ライフサイエンスコーパス: lymphocytic leukemia

1 ations (myelodysplastic syndrome and chronic lymphocytic leukemia).

2 s-of-function mutations recurrent in chronic lymphocytic leukemia.

3 ich develop disease resembling human chronic lymphocytic leukemia.

4 f a specific subset of patients with chronic lymphocytic leukemia.

5 important in clinical management of chronic lymphocytic leukemia.

6 sed tissues in colorectal cancer and chronic lymphocytic leukemia.

7 ic, brain cancers, neuroblastoma and chronic lymphocytic leukemia.

8 ore than 30 months in a patient with chronic lymphocytic leukemia.

9 tment of B cell malignancies such as chronic lymphocytic leukemia.

10 d therapy over chemoimmunotherapy in chronic lymphocytic leukemia.

11 a BH3 mimetic approved for treating chronic lymphocytic leukemia.

12 nts with acute myelogenous leukemia or acute lymphocytic leukemia.

13 2 loss in the pathogenesis of B-cell chronic lymphocytic leukemia.

14 penetrance of cutaneous melanoma and chronic lymphocytic leukemia.

15 ine-rituximab in relapsed/refractory chronic lymphocytic leukemia.

16 as diffuse large B cell lymphoma and chronic lymphocytic leukemia.

17 -derived curative therapy in childhood acute lymphocytic leukemia.

18 dgkin lymphoma (3.53 [.48-25.9]) and chronic lymphocytic leukemia (1.45 [.45-4.66]) were increased bu

19 e, 43-83 years), and 14 patients had chronic lymphocytic leukemia, 2 had classic Hodgkin lymphoma, an

20 cording to International Workshop on Chronic Lymphocytic Leukemia 2008 criteria.

21 P) mutation is found in 2% to 10% of chronic lymphocytic leukemia, 29% of activated B-cell type diffu

22 e evaluation of clinical response in chronic lymphocytic leukemia according to the 2008 International

23 Conclusion Relapse of chronic lymphocytic leukemia after ibrutinib is an issue of incr

24 er mTOR-containing complex is toxic to acute lymphocytic leukemia (ALL) cells and identify 2 previous

25 Acute lymphocytic leukemia (ALL) is the most prevalent pediatr

26 a1i is cytotoxic to primary cells from acute lymphocytic leukemia (ALL) patients.

27 at residue 1099 (E1099K) in childhood acute lymphocytic leukemia (ALL), and cells harboring this mut

28 role for infection in the etiology of acute lymphocytic leukemia (ALL), and the involvement of the i

29 50% of pre-B-cell receptor (preBCR(+)) acute lymphocytic leukemia (ALL).

30 undred thirty-eight patients (307 with acute lymphocytic leukemia [ALL], 311 with non-Hodgkin's lymph

31 le immunocompromised individual with chronic lymphocytic leukemia and acquired hypogammaglobulinemia.

32 in his early 70s with a diagnosis of chronic lymphocytic leukemia and being treated with prednisone,

33 oader utility in analogous models of chronic lymphocytic leukemia and breast adenocarcinoma and perfo

34 in human xenograft models of resistant acute lymphocytic leukemia and CLL when administered concurren

35 plication of these new techniques to chronic lymphocytic leukemia and examine the insights already at

36 tter understand the heterogeneity of chronic lymphocytic leukemia and how mutations, activation state

37 ly, we uncovered tsRNA signatures in chronic lymphocytic leukemia and lung cancer and demonstrated th

38 Responses also occurred in chronic lymphocytic leukemia and lymphoma.

39 eCyPA also promoted the migration of chronic lymphocytic leukemia and lymphoplasmacytic lymphoma cell

40 nase inhibition by ibrutinib in both chronic lymphocytic leukemia and mantle cell lymphoma (MCL).

41 We find that for transformed murine lymphocytic leukemia and mouse pro-B cell lymphoid cell

42 oma, Waldenstroms macroglobulinemia, chronic lymphocytic leukemia and multiple myeloma.

43 matopoiesis, acute myeloid leukemia, chronic lymphocytic leukemia, and a variety of solid tumors.

44 s tumors including multiple myeloma, chronic lymphocytic leukemia, and DLBCL.

45 kemia, non-Hodgkin lymphomas such as chronic lymphocytic leukemia, and multiple myeloma.

46 owth and proliferation in pancreatic cancer, lymphocytic leukemia, and multiple myeloma.

47 ecules (SFMBT1, CBX7, and EZH1) with chronic lymphocytic leukemia, and supported CDK6 as a disease-sp

48 rosine kinase inhibitor ibrutinib in chronic lymphocytic leukemia, arsenic trioxide in acute promyelo

49 bstantially changed the treatment of chronic lymphocytic leukemia as the first targeted agents to ent

50 We further determined that the chronic lymphocytic leukemia-associated H266L substitution signi

51 92R mutation developed T-cell large granular lymphocytic leukemia at age 14 years.

52 Clonal expansion of B cell chronic lymphocytic leukemia (B-CLL) occurs within lymphoid tiss

53 ed in the peripheral blood of B-cell chronic lymphocytic leukemia (B-CLL) patients, but display low f

54 Clinical progression of B cell chronic lymphocytic leukemia (B-CLL) reflects the clone's Ag rec

55 f B cell neoplasms, including B cell chronic lymphocytic leukemia (B-CLL).

56 and for monocytes from patients with chronic lymphocytic leukemia being treated with ibrutinib.

57 g transcriptome sequencing data from chronic lymphocytic leukemia, breast cancer and uveal melanoma t

58 rically derived treatment of pediatric acute lymphocytic leukemia, can consistently achieve curative

59 of primary, activated murine CD8+ T-cell and lymphocytic leukemia cell line lineages.

60 r mitochondrial membrane potential of single lymphocytic leukemia cells and demonstrate that mitochon

61 red growth efficiency of pseudodiploid mouse lymphocytic leukemia cells during normal proliferation a

62 ity against B cell lines and primary chronic lymphocytic leukemia cells in sera depleted of single co

63 over, PI(3,4)P2 depletion in primary chronic lymphocytic leukemia cells significantly impaired their

64 resistance of glioblastoma and B-cell acute lymphocytic leukemia cells.

65 on of BTK in patient-derived primary chronic lymphocytic leukemia cells.

66 ated, with over two-thirds of B-cell chronic lymphocytic leukemia characterized by the deletion of th

67 inhibitors (BTKi's) are effective in chronic lymphocytic leukemia (CLL) after previous progression on

68 sequencing of multiple myeloma (MM), chronic lymphocytic leukemia (CLL) and acute myeloid leukemia, w

69 hematopoietic stem cells results in chronic lymphocytic leukemia (CLL) and CD8-positive peripheral T

70 cell non-Hodgkin lymphomas (NHLs) or chronic lymphocytic leukemia (CLL) and chronic HCV infection tre

71 of a long-known prognostic marker in chronic lymphocytic leukemia (CLL) and integrates its function w

72 ersely correlated with DNA damage in chronic lymphocytic leukemia (CLL) and lymphoma patient-derived

73 revealed a striking contrast between chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL

74 ractice-changing results in relapsed chronic lymphocytic leukemia (CLL) and non-Hodgkin lymphoma (NHL

75 b has been approved for treatment of chronic lymphocytic leukemia (CLL) and non-Hodgkin lymphoma, but

76 rs, current treatment strategies for chronic lymphocytic leukemia (CLL) are not curative, and the sea

77 ole for tumor-expressed CTLA-4 using chronic lymphocytic leukemia (CLL) as a disease model.

78 r were more effectively activated by chronic lymphocytic leukemia (CLL) B-cell targets opsonized with

79 r progression-free survival (PFS) in chronic lymphocytic leukemia (CLL) based on 3 randomized, phase

80 A subset of chronic lymphocytic leukemia (CLL) BCRs interacts with Ags expre

81 represents a therapeutic advance in chronic lymphocytic leukemia (CLL) but as monotherapy produces f

82 are changing treatment paradigms for chronic lymphocytic leukemia (CLL) but important problems remain

83 ession is a recognized phenomenon in chronic lymphocytic leukemia (CLL) but its biological basis rema

84 escription of the natural history of chronic lymphocytic leukemia (CLL) by David Galton in 1966, the

85 Chronic lymphocytic leukemia (CLL) can be familial; however, thu

86 re present in approximately 4-13% of chronic lymphocytic leukemia (CLL) cases, where they are associa

87 ease (MRD) negativity, defined as <1 chronic lymphocytic leukemia (CLL) cell detectable per 10 000 le

88 rget for translational regulation in chronic lymphocytic leukemia (CLL) cells after B-cell receptor (

89 anced proliferation and migration of chronic lymphocytic leukemia (CLL) cells and that these effects

90 Multiple studies show that chronic lymphocytic leukemia (CLL) cells are heavily dependent o

91 Chronic lymphocytic leukemia (CLL) cells cycle between lymph nod

92 Circulating chronic lymphocytic leukemia (CLL) cells display an abnormal inc

93 Chronic lymphocytic leukemia (CLL) cells express poor levels of

94 croenvironmental glycolytic shift in chronic lymphocytic leukemia (CLL) cells mediated by Notch-c-Myc

95 Chronic lymphocytic leukemia (CLL) cells multiply and become mor

96 The crucial dependence of chronic lymphocytic leukemia (CLL) cells on signals derived from

97 The proliferation of chronic lymphocytic leukemia (CLL) cells requires communication

98 nd ROR1 are expressed in circulating chronic lymphocytic leukemia (CLL) cells, and because in other c

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

100 distinctive subset of patients with chronic lymphocytic leukemia (CLL) defined by the expression of

101 The prognosis of chronic lymphocytic leukemia (CLL) depends on different markers,

102 Human and mouse chronic lymphocytic leukemia (CLL) develops from CD5(+) B cells

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

104 ty and mortality among patients with chronic lymphocytic leukemia (CLL) due to immune dysfunction and

105 sregulation is a cardinal feature of chronic lymphocytic leukemia (CLL) from its early stage and wors

106 l efficacy displayed by ibrutinib in chronic lymphocytic leukemia (CLL) has been challenged by the fr

107 The treatment of chronic lymphocytic leukemia (CLL) has been revolutionized by ta

108 The therapy of relapsed chronic lymphocytic leukemia (CLL) has changed dramatically in t

109 regulator of B and myeloid cells, in chronic lymphocytic leukemia (CLL) has not been well characteriz

110 Treatment of chronic lymphocytic leukemia (CLL) has shifted from chemo-immuno

111 The management of chronic lymphocytic leukemia (CLL) has undergone dramatic change

112 n patients with previously untreated chronic lymphocytic leukemia (CLL) have been limited.

113 clax in patients with poor prognosis chronic lymphocytic leukemia (CLL) highlights the potential of t

114 om 841 treatment-naive patients with chronic lymphocytic leukemia (CLL) identified 89 (11%) patients

115 up substantially since then, and the chronic lymphocytic leukemia (CLL) incidence has increased conti

116 Targeted therapies for chronic lymphocytic leukemia (CLL) include venetoclax, the oral

117 Current treatment strategies for chronic lymphocytic leukemia (CLL) involve a combination of conv

118 Chronic lymphocytic leukemia (CLL) is a common B-cell malignancy

119 Chronic lymphocytic leukemia (CLL) is a common lymphoid malignan

120 Chronic lymphocytic leukemia (CLL) is a disease in which a singl

121 Chronic lymphocytic leukemia (CLL) is a heterogenous disease tha

122 Chronic lymphocytic leukemia (CLL) is a malignancy of mature B c

123 Chronic lymphocytic leukemia (CLL) is a malignant disease of sma

124 Chronic lymphocytic leukemia (CLL) is a variable disease; theref

125 Chronic lymphocytic leukemia (CLL) is an incurable disease chara

126 Chronic lymphocytic leukemia (CLL) is characterized by immune dy

127 Chronic lymphocytic leukemia (CLL) is characterized by the accum

128 Chronic lymphocytic leukemia (CLL) is characterized by the expan

129 The treatment landscape for chronic lymphocytic leukemia (CLL) is rapidly evolving.

130 The pathogenesis of chronic lymphocytic leukemia (CLL) is stringently associated wit

131 B-cell chronic lymphocytic leukemia (CLL) is the most common adult huma

132 Chronic lymphocytic leukemia (CLL) is the most common adult leuk

133 Chronic lymphocytic leukemia (CLL) is the most common adult leuk

134 Chronic lymphocytic leukemia (CLL) is the most common human leuk

135 Chronic lymphocytic leukemia (CLL) is the most common human leuk

136 B-cell chronic lymphocytic leukemia (CLL) is the most common human leuk

137 B-cell chronic lymphocytic leukemia (CLL) is the most common leukemia i

138 An unresolved issue in chronic lymphocytic leukemia (CLL) is whether IGHV3-21 gene usag

139 erapy represents a paradigm shift in chronic lymphocytic leukemia (CLL) management, but data on pract

140 aD910A/D910A) in the Emu-TCL1 murine chronic lymphocytic leukemia (CLL) model impaired B cell recepto

141 Chronic lymphocytic leukemia (CLL) occurs in 2 major forms: aggr

142 h hypogammaglobulinemia secondary to chronic lymphocytic leukemia (CLL) or multiple myeloma (MM), int

143 for previously treated patients with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma

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

145 NOTCH1 is mutated in 10% of chronic lymphocytic leukemia (CLL) patients and is associated wi

146 Chronic lymphocytic leukemia (CLL) patients assigned to stereoty

147 l blood mononuclear cells (PBMCs) of chronic lymphocytic leukemia (CLL) patients clearly stated a hig

148 morbidities, and immune dysfunction, chronic lymphocytic leukemia (CLL) patients may be at particular

149 ipheral blood mononuclear cells from chronic lymphocytic leukemia (CLL) patients on clinical trials o

150 Chronic lymphocytic leukemia (CLL) patients progressed early on

151 on of long-term nonprogressors among chronic lymphocytic leukemia (CLL) patients suggests the existen

152 nses in relapsed or refractory (R/R) chronic lymphocytic leukemia (CLL) patients treated with CD19-ta

153 In chronic lymphocytic leukemia (CLL) patients with mutated IGHV, 3

154 ces in the therapeutic management of Chronic Lymphocytic Leukemia (CLL) patients, this common B cell

155 or high-risk and relapsed refractory chronic lymphocytic leukemia (CLL) patients.

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

157 ansplantation (SCT) availability for chronic lymphocytic leukemia (CLL) patients.

158 k, untreated, and previously treated chronic lymphocytic leukemia (CLL) patients.

159 irst-line treatment of medically fit chronic lymphocytic leukemia (CLL) patients; however, despite go

160 tinib resistance have suggested that chronic lymphocytic leukemia (CLL) progression on ibrutinib is l

161 receptor (BCR) signaling pathways in chronic lymphocytic leukemia (CLL) provides significant clinical

162 8 previously untreated patients with chronic lymphocytic leukemia (CLL) received 8 cycles of either 1

163 Chronic lymphocytic leukemia (CLL) remains an incurable disease.

164 B-cell chronic lymphocytic leukemia (CLL) results from accumulation of

165 Chronic lymphocytic leukemia (CLL) risk stratification studies t

166 igh-level expression is required for chronic lymphocytic leukemia (CLL) survival.

167 Chronic lymphocytic leukemia (CLL) therapy has changed dramatica

168 re established prognostic factors in chronic lymphocytic leukemia (CLL) treated with chemoimmunothera

169 Disease progression in patients with chronic lymphocytic leukemia (CLL) treated with ibrutinib has be

170 een CD4(+) T cells and proliferating chronic lymphocytic leukemia (CLL) tumor B cells occurs within l

171 rituximab in patients with relapsed chronic lymphocytic leukemia (CLL) was terminated early because

172 ied the effect of USP7 inhibition in chronic lymphocytic leukemia (CLL) where the ataxia telangiectas

173 Patients with chronic lymphocytic leukemia (CLL) who achieve blood or bone mar

174 CAR-T) cell therapy in patients with chronic lymphocytic leukemia (CLL) who had previously received i

175 identify a subgroup of patients with chronic lymphocytic leukemia (CLL) who have an exceptionally goo

176 Emu-TCL1 transgenic mice resulted in chronic lymphocytic leukemia (CLL) with a biased repertoire, inc

177 Genetic instability is a feature of chronic lymphocytic leukemia (CLL) with adverse prognosis.

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

179 Treatment of patients with chronic lymphocytic leukemia (CLL) with inhibitors of Bruton's t

180 en used to treat relapsed/refractory chronic lymphocytic leukemia (CLL) with prolongation of progress

181 th resistance to targeted therapy of chronic lymphocytic leukemia (CLL) with the Bruton's tyrosine ki

182 e consider the targeted treatment of chronic lymphocytic leukemia (CLL) with tyrosine kinase inhibito

183 Chronic lymphocytic leukemia (CLL) with unmutated (U-CLL) or mut

184 In chronic lymphocytic leukemia (CLL), acquired T-cell dysfunction

185 In chronic lymphocytic leukemia (CLL), AID is overexpressed in the

186 enotype and outcome in patients with chronic lymphocytic leukemia (CLL), breast, or lung cancers.

187 outcomes for patients with relapsed chronic lymphocytic leukemia (CLL), but complete remissions rema

188 are associated with poor outcome in chronic lymphocytic leukemia (CLL), but how these contribute to

189 has shown activity in patients with chronic lymphocytic leukemia (CLL), but its efficacy in combinat

190 SF3B1 is recurrently mutated in chronic lymphocytic leukemia (CLL), but its role in the pathogen

191 leukemia but are less effective for chronic lymphocytic leukemia (CLL), focusing attention on improv

192 re associated with increased risk of chronic lymphocytic leukemia (CLL), follicular lymphoma (FL), an

193 We found that in chronic lymphocytic leukemia (CLL), HIF-1alpha is a novel regula

194 ute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL), including the expansion and

195 In chronic lymphocytic leukemia (CLL), intra-tumoral DNA methylatio

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

197 In chronic lymphocytic leukemia (CLL), neoplastic B cells evade apo

198 ndolent non-Hodgkin lymphoma (iNHL), chronic lymphocytic leukemia (CLL), or T-cell lymphoma (TCL) wer

199 hibitors have transformed therapy in chronic lymphocytic leukemia (CLL), patients with high-risk gene

200 is the most common genetic lesion in chronic lymphocytic leukemia (CLL), promoting overexpression of

201 Within chronic lymphocytic leukemia (CLL), responses to 62% of drugs we

202 In chronic lymphocytic leukemia (CLL), signaling through several pr

203 In chronic lymphocytic leukemia (CLL), the immunoglobulin heavy-cha

204 In chronic lymphocytic leukemia (CLL), the increment in PBLs is slo

205 In human chronic lymphocytic leukemia (CLL), tumor B cells lodge in lymph

206 gnant B cells from 268 patients with chronic lymphocytic leukemia (CLL), we showed that tumors derive

207 nd bendamustine in older adults with chronic lymphocytic leukemia (CLL).

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

209 opsonized B cells from patients with chronic lymphocytic leukemia (CLL).

210 mportant role in the pathogenesis of chronic lymphocytic leukemia (CLL).

211 ion and function and is disturbed in chronic lymphocytic leukemia (CLL).

212 amatically changed the management of chronic lymphocytic leukemia (CLL).

213 largest disease categories: AML and chronic lymphocytic leukemia (CLL).

214 re now prominent in the treatment of chronic lymphocytic leukemia (CLL).

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

216 g clinical activity in patients with chronic lymphocytic leukemia (CLL).

217 al evolution, and chemoresistance in chronic lymphocytic leukemia (CLL).

218 ab, in the majority of patients with chronic lymphocytic leukemia (CLL).

219 rapy for fit patients with untreated chronic lymphocytic leukemia (CLL).

220 the treatment of relapsed/refractory chronic lymphocytic leukemia (CLL).

221 ontributes to disease progression in chronic lymphocytic leukemia (CLL).

222 or treatment of B-cell lymphomas and chronic lymphocytic leukemia (CLL).

223 th single-agent activity in relapsed chronic lymphocytic leukemia (CLL).

224 to analyze CSs and apply it to study chronic lymphocytic leukemia (CLL).

225 is pathway fail to control growth of chronic lymphocytic leukemia (CLL).

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

227 apeutic advance for the treatment of chronic lymphocytic leukemia (CLL).

228 or barrier to effective treatment of chronic lymphocytic leukemia (CLL).

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

230 orambucil for the initial therapy of chronic lymphocytic leukemia (CLL).

231 significant treatment advancement in chronic lymphocytic leukemia (CLL).

232 idity and mortality in patients with chronic lymphocytic leukemia (CLL).

233 g of the genomic alterations driving chronic lymphocytic leukemia (CLL).

234 he outcome of patients with relapsed chronic lymphocytic leukemia (CLL).

235 s of MBL have the immunophenotype of chronic lymphocytic leukemia (CLL).

236 gy in B-cell malignancies, including chronic lymphocytic leukemia (CLL).

237 a remarkable prognostic biomarker of chronic lymphocytic leukemia (CLL).

238 kemia (T-ALL) and RPS15 mutations in chronic lymphocytic leukemia (CLL).

239 patients with relapsed or refractory chronic lymphocytic leukemia (CLL).

240 effective therapy for patients with chronic lymphocytic leukemia (CLL).

241 eviously untreated (first line [1L]) chronic lymphocytic leukemia (CLL).

242 improved outcomes for patients with chronic lymphocytic leukemia (CLL).

243 ant for treatment decision-making in chronic lymphocytic leukemia (CLL).

244 inherited genetic predisposition to chronic lymphocytic leukemia (CLL).

245 n in many types of cancer, including chronic lymphocytic leukemia (CLL).

246 formed the therapeutic landscape for chronic lymphocytic leukemia (CLL).

247 r patients with previously untreated chronic lymphocytic leukemia (CLL).

248 have been approved for patients with chronic lymphocytic leukemia (CLL).

249 chemoimmunotherapy in patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma

250 tive-site occupancy in patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (S

251 survival outcomes for patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (S

252 e for the treatment of patients with chronic lymphocytic leukemia (CLL); however, their high cost has

253 antibody (mAb), recently approved in chronic lymphocytic leukemia (CLL; B-cell CLL) and follicular ly

254 ow-grade B-cell lymphoma (n = 8), or chronic lymphocytic leukemia (CLL; n = 7).

255 ma [NHL], Hodgkin lymphoma [HL], and chronic lymphocytic leukemia [CLL]) outside of rare hereditary s

256 e cancers (non-Hodgkin's lymphoma or chronic lymphocytic leukemia [CLL]).

257 o the 2008 International Workshop on Chronic Lymphocytic Leukemia criteria.

258 treated with chemoimmunotherapy for chronic lymphocytic leukemia experienced a 9-week course of COVI

259 Unlike cells of chronic lymphocytic leukemia, FL cells expressed relatively high

260 Risks of chronic lymphocytic leukemia, follicular lymphoma, and mantle ce

261 8 Modified International Workshop on Chronic Lymphocytic Leukemia guidelines) from 31 centres in the

262 ria of the International Workshop on Chronic Lymphocytic Leukemia, had received at least three cycles

263 osine kinase (BTK) with ibrutinib in chronic lymphocytic leukemia has led to a paradigm shift in ther

264 ility Genes, Genetic Epidemiology of Chronic Lymphocytic Leukemia, Impact of Remote Familial Colorect

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

266 cancer, acute myeloid leukemia, and chronic lymphocytic leukemia, in which the authors reconstructed

267 In Emu-TCL1 mice with chronic lymphocytic leukemia, injection of the STING agonist 3'3

268 e show that venetoclax resistance in chronic lymphocytic leukemia is associated with complex clonal s

269 o the 2008 International Workshop on Chronic Lymphocytic Leukemia (IWCLL) criteria and an Eastern Coo

270 e [PR]) by International Workshop on Chronic Lymphocytic Leukemia (IWCLL) criteria was 71% (17 of 24)

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

272 patients with acute myeloid leukemia, acute lymphocytic leukemia, multiple myeloma, non-Hodgkin lymp

273 ymphoblastic leukemia (ALL; n = 47), chronic lymphocytic leukemia (n = 24), and non-Hodgkin lymphoma

274 fractory kappa+ non-Hodgkin lymphoma/chronic lymphocytic leukemia (NHL/CLL) or multiple myeloma (MM)

275 highly effective targeted agents for chronic lymphocytic leukemia offers the potential for fixed-dura

276 ymphoproliferative disorders such as chronic lymphocytic leukemia or large granular lymphocyte leukem

277 ype-specific analyses indicated that chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL/

278 tion for relapsed or refractory (RR) chronic lymphocytic leukemia or small lymphocytic lymphoma (SLL)

279 d a marked association of sCD23 with chronic lymphocytic leukemia (ORSlope = 28, Ptrend = 7.279 x 10(

280 ctors for basal cell carcinomas were chronic lymphocytic leukemia (P = 0.003), reduced-intensity cond

281 mas were increased age (P < 0.0001), chronic lymphocytic leukemia (P = 0.02), and chronic graft-versu

282 erogeneity within primary cells from chronic lymphocytic leukemia patients, but it can be adapted to

283 ceptor (CAR) can produce dramatic results in lymphocytic leukemia patients; however, therapeutic stra

284 UNX1 carriers develop precursor B-cell acute lymphocytic leukemia (pB-ALL), the underlying genetic ba

285 T3 protein expression was reduced in chronic lymphocytic leukemia primary samples and malignant B cel

286 (DLBCL; n = 34), DLBCL arising from chronic lymphocytic leukemia (Richter transformation; n = 7), Wa

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

288 A expression was decreased in B cell chronic lymphocytic leukemia samples compared with healthy contr

289 survivors of NHL, including 91 after chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL

290 Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL

291 patients with relapsed or refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (RR-CLL/

292 vely associated with the risk of the chronic lymphocytic leukemia/small lymphocytic lymphoma subtype

293 In B-cell chronic lymphocytic leukemia, this is associated with poor progn

294 od and Drug Administration-approved drug for lymphocytic leukemia treatment, was administered intrape

295 tors killed 98% of ex vivo primary chronic B-lymphocytic leukemia tumor cells while sparing healthy B

296 Crohn's disease, multiple sclerosis, chronic lymphocytic leukemia, veno-occlusive disease with immuno

297 with B cell non-Hodgkin lymphoma or chronic lymphocytic leukemia were treated on a phase 1 dose esca

298 l lymphoma, follicular lymphoma, and chronic lymphocytic leukemia, were enrolled.

299 agonist, venetoclax, was approved in chronic lymphocytic leukemia, where it has proven to be highly a

300 ribe a case involving a patient with chronic lymphocytic leukemia who developed invasive A. butzleri