ライフサイエンスコーパス: lymphocytic

1 Using a mouse lacking the signalling lymphocytic activation molecule (SLAM) family of homotyp

2 Signaling lymphocytic activation molecule (SLAM) family receptors

3 n is notable as it is found at the signaling lymphocytic activation molecule (SLAM) receptor-binding

4 extrafollicular pathway, we used a signaling lymphocytic activation molecule (SLAM)-associated protei

5 Signaling lymphocytic activation molecule family 3 (SLAMF3/Ly9) is

6 Signaling lymphocytic activation molecule family cell surface rece

7 ptors and the X-chromosome-defined signaling lymphocytic activation molecule-associated protein (SAP)

8 Among these proteins, signaling lymphocytic activation molecule-associated protein (SAP)

9 The compounds inducing lymphocytic activation were shown to elute, mainly near

10 characterized by a marked decrease in B cell lymphocytic aggregates.

11 s an immunologic lung disease resulting from lymphocytic and frequently granulomatous inflammation of

12 ts immunoregulatory functional activities on lymphocytic and nonlymphocytic cells during infection, a

13 nscriptional activity of CD74-ICD in chronic lymphocytic B cells.

14 led to increased infiltration of the virus, lymphocytic bronchiolitis and reduced survival of Pgam5

15 e studies (PubMed, 1990-2015) analyzed tumor lymphocytic, CD8+, and FOXP3+ cellular infiltrates, and

16 peripheral blood lymphocytes (PBLs) and a B lymphocytic cell line (B-LCL).

17 ies analyzed viruses produced by transformed lymphocytic cell lines chronically infected with HTLV-1,

18 high levels of TIL and assess variations in lymphocytic cell subsets across breast cancer subtypes.

19 We measure the growth of single lymphocytic cells, mouse and human T cells, primary huma

20 clearance of murine gamma-herpesvirus 68 and lymphocytic choriomeningitis clone 13 and reversed T cel

21 f HIV infection in humans and during chronic lymphocytic choriomeningitis infection in mice.

22 -deficient (Prf1(--)) mice are infected with lymphocytic choriomeningitis virus (LCMV) and secondary

23 Here we show that the arenaviruses lymphocytic choriomeningitis virus (LCMV) and the clinic

24 eoproteins (NPs) of the Old World arenavirus lymphocytic choriomeningitis virus (LCMV) and the New Wo

25 te viral infections, such as infections with lymphocytic choriomeningitis virus (LCMV) and vaccinia v

26 In this study, using lymphocytic choriomeningitis virus (LCMV) and Zika virus

27 effector CD8 T cells from mice infected with lymphocytic choriomeningitis virus (LCMV) clone 13 into

28 During chronic infection with lymphocytic choriomeningitis virus (LCMV) clone 13, miR-

29 this study we found that mice infected with lymphocytic choriomeningitis virus (LCMV) exhibit global

30 we immunized mice with Ad5 vectors encoding lymphocytic choriomeningitis virus (LCMV) glycoprotein (

31 found that during the first week of chronic lymphocytic choriomeningitis virus (LCMV) infection, bef

32 (+) T-cell formation following immunization, lymphocytic choriomeningitis virus (LCMV) infection, or

33 evidence that infection of mice with either lymphocytic choriomeningitis virus (LCMV) or pneumonia v

34 t isografts using RIP-LCMV mice expressing a lymphocytic choriomeningitis virus (LCMV) protein in the

35 worldwide-distributed prototypic arenavirus, lymphocytic choriomeningitis virus (LCMV), is a neglecte

36 d by coinfecting mice with L. guyanensis and lymphocytic choriomeningitis virus (LCMV), or the sand f

37 The prototypic arenavirus, lymphocytic choriomeningitis virus (LCMV), provides inve

38 e in perforin-deficient mice is triggered by lymphocytic choriomeningitis virus (LCMV).

39 f cells) during acute infection of mice with lymphocytic choriomeningitis virus (LCMV).

40 at recombinants of the prototypic arenavirus lymphocytic choriomeningitis virus (rLCMVs), whose S-IGR

41 maintained on CD8(+) T cells during chronic lymphocytic choriomeningitis virus and hepatitis C virus

42 only two mammarenaviruses, the widely spread lymphocytic choriomeningitis virus and the recently desc

43 pecific CD8 T cells during acute and chronic lymphocytic choriomeningitis virus challenges, but did n

44 Pathogenic HIV or lymphocytic choriomeningitis virus chronic infections di

45 n PTPN22 resist chronic viral infection with lymphocytic choriomeningitis virus clone 13 (LCMV cl13).

46 isella strains expressing well-characterized lymphocytic choriomeningitis virus epitopes, we found th

47 Consistent with this finding, we show that lymphocytic choriomeningitis virus infection can directl

48 s in virus-specific CD8 T cells during acute lymphocytic choriomeningitis virus infection in mice.

49 cell-extrinsic manner early following acute lymphocytic choriomeningitis virus infection to suppress

50 rvation of antiviral immune responses, acute lymphocytic choriomeningitis virus infection was used.

51 In chronic lymphocytic choriomeningitis virus infection, blockade o

52 Following acute lymphocytic choriomeningitis virus infection, memory CD8

53 CD8(+) T cells to mount a robust response to lymphocytic choriomeningitis virus infection, with both

54 risk of developing HLH immunopathology after lymphocytic choriomeningitis virus infection.

55 ephalitis, and defective immune responses to lymphocytic choriomeningitis virus infection.

56 TE/TEM and TRM subsets was overcome by acute lymphocytic choriomeningitis virus infection; neverthele

57 CD8 T cells responding to acute and chronic lymphocytic choriomeningitis virus infections.

58 To improve upon this, we used the murine lymphocytic choriomeningitis virus model and adenoviral

59 for JUNV and for vesicular stomatitis virus, lymphocytic choriomeningitis virus, and dengue virus but

60 contraction phase of an acute infection with lymphocytic choriomeningitis virus, we found that virus-

61 theless, neither germinal center B cells nor lymphocytic choriomeningitis virus-specific Ab levels we

62 T cell responses during acute infection with lymphocytic choriomeningitis virus.

63 for diabetes antigen tetramers and to LCMV (lymphocytic choriomeningitis)-reactive CD8+ T cells.

64 Although the lymphocytic CNS inflammation in these macaques shared mo

65 Lymphocytic immune responses to tumor antigens also tren

66 Interestingly, biopsy variability of lymphocytic infiltrate differs considerably among breast

67 lium with a striking subepithelial lichenoid lymphocytic infiltrate extending into the muscularis muc

68 cally investigate biopsy variability for the lymphocytic infiltrate in 998 breast tumours using a nov

69 te, while the original study observed sparse lymphocytic infiltrate in IgG-treated tumors and increas

70 between the biopsy and whole-tumour score of lymphocytic infiltrate with increasing number of biopsie

71 ly, there was a variable superficial stromal lymphocytic infiltrate, involving the epithelium in more

72 eated tumors resulted in minimal to moderate lymphocytic infiltrate, while the original study observe

73 Tumor lymphocytic infiltration (TLI) has differing prognostic

74 e detailed understanding of the variation in lymphocytic infiltration in breast cancer may aid in ide

75 Finally, AT-RvD1 decreases lymphocytic infiltration into the salivary glands when u

76 chronic autoimmune disease characterized by lymphocytic infiltration of exocrine glands, mainly sali

77 CXCR3 is associated with monocytic and lymphocytic infiltration of inflamed or tumor-bearing lu

78 a common autoimmune disease characterized by lymphocytic infiltration of the salivary gland and loss

79 umor necrosis factor-alpha levels, decreased lymphocytic infiltration, and decreased nuclear factor (

80 entral nervous system characterized by focal lymphocytic infiltration, demyelination and neurodegener

81 Intense lymphocytic infiltration, found in a minority of tumors,

82 gnosis and are found in environments of high lymphocytic infiltration.

83 Chronic lymphocytic inflammation with pontine perivascular enhan

84 patients with relapsed or refractory chronic lymphocytic leukaemia (according to the 2008 Modified In

85 with del(17p) relapsed or refractory chronic lymphocytic leukaemia (as defined by 2008 Modified Inter

86 A key feature of chronic lymphocytic leukaemia (CLL) cells is overexpressed prote

87 treatment of patients with relapsed chronic lymphocytic leukaemia (CLL) in combination with rituxima

88 Chronic lymphocytic leukaemia (CLL) is a clonal disorder of matu

89 Chronic lymphocytic leukaemia (CLL) is a frequent B-cell maligna

90 Chronic lymphocytic leukaemia (CLL) is characterized by substant

91 Pathogenesis of chronic lymphocytic leukaemia (CLL) is contingent upon antigen r

92 Chronic lymphocytic leukaemia (CLL) is the most common clonal B-

93 Several chronic lymphocytic leukaemia (CLL) susceptibility loci have bee

94 the quality of life of patients with chronic lymphocytic leukaemia (CLL) who do not require systemic

95 ion factor that has been linked with chronic lymphocytic leukaemia (CLL), but its functions in CLL ma

96 nces in the proportion of cases with chronic lymphocytic leukaemia (CLL)-phenotype MBL and CD5-negati

97 in patients with advanced stages of chronic lymphocytic leukaemia (CLL).

98 e of the neoplastic B lymphocytes in chronic lymphocytic leukaemia (CLL).

99 re associated with poor prognosis in chronic lymphocytic leukaemia (CLL).

100 d genome-wide association studies of chronic lymphocytic leukaemia (CLL, N = 1,842), Hodgkin lymphoma

101 T-cell large granular lymphocytic leukaemia (T-LGL) is a lymphoproliferative d

102 g modified International Workshop on Chronic Lymphocytic Leukaemia 2008 criteria.

103 lation per International Workshop on Chronic Lymphocytic Leukaemia 2008 response criteria modified fo

104 older with a documented diagnosis of chronic lymphocytic leukaemia according to the 2008 Internationa

105 patients with relapsed or refractory chronic lymphocytic leukaemia achieved an overall response.

106 patients with relapsed or refractory chronic lymphocytic leukaemia and could allow some patients to m

107 he treatment of patients with del17p chronic lymphocytic leukaemia and has been incorporated into tre

108 GH and AID off-target sites in human chronic lymphocytic leukaemia and mantle cell lymphoma cell line

109 sion body myositis and T cell large granular lymphocytic leukaemia are rare diseases involving pathog

110 some 17p (del[17p]) in patients with chronic lymphocytic leukaemia confers very poor prognosis when t

111 ong treatment-free survival (TFS) in chronic lymphocytic leukaemia have been investigated, most have

112 Patients with 17p deletion (del17p) chronic lymphocytic leukaemia have poor responses and survival a

113 nt groups (one [2%] patient with fatal acute lymphocytic leukaemia in the lenalidomide group and one

114 second-line therapy in patients with chronic lymphocytic leukaemia is unknown.

115 ears) with previously treated del17p chronic lymphocytic leukaemia or small lymphocytic lymphoma rece

116 Most patients with chronic lymphocytic leukaemia or small lymphocytic lymphoma rela

117 st difficult subset of patients with chronic lymphocytic leukaemia or small lymphocytic lymphoma.

118 d or refractory patients with del17p chronic lymphocytic leukaemia or small lymphocytic lymphoma.

119 in patients with previously treated chronic lymphocytic leukaemia or small lymphocytic lymphoma.

120 sistance in serial samples from five chronic lymphocytic leukaemia patients.

121 8 years) with relapsed or refractory chronic lymphocytic leukaemia requiring treatment who had measur

122 rituximab should allow patients with chronic lymphocytic leukaemia to receive clinical benefit from t

123 and Sept 29, 2015, 314 patients with chronic lymphocytic leukaemia were enrolled and randomly assigne

124 patients with relapsed or refractory chronic lymphocytic leukaemia were enrolled from 15 sites across

125 ged 18 years or older with untreated chronic lymphocytic leukaemia were randomly assigned, via an int

126 8 previously untreated patients with chronic lymphocytic leukaemia were screened for the study; 379 (

127 tients with recurrent or progressive chronic lymphocytic leukaemia who are in complete or partial res

128 afety of venetoclax in patients with chronic lymphocytic leukaemia who are refractory to or relapse d

129 gression in first-line patients with chronic lymphocytic leukaemia who do not achieve minimal residua

130 e treatment option for patients with chronic lymphocytic leukaemia who do not have access to kinase i

131 ith previously untreated progressive chronic lymphocytic leukaemia who had an Eastern Cooperative Onc

132 patients with relapsed or refractory chronic lymphocytic leukaemia whose disease progressed during or

133 with immunophenotypically confirmed chronic lymphocytic leukaemia with active disease, who responded

134 ual disease identifies patients with chronic lymphocytic leukaemia with poor outcome after first-line

135 y of the 2000 mg dose established in chronic lymphocytic leukaemia, the study was amended on Dec 9, 2

136 dverse events (four pneumonia, three chronic lymphocytic leukaemia, two Richter's syndrome, two sepsi

137 ted in familial glioma, melanoma and chronic lymphocytic leukaemia.

138 patients with relapsed or refractory chronic lymphocytic leukaemia.

139 patients with relapsed or refractory chronic lymphocytic leukaemia.

140 patients with relapsed or refractory chronic lymphocytic leukaemia.

141 urther advance treatment of del(17p) chronic lymphocytic leukaemia.

142 tuximab 500 mg/m(2) in patients with chronic lymphocytic leukaemia.

143 with relapsed or refractory del(17p) chronic lymphocytic leukaemia.

144 nib has transformed the treatment of chronic lymphocytic leukaemia.

145 in patients with previously treated chronic lymphocytic leukaemia.

146 patients with relapsed or refractory chronic lymphocytic leukaemia.

147 Patients were eligible if they had chronic lymphocytic leukaemia; were aged 18 years or older; had

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 Chronic lymphocytic leukemia (CLL) patients assigned to stereoty

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

187 Chronic lymphocytic leukemia (CLL) patients progressed early on

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

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

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

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

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

193 8 previously untreated patients with chronic lymphocytic leukemia (CLL) received 8 cycles of either 1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

246 Responses also occurred in chronic lymphocytic leukemia and lymphoma.

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

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

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

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

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

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

253 8 Modified International Workshop on Chronic Lymphocytic Leukemia guidelines) from 31 centres in the

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

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

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

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

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

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

260 ations (myelodysplastic syndrome and chronic lymphocytic leukemia).

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

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

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

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

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

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

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

268 important in clinical management of chronic lymphocytic leukemia.

269 sed tissues in colorectal cancer and chronic lymphocytic leukemia.

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

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

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

273 a BH3 mimetic approved for treating chronic lymphocytic leukemia.

274 nts with acute myelogenous leukemia or acute lymphocytic leukemia.

275 ich develop disease resembling human chronic lymphocytic leukemia.

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

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

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

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

280 d that chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL/SLL) was the principal NHL sub

281 efractory chronic lymphocytic leukemia/small lymphocytic lymphoma (RR-CLL/SLL), irrespective of risk

282 ith chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) that was maintained at 24 hou

283 nts with relapsed or refractory CLL or small lymphocytic lymphoma (SLL) to assess safety, pharmacokin

284 patients with relapsed/refractory CLL/small lymphocytic lymphoma harboring ATM deletions/mutations;

285 el17p chronic lymphocytic leukaemia or small lymphocytic lymphoma received oral ibrutinib 420 mg once

286 with chronic lymphocytic leukaemia or small lymphocytic lymphoma relapse after initial therapy.

287 sk of the chronic lymphocytic leukemia/small lymphocytic lymphoma subtype among women only (253 cases

288 ational Workshop on CLL guidelines) or small lymphocytic lymphoma were eligible for this phase 1b, do

289 with chronic lymphocytic leukaemia or small lymphocytic lymphoma.

290 el17p chronic lymphocytic leukaemia or small lymphocytic lymphoma.

291 eated chronic lymphocytic leukaemia or small lymphocytic lymphoma.

292 f its potential target genes, B-cell chronic lymphocytic /lymphoma 11B (BCL11B) was predicted.

293 mphomas, 2 follicular lymphomas, 4 CLL/small lymphocytic lymphomas (CLL/SLLs), and 1 low-grade NHL no

294 id examinations were consistent with chronic lymphocytic meningitis, but no definitive cause was iden

295 Cerebrospinal fluid (CSF) analysis revealed lymphocytic/monocytic pleocytosis, elevated protein conc

296 sies (especially for patchy diseases such as lymphocytic myocarditis and sarcoidosis) using the gold-

297 y cardiomyopathies in developed countries is lymphocytic myocarditis most commonly caused by a viral

298 ontrol signatures were enriched for immature lymphocytic patterns.

299 a provide information about the cytokine and lymphocytic responses to VZV infection of RPE cells, the

300 Levels of lymphocytic subpopulations may identify breast cancers m