and primary mediastinal B-cell lymphoma.

7 orting its use as a strong prognosticator in lymphoma.

8 he transformation of the underlying indolent lymphoma.

9 is the etiologic agent of PEL-an aggressive lymphoma.

10 ith previously untreated advanced follicular lymphoma.

11 a clinically validated target in mantle cell lymphoma.

12 ether TLR3 has same function against chicken lymphoma.

13 velopment, which could lead to lethal thymic lymphoma.

14 isk of human herpesvirus 8 (HHV8)-associated lymphoma.

15 strains derived from an HCV-positive B-cell lymphoma.

16 utic intervention in autoimmune diseases and lymphoma.

17 idepsin in patients with relapsed/refractory lymphoma.

18 lvement, orbital lymphoma, or other systemic lymphoma.

19 rnal older ages were associated with risk of lymphoma.

20 nd causes cell death in EBNA1-induced B cell lymphomas.

21 osensitive malignancies, particularly B-cell lymphomas.

22 well as MF, are frequently secondary eyelid lymphomas.

23 yet devastating complication of non-Hodgkin lymphomas.

24 ed enzymatic function of mutant EZH2 in some lymphomas.

25 wing intralesional treatment of murine A20 B-lymphomas.

26 pressed in normal naive B cells and ABC type lymphomas.

27 s favorable as the treatment results of MALT lymphomas.

28 (T-ALL) and in a subset of peripheral T-cell lymphomas.

29 are associated with cancer, including B cell lymphomas.

30 o-occurrence of MYD88 and CD79B mutations in lymphomas.

31 was confirmed in 5 patients (0.7%; 2 lung, 1 lymphoma, 1 thyroid, and 1 base of tongue).

32 sarcoma [498.11, 477.82-519.03], non-Hodgkin lymphoma [11.51, 11.14-11.89], and cervix [3.24, 2.94-3.

33 rase II, B-cell chronic lymphocytic leukemia/lymphoma 2 (BCL2), and many tyrosine kinase inhibitors (

34 ted levels of Mcl-1, an antiapoptotic B-cell lymphoma 2 family member, with selective reduction of de

35 The Bcl-2 (B-cell lymphoma 2) protein Bax (Bcl-2 associated X, apoptosis r

36 n of downstream genes, such as Bcl-2 (B-cell lymphoma 2), c-Myc, MMP7 (matrix metalloproteinase-7), a

37 Purpose B-cell leukemia/lymphoma-2 (BCL-2) overexpression is common in many non-

38 ortions for malignant lesions (carcinoma and lymphoma; 27/76, 36%) and benign dacryoadenitis (15%) we

39 ples comprised 36,920 newly diagnosed mature lymphomas, 321 precursor lymphoid neoplasms, 314 myeloid

40 n 6 of 14 patients with diffuse large B-cell lymphoma (43%; 95% CI, 18 to 71) and 10 of 14 patients w

41 s conducted of 115 consecutive patients with lymphomas (45 females, 70 males; mean age of 46 years).

42 B cell lymphoma-6 (Bcl-6) is a transcriptional repressor that i

43 .03], liver [3.21, 3.02-3.41], and Hodgkin's lymphoma [7.70, 7.20-8.23]), and some virus-unrelated ca

44 to 71) and 10 of 14 patients with follicular lymphoma (71%; 95% CI, 42 to 92).

45 cancer (92 patients, 426 scans), non-Hodgkin lymphoma (77 patients, 208 scans), Hodgkin disease (41 p

46 occur, and in studies reporting only on MALT lymphomas (884 patients), the 5-year and 10-year disease

47 27 [3%]), including melanoma (18 [2.2%]) and lymphoma (9 [1.1%]).

48 histologic subtypes of lymphoma or non-MALT lymphomas (988 patients) reported local control rates to

49 pooled data from 2 phase 3 clinical trials (Lymphoma Academic Research Organization-CORAL and Canadi

50 lity for staging and treatment assessment in lymphoma according to the Lugano classification.

51 (WBCT) in staging and response assessment in lymphoma according to the Lugano classification.

52 s for thyroid, Hodgkin lymphoma, non-Hodgkin lymphoma, acute myeloid leukemia, soft-tissue sarcoma, a

53 gkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL) has had profound clinical success.

54 n underlying pediatric anaplastic large cell lymphomas (ALCL) and inflammatory myofibroblastic tumors

55 mphoma kinase (ALK)(-) anaplastic large cell lymphomas (ALCLs).

56 An EL4 mouse model of non-Hodgkin lymphoma and a B16 mouse model of subcutaneous melanoma

57 onstrated promising results in patients with lymphoma and are being tested in combination therapy tri

58 -W was overexpressed in diffuse large B cell lymphoma and correlated with decreased patient survival.

59 allenge the assumed two-hit model of Emu-Myc lymphoma and demonstrate a functional in vivo role for B

60 0, 2014, 11 patients (three with mantle cell lymphoma and eight with follicular lymphoma) were enroll

61 relapsed or refractory diffuse large B-cell lymphoma and follicular lymphoma.

62 ons have been discovered in primary leukemia/lymphoma and gastric cancer by human cancer genome seque

63 ved in lymphoma impact the classification of lymphoma and have significant implications for the diagn

64 ents presented with EBV-associated Hodgkin's lymphoma and hypogammaglobulinemia; one also had severe

65 ach as a screening technique for non-Hodgkin lymphoma and melanoma skin cancer.

66 at has been associated with primary effusion lymphoma and multicentric Castleman's disease, as well a

67 In patients with Hodgkin's lymphoma and peripheral T-cell lymphoma, treatment with

68 herapy in patients with diffuse large B-cell lymphoma and primary mediastinal B-cell lymphoma.

69 ding the biology and genetics of non-Hodgkin lymphoma and the availability of new diagnostic methods

70 sease are variable and depend on the type of lymphoma and/ or presence of adrenal insufficiency.

71 ruses are associated with the development of lymphomas and lymphoproliferative diseases, as well as s

72 A051201 (mantle cell lymphoma) and A051202 (follicular lymphoma) were phase 1

73 s were acute lymphoblastic leukemia, Hodgkin lymphoma, and astrocytoma.

74 sformation, mantle cell lymphoma, follicular lymphoma, and chronic lymphocytic leukemia, were enrolle

75 s the standard of care in B-cell non-Hodgkin lymphoma, and is administered over 1.5-6 h.

76 that BCL-W profoundly contributes to B cell lymphoma, and its expression could serve as a biomarker

77 in acute myeloid leukemia (AML), non-Hodgkin lymphoma, and multiple myeloma cells.

78 y lysed primary B-cell leukemia, mantle cell lymphoma, and multiple myeloma in vitro.

79 MYC in Burkitt lymphoma, BCL2 in follicular lymphoma, and MYC/BCL2/BCL6 in high-grade B-cell lymphom

80 at is highly expressed on B-cells and B cell lymphomas, and is a validated target for antibody and na

81 tment of advanced stages of this non-Hodgkin lymphoma are clearly warranted.

82 homa, and MYC/BCL2/BCL6 in high-grade B-cell lymphomas are essential for diagnosis.

83 cell cancers, although data regarding B-cell lymphomas are limited.

84 mpare in a large series of peripheral T cell lymphoma, as a model of diffuse disease, the prognostic

85 or relapsed and refractory peripheral T-cell lymphomas based on their activity, although they do not

86 stic rearrangements involving MYC in Burkitt lymphoma, BCL2 in follicular lymphoma, and MYC/BCL2/BCL6

87 ed B cell proliferations including Hodgkin's lymphoma because of a deficiency in CD70, the ligand of

88 colorectal, non-small-cell lung, non-Hodgkin lymphoma, breast, uterine, or cervical) from 2010 to 201

89 rs and is strongly associated with Hodgkin's lymphoma, Burkitt's lymphoma, diffuse large B-cell lymph

90 little effect on the ability of EBV to cause lymphomas but delays tumor onset.

91 promising clinical response rates in several lymphomas, but is not curative as monotherapy.

92 ising clinical activity in breast cancer and lymphomas, but it is not clear which additional Rb-posit

93 we discover neoantigens in human mantle-cell lymphomas by using an integrated genomic and proteomic s

94 Lymphomas can affect any organ in the body, present with

95 bring us closer to the goal of personalized lymphoma care.

96 Overall, 336 lymphoma cases occurred: 220 in unexposed patients (inci

97 egative control IgG2 in a CD20(+) human Raji lymphoma cell line.

98 usokine treatment led to direct apoptosis of lymphoma cell lines and primary tumors that otherwise we

99 hronic lymphocytic leukaemia and mantle cell lymphoma cell lines, and patients treated with idelalisi

100 mammary carcinoma cells, OVA-expressing EG7 lymphoma cells and CMS5 MCA-induced fibrosarcoma cells n

101 The lymphoma cells demonstrated chromosome instability along

102 Lymphoma cells from diffuse large B-cell lymphoma patien

103 sion diminished proliferation in primary and lymphoma cells in vitro.

104 measured signaling nodes, whereas follicular lymphoma cells represented the opposite pattern with no

105 increasing the sensitivity of receptor-less lymphoma cells to nutrient restriction.

106 unctional testing of primary patient-derived lymphoma cells using a library of 106 US Food and Drug A

107 se cells could mediate killing of autologous lymphoma cells.

108 yeloid cell leukemia 1 (MCL-1) and BCL-XL in lymphoma cells.

109 nd Reed-Sternberg cells of classical Hodgkin lymphoma (CHL) (uniform CD50 and variable CD58 for NLPHL

110 elapse (LR) in patients with classic Hodgkin lymphoma (cHL) are poorly understood.

111 ed-Sternberg (RS) cells of classical Hodgkin lymphoma (cHL) express multiple immunoregulatory protein

112 vade antitumor immunity in classical Hodgkin lymphoma (cHL).

113 -cell lymphomas, including classical Hodgkin lymphoma (cHL).

114 statistically significant increased risk of lymphoma compared with exposure to neither medication, a

115 Lymphoma, compared with BRLH, was associated with larger

116 Non-Hodgkin lymphoma comprises a variety of neoplasms, many of which

117 nvolvement in patients with cutaneous T-cell lymphoma (CTCL) portend a worse clinical outcome.

118 interleukin 21 (IL-21), which induces direct lymphoma cytotoxicity and activates immune effector cell

119 le-hit lymphomas (DHLs) and double-expressor lymphomas (DELs) are subtypes of diffuse large B-cell ly

120 utations in JAK2, CALR, or MPL In the B-cell lymphomas, detection of characteristic rearrangements in

121 l activation seemed to play a role in B-cell lymphoma development at early stages across different su

122 loss profoundly delayed MYC-mediated B cell lymphoma development due to increased MYC-induced B cell

123 In this article, we report rapid lymphoma development in Id2/Id3 double-knockout mice tha

124 Purpose Double-hit lymphomas (DHLs) and double-expressor lymphomas (DELs) a

125 ssociated with Hodgkin's lymphoma, Burkitt's lymphoma, diffuse large B-cell lymphomas, nasopharyngeal

126 (DELs) are subtypes of diffuse large B-cell lymphoma (DLBCL) associated with poor outcomes after sta

127 Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgk

128 Primary diffuse large B-cell lymphoma (DLBCL) of the ocular region is rare, and the u

129 r B-cell-like (non-GCB) diffuse large B-cell lymphoma (DLBCL).

130 naling in cell lines of diffuse large B-cell lymphoma (DLBCL).

131 role of this pathway in diffuse large B-cell lymphoma (DLBCL).

132 cular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL).

133 B cell-like subtypes of diffuse large B cell lymphoma (DLBCL).

134 trials of patients with diffuse large B-cell lymphoma (DLBCL).

135 lymphoma (FL; n = 29), diffuse large B-cell lymphoma (DLBCL; n = 34), DLBCL arising from chronic lym

136 reclassify a subset of diffuse large B-cell lymphomas (DLBCLs) and HGBLs with features intermediate

137 , CD20-positive grade 1, 2, or 3a follicular lymphoma; Eastern Co-operative Oncology Group performanc

138 about the function of TLR3 in chicken T-cell lymphoma, especially in signal pathway.

139 articularly poor compared with vitreoretinal lymphomas even in response to chemotherapy.

140 We also identified B-cell lymphoma-extra large (Bcl-xL) as a key survival factor i

141 iated gain-of-function alterations in B-cell lymphoma-extra large (Bcl-xL), Mdm4, and two TP53 family

142 eted by inactivating mutations in follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL).

143 Follicular lymphoma (FL) is a clinically and molecularly highly het

144 Purpose Follicular lymphoma (FL) is an indolent cancer, with effective but

145 Follicular lymphoma (FL) is an indolent malignancy of germinal cent

146 l event in the clinical course of follicular lymphoma (FL) patients.

147 ntle cell lymphoma (MCL; n = 28), follicular lymphoma (FL; n = 29), diffuse large B-cell lymphoma (DL

148 phoma, Richter's transformation, mantle cell lymphoma, follicular lymphoma, and chronic lymphocytic l

149 with RCDII, these Lin(-)IELs develop into a lymphoma for which no effective treatment is available.

150 comparing senescent and non-senescent B-cell lymphomas from Emu-Myc transgenic mice revealed substant

151 ctive, label-free sensor for the non-Hodgkin lymphoma gene, with an aM detection limit, utilizing ele

152 odgkin's lymphoma or anaplastic large-T-cell lymphoma, had biopsy-proven CD30-positive tumours, had a

153 nsify chemotherapy in aggressive non-Hodgkin lymphomas have, however, proved ineffective in patients

154 d 10% had an immune-mediated encephalopathy; lymphoma, hepatic encephalopathy and progressive multifo

155 ss immune evasion mechanisms in leukemia and lymphoma, highlighting key differences from solid tumors

156 g CD30 with monoclonal antibodies in Hodgkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL)

157 nt and end of treatment in pediatric Hodgkin lymphoma (HL) are limited.

158 or patients with relapsed/refractory Hodgkin lymphoma (HL) is essential for optimizing therapy with r

159 T) in children and young adults with Hodgkin lymphoma (HL) or non-Hodgkin lymphoma (NHL) and compared

160 Hodgkin lymphoma (HL) survivors treated with radiotherapy and/or

161 the standard of care in early-stage Hodgkin lymphoma (HL), and treatment intensity has been reduced

162 lapsed or refractory (R/R) classical Hodgkin lymphoma (HL).

163 patients with relapsed or refractory Hodgkin lymphoma (HL).

164 phocytic leukaemia (CLL, N = 1,842), Hodgkin lymphoma (HL, N = 1,465) and multiple myeloma (MM, N = 3

165 rucial part of the pathophysiology of B-cell lymphomas; however, several early attempts to target thi

166 time for patients with diffuse large B-cell lymphoma, illustrate the behavior of our methodology on

167 into the pathogenetic mechanisms involved in lymphoma impact the classification of lymphoma and have

168 Significant increases in lymphoma in both men (10-fold increase, P < .001) and wo

169 /or the screening and monitoring of indolent lymphoma in individual patients.

170 at an LMP1-deleted EBV mutant induces B cell lymphomas in a newly developed cord blood-humanized mous

171 us (EBV) infection is associated with B cell lymphomas in humans.

172 It causes lymphomas in individuals with acquired and innate immune

173 e ability to cause aggressive leukaemias and lymphomas in non-natural hosts, expresses seven small nu

174 disease response assessment in patients with lymphoma, including positron emission tomography and com

175 athways is a hallmark of a variety of B-cell lymphomas, including classical Hodgkin lymphoma (cHL).

176 The MALT-lymphoma International Prognostic Index (MALT-IPI) also

177 Randomisation was stratified by Follicular Lymphoma International Prognostic Index risk group and g

178 tratified by country, gender, and Follicular Lymphoma International Prognostic Index score (0-2 vs 3-

179 tures intermediate between DLBCL and Burkitt lymphoma into this new category.

180 Transformation to aggressive lymphoma is a critical event in the clinical course of f

181 s already approved to treat cutaneous T-cell lymphoma, it could potentially be used as a therapy for

182 Anaplastic lymphoma kinase (Alk) and leucocyte tyrosine kinase (Ltk

183 Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase phys

184 ransformation of T cells that are anaplastic lymphoma kinase (ALK) negative and CD30 positive.

185 ny T-cell malignancies, including anaplastic lymphoma kinase (ALK)(-) anaplastic large cell lymphomas

186 racterized in primary cutaneous large B-cell lymphoma, leg type.

187 n of low-signal-intensity regions (LSIRs) in lymphoma lesions and to compare these to fluorodeoxygluc

188 d rates of lung, kidney, and bladder cancer, lymphoma, leukemia, and unspecified metastatic cancer.

189 For MALT lymphomas, local control, disease-free survival, and ove

190 ed a comprehensive analysis of LR of Hodgkin lymphoma (LR-HL).

191 able deaths were associated with non-Hodgkin lymphoma, lung cancer, and liver cancer.

192 In 15 non-Hodgkin lymphomas, many more sst2 sites were labeled with the an

193 Double-hit lymphomas may arise as a consequence of the transformati

194 ucleotide antagonist of eIF4E in mantle cell lymphoma (MCL) cells.

195 SOX11 overexpression in mantle cell lymphoma (MCL) has been associated with more aggressive

196 Mantle cell lymphoma (MCL) may be 1 of the few cancers for which mul

197 ress-mediated drug resistance in mantle cell lymphoma (MCL); however, the biological functions of BAC

198 Results NHL subtypes included mantle cell lymphoma (MCL; n = 28), follicular lymphoma (FL; n = 29)

199 hanges (2.3%) mostly consisted of follicular lymphoma misgrading and diffuse large B-cell lymphoma su

200 ntly reduced tumor burden in a murine B-cell lymphoma model.

201 ation (IR)-induced replication stress T-cell lymphoma mouse model, we observed a significant inhibiti

202 mesothelioma; Hodgkin lymphoma; non-Hodgkin lymphoma; multiple myeloma; leukemia; and all other canc

203 stage IA through stage IIA) cutaneous T-cell lymphoma, mycosis fungoides (MF) type, resulted in clini

204 Marginal zone lymphoma (MZL) is a heterogeneous B-cell malignancy for

205 macroglobulinemia (n = 4), and marginal zone lymphoma (n = 3).

206 A-MCL frequently presented with disseminated lymphoma (n = 34 of 55; 62%), and were likely to experie

207 ma, Burkitt's lymphoma, diffuse large B-cell lymphomas, nasopharyngeal carcinoma (NPC), and lymphomas

208 ts with Hodgkin lymphoma (HL) or non-Hodgkin lymphoma (NHL) and compared the biodistribution of (11)C

209 ith relapsed or refractory (R/R) non-Hodgkin lymphoma (NHL) have a poor prognosis and limited treatme

210 ), we studied PCNSL and systemic non-Hodgkin lymphoma (NHL) in 288 029 solid organ transplant recipie

211 Non-Hodgkin lymphoma (NHL) is the most common AIDS-defining conditio

212 ary fat intake may contribute to non-Hodgkin lymphoma (NHL) pathogenesis by influencing carcinogen ex

213 overexpression is common in many non-Hodgkin lymphoma (NHL) subtypes.

214 failure (HF) among survivors of non-Hodgkin lymphoma (NHL).

215 NK cell lymphoma (NKCL) did not express significant levels of TC

216 Nodular lymphocyte Hodgkin lymphoma (NLPHL) is a rare disease for which the optimal

217 unger vs older patients for thyroid, Hodgkin lymphoma, non-Hodgkin lymphoma, acute myeloid leukemia,

218 rvous system; thyroid; mesothelioma; Hodgkin lymphoma; non-Hodgkin lymphoma; multiple myeloma; leukem

219 clinical activity of TGR-1202 in aggressive lymphoma not found with idelalisib.

220 gnostic indices for extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT).

221 cases reported were extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT).

222 stage (Ann Arbor stage III or IV) follicular lymphoma of WHO histological grades 1, 2, or 3a were ran

223 y confirmed relapsed or refractory Hodgkin's lymphoma or anaplastic large-T-cell lymphoma, had biopsy

224 to treat patients with diffuse large B-cell lymphoma or follicular lymphoma that had relapsed or was

225 uded data on multiple histologic subtypes of lymphoma or non-MALT lymphomas (988 patients) reported l

226 emotherapy (OR = 0.19, 95% CI 0.11-0.32) and lymphoma (OR = 0.18, 95% CI 0.11-0.28).

227 nd a diagnosis of breast cancer, non-Hodgkin lymphoma, or gynecologic cancers.

228 iteria were intraocular involvement, orbital lymphoma, or other systemic lymphoma.

229 present in lymph node biopsies of follicular lymphoma patents.

230 ated our results on human serum samples from lymphoma patients and healthy control subjects.

231 Moreover, CD8(+) T cells isolated from lymphoma patients express higher levels of Grail and low

232 Lymphoma cells from diffuse large B-cell lymphoma patients had high basal phosphorylation levels

233 ned by merging 3 independent cohorts of MALT lymphoma patients.

234 Primary central nervous system (CNS) lymphoma (PCNSL) and primary testicular lymphoma (PTL) a

235 Primary CNS lymphoma (PCNSL) is a rare form of extranodal non-Hodgki

236 the survival and growth of primary effusion lymphoma (PEL) cells.

237 Primary effusion lymphoma (PEL) is a highly aggressive B-cell malignancy

238 Primary effusion lymphoma (PEL) is a lymphogenic disorder associated with

239 rvival and proliferation of primary effusion lymphoma (PEL), an aggressive malignancy associated with

240 xal mucosa-associated lymphoid tissue (MALT) lymphoma (POAML) is the most common orbital tumor, there

241 icantly associated with diffuse large B cell lymphoma (pooled HR per SD: 1.47; 95% CI: 1.06, 2.05), w

242 re form of B cell lymphoma (primary effusion lymphoma) primarily observed in HIV-infected individuals

243 's disease, as well as a rare form of B cell lymphoma (primary effusion lymphoma) primarily observed

244 ally treated with R-CVP had a higher risk of lymphoma progression compared with those receiving R-CHO

245 domide 25 mg per day for 21 of 28 days until lymphoma progression or unacceptable toxicity (severely

246 to treatment with rituximab according to the lymphoma protocol (4 weekly infusions of 375 mg/m2).

247 Peripheral T-cell lymphomas (PTCL) are aggressive diseases with poor respo

248 CNS) lymphoma (PCNSL) and primary testicular lymphoma (PTL) are rare extranodal large B-cell lymphoma

249 th overall survival in primary vitreoretinal lymphoma (PVRL) and ocular adnexal (OA)-uveal DLBCL.

250 ; P < .001; lung cancer: R = 0.73; P < .001; lymphoma: R = 0.51; P < .001; melanoma: R = 0.36; P = .0

251 ge-matched controls if they were treated for lymphoma, received combination chemotherapy, and did not

252 Lymphomas represent a striking spectrum of clinical beha

253 Lymphomas represent clonal proliferations of lymphocytes

254 Non-Hodgkin lymphoma represents a wide spectrum of illnesses that va

255 histologies, including diffuse large B-cell lymphoma, Richter's transformation, mantle cell lymphoma

256 6 in HLA-DRB1) and mixed cellularity Hodgkin lymphoma (rs1633096, rs13196329, Val86 in HLA-DRB1).

257 n are observed for nodular sclerosis Hodgkin lymphoma (rs9269081, HLA-DPB1*03:01, Val86 in HLA-DRB1)

258 ransforming retrovirus AKT8 in rodent T-cell lymphoma/signal transducer and activator of transcriptio

259 lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) that was maintained at 24 hours.

260 er Center and University of Iowa/Mayo Clinic Lymphoma Specialized Program of Research Excellence).

261 national randomized International Extranodal Lymphoma Study Group 19 (IELSG-19) trial.

262 PI 2,3) of the German High-Grade Non-Hodgkin Lymphoma Study Group were analyzed with the Lymph2Cx ass

263 lymphoma misgrading and diffuse large B-cell lymphoma subtype misclassification.

264 ent, and the characteristics of the specific lymphoma subtype reflect those of the cell from which th

265 n slope and risk were strongest for indolent lymphoma subtypes.

266 e for treatment success or failure in common lymphoma subtypes.

267 dult mice induces T-cell acute lymphoblastic lymphoma (T-ALL), a tumor type known to carry CIC mutati

268 absence of gene amplification, e.g., T cell lymphoma (TCL).

269 diffuse large B-cell lymphoma or follicular lymphoma that had relapsed or was refractory to previous

270 SL) is a rare form of extranodal non-Hodgkin lymphoma that is typically confined to the brain, eyes,

271 mphomas, nasopharyngeal carcinoma (NPC), and lymphomas that develop in organ transplant recipients.

272 However, in many subtypes of lymphoma, the application of MRD assessment techniques,

273 re we sequence spontaneously arising Emu-Myc lymphomas to define transgene architecture, somatic muta

274 ith Hodgkin's lymphoma and peripheral T-cell lymphoma, treatment with bendamustine alone only achieve

275 ells that have infiltrated into transplanted lymphoma tumours, and Grail deficiency confers long-term

276 ad genomics findings that characterize these lymphoma types and discuss new therapeutic opportunities

277 The malignant cells also gave rise to lymphomas upon transfer to Rag-deficient and wild-type h

278 The results of treatment of non-MALT lymphomas using radiotherapy also were good, but they we

279 A mouse model of human B-cell lymphoma was utilized to test in vivo efficacy of AR160

280 are closely linked to MC and HCV-associated lymphomas, was specifically seen among IgM(+) memory B c

281 shop on CLL guidelines) or small lymphocytic lymphoma were eligible for this phase 1b, dose-escalatio

282 ents with relapsed or refractory mantle cell lymphoma were enrolled and all patients received treatme

283 m patients with newly diagnosed or suspected lymphomas were reviewed, according to the 2008 WHO class

284 ntle cell lymphoma and eight with follicular lymphoma) were enrolled.

285 ary body, lacrimal gland, or orbit (OA-uveal lymphoma) were included.

286 antle cell lymphoma) and A051202 (follicular lymphoma) were phase 1 trials.

287 s, 86% of patients with diffuse large B-cell lymphoma who had a response (95% CI, 33 to 98) and 89% o

288 3 to 98) and 89% of patients with follicular lymphoma who had a response (95% CI, 43 to 98) had maint

289 s or primary cutaneous anaplastic large-cell lymphoma who had been previously treated.

290 iesis in an external cohort of patients with lymphoma who were treated in a randomised trial of front

291 all survival among patients with mantle-cell lymphoma who were younger than 66 years of age at diagno

292 andard of care for patients with HIV-related lymphomas who otherwise meet standard transplant criteri

293 ssment into clinical trials in patients with lymphoma, will be critical to determine how best to depl

294 BCR signaling and is particularly active in lymphomas with mutations altering the BCR subunit CD79B

295 phoma (PTL) are rare extranodal large B-cell lymphomas with similar genetic signatures.

296 n accessibility profiles of cutaneous T cell lymphoma, with dynamic assessments of response and resis

297 .4), followed by CNS tumours (WSR 28.2), and lymphomas (WSR 15.2).

298 re preactivation but infiltrated a Burkitt's lymphoma xenograft and efficiently inhibited tumor growt

299 and macrophages infiltrate a human Burkitt's lymphoma xenograft and inhibit tumor growth, generating

300 und that shows durable tumor regression in a lymphoma xenograft model.