ライフサイエンスコーパス: lymphocytic leukemia

1 ations (myelodysplastic syndrome and chronic lymphocytic leukemia).

2 a BH3 mimetic approved for treating chronic lymphocytic leukemia.

3 nts with acute myelogenous leukemia or acute lymphocytic leukemia.

4 2 loss in the pathogenesis of B-cell chronic lymphocytic leukemia.

5 had indolent lymphomas, and four had chronic lymphocytic leukemia.

6 imary myelofibrosis, and T- and B-cell acute lymphocytic leukemia.

7 utstanding activity in patients with chronic lymphocytic leukemia.

8 ich develop disease resembling human chronic lymphocytic leukemia.

9 arable concentrations efficacious in chronic lymphocytic leukemia.

10 ogression-free survival in high-risk chronic lymphocytic leukemia.

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

12 important in clinical management of chronic lymphocytic leukemia.

13 sed tissues in colorectal cancer and chronic lymphocytic leukemia.

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

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

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

17 balances the activating role of T-cell acute lymphocytic leukemia 1 (TAL1).

18 incipal hematopoietic regulator T-cell acute lymphocytic leukemia-1 (TAL1) is involved in regulating

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

20 ients with asymptomatic, early-stage chronic lymphocytic leukemia; (4) do not test or treat for hepar

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

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

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

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

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

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

27 50% of pre-B-cell receptor (preBCR(+)) acute lymphocytic leukemia (ALL).

28 to metformin in multiple myeloma and chronic lymphocytic leukemia and a number of solid tumors sugges

29 so implicated in the pathogenesis of chronic lymphocytic leukemia and Aicardi-Goutieres syndrome.

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

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

32 receptors to treat relapsed/refractory acute lymphocytic leukemia and cytotoxic T-lymphocyte-associat

33 some of these have activity against chronic lymphocytic leukemia and hairy cell leukemia, in general

34 hows impressive clinical activity in chronic lymphocytic leukemia and indolent B cell non-Hodgkin's l

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

36 Responses also occurred in chronic lymphocytic leukemia and lymphoma.

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

38 III clinical trials in patients with chronic lymphocytic leukemia and mantle-cell lymphoma.

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

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

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

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

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

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

45 ockout mice, a characteristic of the chronic lymphocytic leukemia-associated phenotype found in human

46 92R mutation developed T-cell large granular lymphocytic leukemia at age 14 years.

47 and constitutively active in B-cell chronic lymphocytic leukemia (B-CLL) cells, resulting in a high

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

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

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

51 teracted with the oncoprotein B cell chronic lymphocytic leukemia (BCL6) and induced lysine 63-mediat

52 The finding that in chronic lymphocytic leukemia, BCRs bind to an epitope on the BCR

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

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

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

56 and 3,4,5-trimethoxy derivatives in chronic lymphocytic leukemia cells revealed that co-treatment of

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

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

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

60 n the poor outcomes of patients with chronic lymphocytic leukemia (CLL) after the discontinuation of

61 the most abundantly expressed miR in chronic lymphocytic leukemia (CLL) and affects the threshold for

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

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

64 the microRNAs (miRNAs) expressed in chronic lymphocytic leukemia (CLL) and identified miR-150 as the

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

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

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

68 on between the understood biology of chronic lymphocytic leukemia (CLL) and the therapeutics used to

69 Defining features of chronic lymphocytic leukemia (CLL) are not only its immunophenot

70 altered prognosis for patients with chronic lymphocytic leukemia (CLL) at diagnosis.

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

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

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

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

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

76 (IL)-6 acts as a tumor suppressor in chronic lymphocytic leukemia (CLL) by inhibiting toll-like recep

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

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

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

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

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

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

83 Chronic lymphocytic leukemia (CLL) cells depend on microenvironm

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

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

86 act B-cell-receptor (BCR) signaling, chronic lymphocytic leukemia (CLL) cells fail to undergo termina

87 cal role for homing and retention of chronic lymphocytic leukemia (CLL) cells in tissues such as the

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

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

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

91 BCL2 in cells or induce apoptosis in chronic lymphocytic leukemia (CLL) cells or platelets, which req

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

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

94 s high proapoptotic activity against chronic lymphocytic leukemia (CLL) cells, which may indicate a p

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

96 nancies, as it is known from primary chronic lymphocytic leukemia (CLL) cells.

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

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

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

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

101 Chronic lymphocytic leukemia (CLL) exhibits high remission rates

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

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

104 g B-cell receptor (BCR) signaling in chronic lymphocytic leukemia (CLL) has been successful with dura

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

106 tter understanding of the biology of chronic lymphocytic leukemia (CLL) has led to significant advanc

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

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

109 well established that patients with chronic lymphocytic leukemia (CLL) have an increased risk of dev

110 e-wide association studies (GWAS) of chronic lymphocytic leukemia (CLL) have shown that common geneti

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

112 for detection of miRNA signature of chronic lymphocytic leukemia (CLL) in human serum.

113 is defined as the transformation of chronic lymphocytic leukemia (CLL) into an aggressive lymphoma,

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

115 Chronic lymphocytic leukemia (CLL) is a B cell malignancy associ

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

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

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

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

120 Chronic lymphocytic leukemia (CLL) is a disease of an accumulati

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

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

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

124 Chronic lymphocytic leukemia (CLL) is associated with a tumor-su

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

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

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

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

129 Chronic lymphocytic leukemia (CLL) is characterized by the progr

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

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

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

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

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

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

136 Chronic lymphocytic leukemia (CLL) is the most common leukemia a

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

138 Chronic lymphocytic leukemia (CLL) is the most common leukemia i

139 Chronic lymphocytic leukemia (CLL) is the most common lymphoid n

140 nically relevant question of whether chronic lymphocytic leukemia (CLL) is transmitted through blood

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

142 ations of chromosomal aberrations in chronic lymphocytic leukemia (CLL) led to a better understanding

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

144 ents an unsolved clinical problem of chronic lymphocytic leukemia (CLL) management.

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

146 fraction of patients with high-risk chronic lymphocytic leukemia (CLL) or Richter's transformation (

147 rosine kinase inhibitor ibrutinib in chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma

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

149 Chronic lymphocytic leukemia (CLL) patients assigned to stereoty

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

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

152 Chronic lymphocytic leukemia (CLL) patients progressed early on

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

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

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

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

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

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

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

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

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 ay impair prognosis of patients with chronic lymphocytic leukemia (CLL) receiving frontline therapy,

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

165 uplet has become the backbone of the chronic lymphocytic leukemia (CLL) standard of care.

166 We recently reported that chronic lymphocytic leukemia (CLL) subgroups with distinct clono

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

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

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

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

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

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

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

174 54 patients with relapsed/refractory chronic lymphocytic leukemia (CLL) with adverse characteristics

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

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

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

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

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

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

181 notypic analysis was consistent with chronic lymphocytic leukemia (CLL), and FISH results revealed pr

182 or immune responses are hallmarks of chronic lymphocytic leukemia (CLL), and PD-1/PD-L1 inhibitory si

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

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

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

186 start (CpG+223) predicts outcome in chronic lymphocytic leukemia (CLL), but its impact relative to C

187 ontributes to the clinical course of chronic lymphocytic leukemia (CLL), but to date, only static in

188 In chronic lymphocytic leukemia (CLL), CD8(+) T cells exhibit featu

189 therapeutic efficacy of ibrutinib in chronic lymphocytic leukemia (CLL), complete responses are infre

190 an unfavorable prognostic marker in chronic lymphocytic leukemia (CLL), definitive validation eviden

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

192 ions of CD20 mAb-based therapies for chronic lymphocytic leukemia (CLL), including correlative measur

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

194 aggressive disease in patients with chronic lymphocytic leukemia (CLL), including those cases with a

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

196 Despite the high incidence of chronic lymphocytic leukemia (CLL), metabolism of CLL cells rema

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

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

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

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

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

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

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 LA class I and II ligands of primary chronic lymphocytic leukemia (CLL), we delineated a novel catego

207 nal whole genome sequencing study of chronic lymphocytic leukemia (CLL), we revealed a SAMHD1 mutatio

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

209 gulation of the survival pathways in chronic lymphocytic leukemia (CLL), which is crucial to the path

210 ti et al present novel findings that chronic lymphocytic leukemia (CLL)-derived exosomes and their mo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

227 ymphocytosis (MBL) is a precursor of chronic lymphocytic leukemia (CLL).

228 oantigen)- mediated BCR signaling in chronic lymphocytic leukemia (CLL).

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

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

231 c landscape and clonal complexity of chronic lymphocytic leukemia (CLL).

232 utinib is effective in patients with chronic lymphocytic leukemia (CLL).

233 d progression-free survival (PFS) in chronic lymphocytic leukemia (CLL).

234 ce in B cell malignancies, including chronic lymphocytic leukemia (CLL).

235 urvival (OS) have been identified in chronic lymphocytic leukemia (CLL).

236 massively parallel DNA sequencing of chronic lymphocytic leukemia (CLL).

237 w targeted therapy for patients with chronic lymphocytic leukemia (CLL).

238 icantly improved patient outcomes in chronic lymphocytic leukemia (CLL).

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

240 y agent with therapeutic activity in chronic lymphocytic leukemia (CLL).

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

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

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

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

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

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

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

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

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

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

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

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

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

254 appaB is constitutively activated in chronic lymphocytic leukemia (CLL); however, the implicated mole

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

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

257 subjects with relapsed or refractory chronic lymphocytic leukemia (CLL; n = 41) or non-Hodgkin lympho

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

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

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

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

262 8 Modified International Workshop on Chronic Lymphocytic Leukemia guidelines) from 31 centres in the

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

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

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

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

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

270 nors had low-count MBL, including 99 chronic lymphocytic leukemia-like (66.4%), 22 atypical (14.8%),

271 associated antigen 4 (CTLA4), B-cell chronic lymphocytic leukemia/lymphoma 10 (BCL10), phosphoinositi

272 ficiency selectively impaired B-cell chronic lymphocytic leukemia/lymphoma 10 (BCL10)-mediated innate

273 in family, member 11 (CARD11)-B-cell chronic lymphocytic leukemia/lymphoma 10 (BCL10)-mucosa-associat

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

275 tment-naive older patients with CLL or small lymphocytic leukemia (median age, 71 years; range, 65-90

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

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

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

279 cer types (chronic myeloid leukemia, chronic lymphocytic leukemia, non-Hodgkin lymphoma, and multiple

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

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

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

283 itself unravels a novel concept for chronic lymphocytic leukemia pathogenesis.

284 Twenty-two previously untreated chronic lymphocytic leukemia patients underwent PET/CT for disea

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

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

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

288 -miR-150-5p in normal healthy serum, chronic lymphocytic leukemia Rai stage 1 (CLL-1), and stage 3 (C

289 Patients with relapsed/refractory chronic lymphocytic leukemia received bendamustine and rituximab

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

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

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

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

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

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

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

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

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

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

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