ライフサイエンスコーパス: chronic lymphocytic leukemia

1 F3B1 mutations (myelodysplastic syndrome and chronic lymphocytic leukemia).

2 oclax is a BH3 mimetic approved for treating chronic lymphocytic leukemia.

3 -15b/16-2 loss in the pathogenesis of B-cell chronic lymphocytic leukemia.

4 L), two had indolent lymphomas, and four had chronic lymphocytic leukemia.

5 ib has outstanding activity in patients with chronic lymphocytic leukemia.

6 mice, which develop disease resembling human chronic lymphocytic leukemia.

7 at comparable concentrations efficacious in chronic lymphocytic leukemia.

8 roves progression-free survival in high-risk chronic lymphocytic leukemia.

9 atment of a specific subset of patients with chronic lymphocytic leukemia.

10 gion are important in clinical management of chronic lymphocytic leukemia.

11 nd diseased tissues in colorectal cancer and chronic lymphocytic leukemia.

12 r, gastric, brain cancers, neuroblastoma and chronic lymphocytic leukemia.

13 CR was more than 30 months in a patient with chronic lymphocytic leukemia.

14 in treatment of B cell malignancies such as chronic lymphocytic leukemia.

15 D88(L265P) mutation is found in 2% to 10% of chronic lymphocytic leukemia, 29% of activated B-cell ty

16 s in patients with asymptomatic, early-stage chronic lymphocytic leukemia; (4) do not test or treat f

17 with the evaluation of clinical response in chronic lymphocytic leukemia according to the 2008 Inter

18 Conclusion Relapse of chronic lymphocytic leukemia after ibrutinib is an issue

19 ization to metformin in multiple myeloma and chronic lymphocytic leukemia and a number of solid tumor

20 1 are also implicated in the pathogenesis of chronic lymphocytic leukemia and Aicardi-Goutieres syndr

21 A man in his early 70s with a diagnosis of chronic lymphocytic leukemia and being treated with pred

22 Although some of these have activity against chronic lymphocytic leukemia and hairy cell leukemia, in

23 ibitor shows impressive clinical activity in chronic lymphocytic leukemia and indolent B cell non-Hod

24 ecifically, we uncovered tsRNA signatures in chronic lymphocytic leukemia and lung cancer and demonst

25 Responses also occurred in chronic lymphocytic leukemia and lymphoma.

26 eCyPA also promoted the migration of chronic lymphocytic leukemia and lymphoplasmacytic lymph

27 g phase III clinical trials in patients with chronic lymphocytic leukemia and mantle-cell lymphoma.

28 ll lymphoma, Waldenstroms macroglobulinemia, chronic lymphocytic leukemia and multiple myeloma.

29 numerous tumors including multiple myeloma, chronic lymphocytic leukemia, and DLBCL.

30 cute leukemia, non-Hodgkin lymphomas such as chronic lymphocytic leukemia, and multiple myeloma.

31 ruton tyrosine kinase inhibitor ibrutinib in chronic lymphocytic leukemia, arsenic trioxide in acute

32 aling substantially changed the treatment of chronic lymphocytic leukemia as the first targeted agent

33 f 40% knockout mice, a characteristic of the chronic lymphocytic leukemia-associated phenotype found

34 complex and constitutively active in B-cell chronic lymphocytic leukemia (B-CLL) cells, resulting in

35 n detected in the peripheral blood of B-cell chronic lymphocytic leukemia (B-CLL) patients, but displ

36 Clinical progression of B cell chronic lymphocytic leukemia (B-CLL) reflects the clone'

37 atment of B cell neoplasms, including B cell chronic lymphocytic leukemia (B-CLL).

38 ectly interacted with the oncoprotein B cell chronic lymphocytic leukemia (BCL6) and induced lysine 6

39 The finding that in chronic lymphocytic leukemia, BCRs bind to an epitope on

40 Using transcriptome sequencing data from chronic lymphocytic leukemia, breast cancer and uveal me

41 ir activity against B cell lines and primary chronic lymphocytic leukemia cells in sera depleted of s

42 imethoxy and 3,4,5-trimethoxy derivatives in chronic lymphocytic leukemia cells revealed that co-trea

43 Moreover, PI(3,4)P2 depletion in primary chronic lymphocytic leukemia cells significantly impaire

44 demonstrated, with over two-thirds of B-cell chronic lymphocytic leukemia characterized by the deleti

45 ported on the poor outcomes of patients with chronic lymphocytic leukemia (CLL) after the discontinua

46 150) is the most abundantly expressed miR in chronic lymphocytic leukemia (CLL) and affects the thres

47 ation in hematopoietic stem cells results in chronic lymphocytic leukemia (CLL) and CD8-positive peri

48 olent B-cell non-Hodgkin lymphomas (NHLs) or chronic lymphocytic leukemia (CLL) and chronic HCV infec

49 ctors of poor survival and refractoriness in chronic lymphocytic leukemia (CLL) and have direct impli

50 examined the microRNAs (miRNAs) expressed in chronic lymphocytic leukemia (CLL) and identified miR-15

51 action of a long-known prognostic marker in chronic lymphocytic leukemia (CLL) and integrates its fu

52 of NHL revealed a striking contrast between chronic lymphocytic leukemia (CLL) and mantle cell lymph

53 ovided practice-changing results in relapsed chronic lymphocytic leukemia (CLL) and non-Hodgkin lymph

54 ssociation between the understood biology of chronic lymphocytic leukemia (CLL) and the therapeutics

55 Defining features of chronic lymphocytic leukemia (CLL) are not only its immu

56 hat have altered prognosis for patients with chronic lymphocytic leukemia (CLL) at diagnosis.

57 (ROR1) is an oncoembryonic antigen found on chronic lymphocytic leukemia (CLL) B cells, but not on n

58 point for progression-free survival (PFS) in chronic lymphocytic leukemia (CLL) based on 3 randomized

59 A subset of chronic lymphocytic leukemia (CLL) BCRs interacts with A

60 brutinib represents a therapeutic advance in chronic lymphocytic leukemia (CLL) but as monotherapy pr

61 BT-199) are changing treatment paradigms for chronic lymphocytic leukemia (CLL) but important problem

62 cally fit patients with previously untreated chronic lymphocytic leukemia (CLL) but not in those with

63 first description of the natural history of chronic lymphocytic leukemia (CLL) by David Galton in 19

64 rleukin (IL)-6 acts as a tumor suppressor in chronic lymphocytic leukemia (CLL) by inhibiting toll-li

65 Chronic lymphocytic leukemia (CLL) can be familial; howe

66 kemia) are present in approximately 4-13% of chronic lymphocytic leukemia (CLL) cases, where they are

67 dual disease (MRD) negativity, defined as <1 chronic lymphocytic leukemia (CLL) cell detectable per 1

68 rtant target for translational regulation in chronic lymphocytic leukemia (CLL) cells after B-cell re

69 nt5a enhanced proliferation and migration of chronic lymphocytic leukemia (CLL) cells and that these

70 Multiple studies show that chronic lymphocytic leukemia (CLL) cells are heavily dep

71 Chronic lymphocytic leukemia (CLL) cells depend on micro

72 Circulating chronic lymphocytic leukemia (CLL) cells display an abno

73 Chronic lymphocytic leukemia (CLL) cells express poor le

74 and intact B-cell-receptor (BCR) signaling, chronic lymphocytic leukemia (CLL) cells fail to undergo

75 a critical role for homing and retention of chronic lymphocytic leukemia (CLL) cells in tissues such

76 ate a microenvironmental glycolytic shift in chronic lymphocytic leukemia (CLL) cells mediated by Not

77 Chronic lymphocytic leukemia (CLL) cells multiply and be

78 The crucial dependence of chronic lymphocytic leukemia (CLL) cells on signals deri

79 inhibit BCL2 in cells or induce apoptosis in chronic lymphocytic leukemia (CLL) cells or platelets, w

80 The proliferation of chronic lymphocytic leukemia (CLL) cells requires commun

81 stromal niche exerts a protective effect on chronic lymphocytic leukemia (CLL) cells, thereby also a

82 and shows high proapoptotic activity against chronic lymphocytic leukemia (CLL) cells, which may indi

83 driver of the proliferation and survival of chronic lymphocytic leukemia (CLL) cells.

84 nt malignancies, as it is known from primary chronic lymphocytic leukemia (CLL) cells.

85 B cells that rely on BCR signaling, such as chronic lymphocytic leukemia (CLL) cells.

86 We applied TEDG to a chronic lymphocytic leukemia (CLL) cohort of 70 patients

87 #8 is a distinctive subset of patients with chronic lymphocytic leukemia (CLL) defined by the expres

88 Human and mouse chronic lymphocytic leukemia (CLL) develops from CD5(+)

89 Chronic lymphocytic leukemia (CLL) displays remarkable e

90 A T-cell defect in chronic lymphocytic leukemia (CLL) due to disease and/or

91 Chronic lymphocytic leukemia (CLL) exhibits high remissi

92 mmune dysregulation is a cardinal feature of chronic lymphocytic leukemia (CLL) from its early stage

93 clinical efficacy displayed by ibrutinib in chronic lymphocytic leukemia (CLL) has been challenged b

94 Targeting B-cell receptor (BCR) signaling in chronic lymphocytic leukemia (CLL) has been successful w

95 The therapy of relapsed chronic lymphocytic leukemia (CLL) has changed dramatica

96 A better understanding of the biology of chronic lymphocytic leukemia (CLL) has led to significan

97 egative regulator of B and myeloid cells, in chronic lymphocytic leukemia (CLL) has not been well cha

98 Treatment of chronic lymphocytic leukemia (CLL) has shifted from chem

99 has been well established that patients with chronic lymphocytic leukemia (CLL) have an increased ris

100 Genome-wide association studies (GWAS) of chronic lymphocytic leukemia (CLL) have shown that commo

101 c venetoclax in patients with poor prognosis chronic lymphocytic leukemia (CLL) highlights the potent

102 ns(PEQ)) for detection of miRNA signature of chronic lymphocytic leukemia (CLL) in human serum.

103 ome (RS) is defined as the transformation of chronic lymphocytic leukemia (CLL) into an aggressive ly

104 Current treatment strategies for chronic lymphocytic leukemia (CLL) involve a combination

105 Chronic lymphocytic leukemia (CLL) is a B cell malignanc

106 Chronic lymphocytic leukemia (CLL) is a common B-cell ma

107 Chronic lymphocytic leukemia (CLL) is a common B-cell ma

108 Chronic lymphocytic leukemia (CLL) is a common lymphoid

109 Chronic lymphocytic leukemia (CLL) is a disease in which

110 Chronic lymphocytic leukemia (CLL) is a disease of an ac

111 Chronic lymphocytic leukemia (CLL) is a malignant diseas

112 Chronic lymphocytic leukemia (CLL) is a variable disease

113 Chronic lymphocytic leukemia (CLL) is an incurable disea

114 Chronic lymphocytic leukemia (CLL) is associated with a

115 Chronic lymphocytic leukemia (CLL) is characterized by c

116 Chronic lymphocytic leukemia (CLL) is characterized by i

117 Chronic lymphocytic leukemia (CLL) is characterized by t

118 Chronic lymphocytic leukemia (CLL) is characterized by t

119 Chronic lymphocytic leukemia (CLL) is characterized by t

120 Chronic lymphocytic leukemia (CLL) is characterized by t

121 The efficacy of OFA in patients with chronic lymphocytic leukemia (CLL) is limited by drug re

122 The pathogenesis of chronic lymphocytic leukemia (CLL) is stringently associ

123 B-cell chronic lymphocytic leukemia (CLL) is the most common ad

124 Chronic lymphocytic leukemia (CLL) is the most common ad

125 B-cell chronic lymphocytic leukemia (CLL) is the most common hu

126 Chronic lymphocytic leukemia (CLL) is the most common hu

127 B-cell chronic lymphocytic leukemia (CLL) is the most common le

128 Chronic lymphocytic leukemia (CLL) is the most common le

129 Chronic lymphocytic leukemia (CLL) is the most common le

130 Chronic lymphocytic leukemia (CLL) is the most common ly

131 the clinically relevant question of whether chronic lymphocytic leukemia (CLL) is transmitted throug

132 An unresolved issue in chronic lymphocytic leukemia (CLL) is whether IGHV3-21 g

133 investigations of chromosomal aberrations in chronic lymphocytic leukemia (CLL) led to a better under

134 (KI) therapy represents a paradigm shift in chronic lymphocytic leukemia (CLL) management, but data

135 ) represents an unsolved clinical problem of chronic lymphocytic leukemia (CLL) management.

136 ents with hypogammaglobulinemia secondary to chronic lymphocytic leukemia (CLL) or multiple myeloma (

137 (FDG/PET) in the management of patients with chronic lymphocytic leukemia (CLL) or Richter syndrome (

138 ion in a fraction of patients with high-risk chronic lymphocytic leukemia (CLL) or Richter's transfor

139 ruton tyrosine kinase inhibitor ibrutinib in chronic lymphocytic leukemia (CLL) or small lymphocytic

140 atic nitrogen mustards that selectively kill chronic lymphocytic leukemia (CLL) over normal lymphocyt

141 cR IG) has proved instrumental in dissecting chronic lymphocytic leukemia (CLL) pathogenesis.

142 On real data from a chronic lymphocytic leukemia (CLL) patient, we show that

143 Chronic lymphocytic leukemia (CLL) patients assigned to

144 eripheral blood mononuclear cells (PBMCs) of chronic lymphocytic leukemia (CLL) patients clearly stat

145 Current treatment of chronic lymphocytic leukemia (CLL) patients often result

146 Peripheral blood mononuclear cells from chronic lymphocytic leukemia (CLL) patients on clinical

147 Chronic lymphocytic leukemia (CLL) patients progressed e

148 proportion of long-term nonprogressors among chronic lymphocytic leukemia (CLL) patients suggests the

149 In chronic lymphocytic leukemia (CLL) patients with mutated

150 nt advances in the therapeutic management of Chronic Lymphocytic Leukemia (CLL) patients, this common

151 levels are increased in cells and plasma of chronic lymphocytic leukemia (CLL) patients.

152 cell transplantation (SCT) availability for chronic lymphocytic leukemia (CLL) patients.

153 ilencing of the 13q14 locus in a majority of chronic lymphocytic leukemia (CLL) patients.

154 herapy for high-risk and relapsed refractory chronic lymphocytic leukemia (CLL) patients.

155 CR) is first-line treatment of medically fit chronic lymphocytic leukemia (CLL) patients; however, de

156 B-cell receptor (BCR) signaling pathways in chronic lymphocytic leukemia (CLL) provides significant

157 which 78 previously untreated patients with chronic lymphocytic leukemia (CLL) received 8 cycles of

158 ations may impair prognosis of patients with chronic lymphocytic leukemia (CLL) receiving frontline t

159 Chronic lymphocytic leukemia (CLL) remains an incurable

160 rate that B-cell receptor (BCR) signaling in chronic lymphocytic leukemia (CLL) results in partial ac

161 amide couplet has become the backbone of the chronic lymphocytic leukemia (CLL) standard of care.

162 We recently reported that chronic lymphocytic leukemia (CLL) subgroups with distin

163 s, and high-level expression is required for chronic lymphocytic leukemia (CLL) survival.

164 Disease progression in patients with chronic lymphocytic leukemia (CLL) treated with ibrutini

165 alk between CD4(+) T cells and proliferating chronic lymphocytic leukemia (CLL) tumor B cells occurs

166 we studied the effect of USP7 inhibition in chronic lymphocytic leukemia (CLL) where the ataxia tela

167 fied T (CAR-T) cell therapy in patients with chronic lymphocytic leukemia (CLL) who had previously re

168 able to identify a subgroup of patients with chronic lymphocytic leukemia (CLL) who have an exception

169 ls from Emu-TCL1 transgenic mice resulted in chronic lymphocytic leukemia (CLL) with a biased reperto

170 ated in 54 patients with relapsed/refractory chronic lymphocytic leukemia (CLL) with adverse characte

171 Genetic instability is a feature of chronic lymphocytic leukemia (CLL) with adverse prognosi

172 Adoptive cell therapy of chronic lymphocytic leukemia (CLL) with chimeric antigen

173 , has been used to treat relapsed/refractory chronic lymphocytic leukemia (CLL) with prolongation of

174 iated with resistance to targeted therapy of chronic lymphocytic leukemia (CLL) with the Bruton's tyr

175 aches, we consider the targeted treatment of chronic lymphocytic leukemia (CLL) with tyrosine kinase

176 Chronic lymphocytic leukemia (CLL) with unmutated (U-CLL

177 mmunophenotypic analysis was consistent with chronic lymphocytic leukemia (CLL), and FISH results rev

178 antitumor immune responses are hallmarks of chronic lymphocytic leukemia (CLL), and PD-1/PD-L1 inhib

179 CYP3A genotype and outcome in patients with chronic lymphocytic leukemia (CLL), breast, or lung canc

180 improved outcomes for patients with relapsed chronic lymphocytic leukemia (CLL), but complete remissi

181 mponent, are associated with poor outcome in chronic lymphocytic leukemia (CLL), but how these contri

182 cription start (CpG+223) predicts outcome in chronic lymphocytic leukemia (CLL), but its impact relat

183 icking contributes to the clinical course of chronic lymphocytic leukemia (CLL), but to date, only st

184 In chronic lymphocytic leukemia (CLL), CD8(+) T cells exhib

185 ite the therapeutic efficacy of ibrutinib in chronic lymphocytic leukemia (CLL), complete responses a

186 CD49d is an unfavorable prognostic marker in chronic lymphocytic leukemia (CLL), definitive validatio

187 We found that in chronic lymphocytic leukemia (CLL), HIF-1alpha is a nove

188 vestigations of CD20 mAb-based therapies for chronic lymphocytic leukemia (CLL), including correlativ

189 -cell acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL), including the expans

190 ith more aggressive disease in patients with chronic lymphocytic leukemia (CLL), including those case

191 and Drug Administration for the treatment of chronic lymphocytic leukemia (CLL), mantle cell lymphoma

192 Despite the high incidence of chronic lymphocytic leukemia (CLL), metabolism of CLL ce

193 In chronic lymphocytic leukemia (CLL), neoplastic B cells e

194 pecific CD8+ T-cell function is preserved in chronic lymphocytic leukemia (CLL), on a background of g

195 s with indolent non-Hodgkin lymphoma (iNHL), chronic lymphocytic leukemia (CLL), or T-cell lymphoma (

196 h BTK inhibitors have transformed therapy in chronic lymphocytic leukemia (CLL), patients with high-r

197 R-15/16 is the most common genetic lesion in chronic lymphocytic leukemia (CLL), promoting overexpres

198 Within chronic lymphocytic leukemia (CLL), responses to 62% of

199 In chronic lymphocytic leukemia (CLL), the immunoglobulin h

200 In chronic lymphocytic leukemia (CLL), the increment in PBL

201 irst-line treatment of younger patients with chronic lymphocytic leukemia (CLL), there is little info

202 In human chronic lymphocytic leukemia (CLL), tumor B cells lodge

203 sented HLA class I and II ligands of primary chronic lymphocytic leukemia (CLL), we delineated a nove

204 ongitudinal whole genome sequencing study of chronic lymphocytic leukemia (CLL), we revealed a SAMHD1

205 to malignant B cells from 268 patients with chronic lymphocytic leukemia (CLL), we showed that tumor

206 the deregulation of the survival pathways in chronic lymphocytic leukemia (CLL), which is crucial to

207 , Paggetti et al present novel findings that chronic lymphocytic leukemia (CLL)-derived exosomes and

208 genome sequencing of bulk tumors, including chronic lymphocytic leukemia (CLL).

209 ibody with single-agent activity in relapsed chronic lymphocytic leukemia (CLL).

210 ti-CD20-opsonized B cells from patients with chronic lymphocytic leukemia (CLL).

211 ts in this pathway fail to control growth of chronic lymphocytic leukemia (CLL).

212 gnaling is a central pathogenetic pathway in chronic lymphocytic leukemia (CLL).

213 ant therapeutic advance for the treatment of chronic lymphocytic leukemia (CLL).

214 is a major barrier to effective treatment of chronic lymphocytic leukemia (CLL).

215 athways plays a major role in progression of chronic lymphocytic leukemia (CLL).

216 with chlorambucil for the initial therapy of chronic lymphocytic leukemia (CLL).

217 ented a significant treatment advancement in chronic lymphocytic leukemia (CLL).

218 of morbidity and mortality in patients with chronic lymphocytic leukemia (CLL).

219 ays an important role in the pathogenesis of chronic lymphocytic leukemia (CLL).

220 rstanding of the genomic alterations driving chronic lymphocytic leukemia (CLL).

221 proved the outcome of patients with relapsed chronic lymphocytic leukemia (CLL).

222 of cases of MBL have the immunophenotype of chronic lymphocytic leukemia (CLL).

223 B-cell lymphocytosis (MBL) is a precursor of chronic lymphocytic leukemia (CLL).

224 and (autoantigen)- mediated BCR signaling in chronic lymphocytic leukemia (CLL).

225 ctivity in patients with relapsed/refractory chronic lymphocytic leukemia (CLL).

226 cascade in the initiation and maintenance of chronic lymphocytic leukemia (CLL).

227 e genetic landscape and clonal complexity of chronic lymphocytic leukemia (CLL).

228 itor ibrutinib is effective in patients with chronic lymphocytic leukemia (CLL).

229 prolonged progression-free survival (PFS) in chronic lymphocytic leukemia (CLL).

230 ic advance in B cell malignancies, including chronic lymphocytic leukemia (CLL).

231 verall survival (OS) have been identified in chronic lymphocytic leukemia (CLL).

232 e-scale massively parallel DNA sequencing of chronic lymphocytic leukemia (CLL).

233 is a new targeted therapy for patients with chronic lymphocytic leukemia (CLL).

234 s significantly improved patient outcomes in chronic lymphocytic leukemia (CLL).

235 tinguish from mantle cell lymphoma (MCL) and chronic lymphocytic leukemia (CLL).

236 odulatory agent with therapeutic activity in chronic lymphocytic leukemia (CLL).

237 ociated with malignant progression of B cell chronic lymphocytic leukemia (CLL).

238 berrations or deregulated gene expression in chronic lymphocytic leukemia (CLL).

239 The most common leukemia is chronic lymphocytic leukemia (CLL).

240 excellent clinical activity in patients with chronic lymphocytic leukemia (CLL).

241 ignaling plays a key role in the behavior of chronic lymphocytic leukemia (CLL).

242 b has dramatically changed the management of chronic lymphocytic leukemia (CLL).

243 the two largest disease categories: AML and chronic lymphocytic leukemia (CLL).

244 (BCR) are now prominent in the treatment of chronic lymphocytic leukemia (CLL).

245 revealed the complex clonal heterogeneity of chronic lymphocytic leukemia (CLL).

246 promising clinical activity in patients with chronic lymphocytic leukemia (CLL).

247 ty, clonal evolution, and chemoresistance in chronic lymphocytic leukemia (CLL).

248 rituximab, in the majority of patients with chronic lymphocytic leukemia (CLL).

249 dard therapy for fit patients with untreated chronic lymphocytic leukemia (CLL).

250 acy for the treatment of relapsed/refractory chronic lymphocytic leukemia (CLL).

251 tissue contributes to disease progression in chronic lymphocytic leukemia (CLL).

252 mumab) for treatment of B-cell lymphomas and chronic lymphocytic leukemia (CLL).

253 classic chemoimmunotherapy in patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lym

254 d BTK active-site occupancy in patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lym

255 NF-kappaB is constitutively activated in chronic lymphocytic leukemia (CLL); however, the implica

256 t advance for the treatment of patients with chronic lymphocytic leukemia (CLL); however, their high

257 oclonal antibody (mAb), recently approved in chronic lymphocytic leukemia (CLL; B-cell CLL) and folli

258 nrolled subjects with relapsed or refractory chronic lymphocytic leukemia (CLL; n = 41) or non-Hodgki

259 n lymphoma [NHL], Hodgkin lymphoma [HL], and chronic lymphocytic leukemia [CLL]) outside of rare here

260 We applied our computational pipeline to 91 chronic lymphocytic leukemias (CLLs) that underwent whol

261 ording to the 2008 International Workshop on Chronic Lymphocytic Leukemia criteria.

262 onoclonal antibody alemtuzumab for high-risk chronic lymphocytic leukemia, defined as at least 1 of t

263 Unlike cells of chronic lymphocytic leukemia, FL cells expressed relativ

264 Risks of chronic lymphocytic leukemia, follicular lymphoma, and m

265 d by 2008 Modified International Workshop on Chronic Lymphocytic Leukemia guidelines) from 31 centres

266 uton tyrosine kinase (BTK) with ibrutinib in chronic lymphocytic leukemia has led to a paradigm shift

267 30 (60%), multiple myeloma in 17 (34%), and chronic lymphocytic leukemia in 3 (6%) patients.

268 ed from NK cells isolated from patients with chronic lymphocytic leukemia in an autologous setting.

269 ell lung cancer, acute myeloid leukemia, and chronic lymphocytic leukemia, in which the authors recon

270 In Emu-TCL1 mice with chronic lymphocytic leukemia, injection of the STING ago

271 ording to the 2008 International Workshop on Chronic Lymphocytic Leukemia (IWCLL) criteria and an Eas

272 response [PR]) by International Workshop on Chronic Lymphocytic Leukemia (IWCLL) criteria was 71% (1

273 e 149 donors had low-count MBL, including 99 chronic lymphocytic leukemia-like (66.4%), 22 atypical (

274 phocyte-associated antigen 4 (CTLA4), B-cell chronic lymphocytic leukemia/lymphoma 10 (BCL10), phosph

275 XIAP deficiency selectively impaired B-cell chronic lymphocytic leukemia/lymphoma 10 (BCL10)-mediate

276 ent domain family, member 11 (CARD11)-B-cell chronic lymphocytic leukemia/lymphoma 10 (BCL10)-mucosa-

277 ompounds, including topoisomerase II, B-cell chronic lymphocytic leukemia/lymphoma 2 (BCL2), and many

278 acute lymphoblastic leukemia (ALL; n = 47), chronic lymphocytic leukemia (n = 24), and non-Hodgkin l

279 ed or refractory kappa+ non-Hodgkin lymphoma/chronic lymphocytic leukemia (NHL/CLL) or multiple myelo

280 by 4 cancer types (chronic myeloid leukemia, chronic lymphocytic leukemia, non-Hodgkin lymphoma, and

281 tosus; lymphoproliferative disorders such as chronic lymphocytic leukemia or large granular lymphocyt

282 Subtype-specific analyses indicated that chronic lymphocytic leukemia or small lymphocytic lympho

283 We noted a marked association of sCD23 with chronic lymphocytic leukemia (ORSlope = 28, Ptrend = 7.2

284 the BCR itself unravels a novel concept for chronic lymphocytic leukemia pathogenesis.

285 Twenty-two previously untreated chronic lymphocytic leukemia patients underwent PET/CT f

286 her, SIRT3 protein expression was reduced in chronic lymphocytic leukemia primary samples and maligna

287 and hsa-miR-150-5p in normal healthy serum, chronic lymphocytic leukemia Rai stage 1 (CLL-1), and st

288 Patients with relapsed/refractory chronic lymphocytic leukemia received bendamustine and r

289 lymphoma (DLBCL; n = 34), DLBCL arising from chronic lymphocytic leukemia (Richter transformation; n

290 eatment of patients with relapsed refractory chronic lymphocytic leukemia (RR-CLL).

291 d among survivors of NHL, including 91 after chronic lymphocytic leukemia/small lymphocytic lymphoma

292 e positively associated with the risk of the chronic lymphocytic leukemia/small lymphocytic lymphoma

293 79% of patients with relapsed or refractory chronic lymphocytic leukemia/small lymphocytic lymphoma

294 e in several lymphoid malignancies (T-ALL, B-chronic lymphocytic leukemia, splenic marginal zone lymp

295 new prognostic score published by the German Chronic Lymphocytic Leukemia Study Group (GCLLSG).

296 ween 2000-2014 were found using the keywords chronic lymphocytic leukemia, upfront therapy, upfront t

297 ntle cell lymphoma, follicular lymphoma, and chronic lymphocytic leukemia, were enrolled.

298 CL-2 antagonist, venetoclax, was approved in chronic lymphocytic leukemia, where it has proven to be

299 We describe a case involving a patient with chronic lymphocytic leukemia who developed invasive A. b

300 We report on 237 patients with chronic lymphocytic leukemia who received first-line FCR