ライフサイエンスコーパス: CLL

1 CLL cell death in vitro and the depth of clinical respon

2 CLL cell proliferation in vitro correlated with RANK exp

3 CLL tumors had elevated basal levels for the phosphoryla

4 CLL with high-level expression of ROR1 also have high-le

5 CLL-1 is prevalent in AML and, unlike other targets such

6 CLL-phenotype MBL was detected in three (1%) Ugandan par

7 ut of 9 RT patients (44%) and in 0 out of 16 CLL patients (0%).

8 macytic lymphomas, 2 follicular lymphomas, 4 CLL/small lymphocytic lymphomas (CLL/SLLs), and 1 low-gr

9 provide experimental evidence that subset #4 CLL cells show low IgG levels, constitutive ERK1/2 activ

10 were examined in longitudinal samples of 48 CLL patients.

11 n the Emu-Tcl1 (Tcl1) CLL mouse model and 68 CLL patients.

12 proach to the evaluation and management of a CLL patient starting on ibrutinib, with the goal of mini

13 Additional CLL trial data are required to establish a more precise

14 erefore studied the activity of MI-2 against CLL and ibrutinib-resistant CLL.

15 ted IGHV Notably, MI-2 was effective against CLL cells collected from patients harboring mutations co

16 BCR cross-linking and was effective against CLL cells harboring features associated with poor outcom

17 ted a role for RPS15 mutations in aggressive CLL, with one-third of RPS15-mutant cases also carrying

18 Thus, we generate two aggressive CLL models and provide a preclinical rational for the us

19 leen colonization in xenograft and allograft CLL mouse models, and prolongs survival in mice.

20 with CTL019 in 2 different diseases (ALL and CLL).

21 Expanded analyses of patients with AML and CLL revealed specific patterns of ex vivo drug combinati

22 T cell phenotype, immune function, and CLL cell immunosuppressive capacity were evaluated.

23 efine a gene expression signature of anergic CLL cells consisting of several NFAT2-dependent genes in

24 d a high-affinity monkey cross-reactive anti-CLL-1 arm and tested several anti-CD3 arms that varied i

25 the anti-FcmuR CAR, purged their autologous CLL cells in vitro without reducing the number of health

26 an RTX in vitro in both normal B cells and B-CLL cells.

27 In contrast, ATA B-CLL did not develop from other B cell subsets, even when

28 1-mediated CD19 and CD20 trogocytosis from B-CLL cells is associated with its ability to induce homot

29 is similar to the aggressive type of human B-CLL, and this valuable model has been widely used for te

30 uding B cell chronic lymphocytic leukemia (B-CLL).

31 of these anti-CD20 Abs appear specific to B-CLL cells.

32 1 B cells bearing restricted BCRs can become CLL during aging.

33 re hypothesized that CD84 may bridge between CLL cells and their microenvironment, promoting cell sur

34 This study suggests an interaction between CLL cells and stromal elements able to simultaneously im

35 The degree of HA varies between CLL patients and positively correlates with the expressi

36 Scores on the Brief Fatigue Inventory (BFI), CLL module of the MD Anderson Symptom Inventory (MDASI)

37 ble in approximately 50% of peripheral blood CLL cases lacking gene mutations.

38 gnaling in freshly isolated peripheral blood CLL cells and in CLL cells cultured with nurselike cells

39 ly resemble the egress phenotype taken on by CLL cells treated with idelalisib.

40 D200 and BTLA as well as IL-10 production by CLL cells.

41 in chronic lymphocytic leukemia (CLL; B-cell CLL) and follicular lymphoma (FL).

42 inker of activation of T cells (LAT); B-cell CLL/lymphoma 11B (BCL11B); RGD, leucine-rich repeat, tro

43 B-cell CLL/lymphoma 6 (BCL6) exerts oncogenic effects in severa

44 nd that, compared with normal naive B cells, CLL cells express a low level of total CD79b protein but

45 domised, double-blind, phase 3 study (CLLM1; CLL Maintenance 1 of the German CLL Study Group), patien

46 In TP53- or ATM-defective CLL cells, inhibition of ATR signaling by AZD6738 led to

47 rate mouse models of Tp53- and Atm-defective CLL mimicking the high-risk form of human disease and sh

48 of human disease and show that Atm-deficient CLL is sensitive to PARP1 inhibition.

49 two mouse models of Atm- and Trp53-deficient CLL.

50 tests for all patients with newly diagnosed CLL in those countries with the resources to do so.

51 an activator of the NFkappaB pathway during CLL progression and suggest that the leukemic clone can

52 eating a cohesive expression profile in each CLL sample despite the presence of genetic heterogeneity

53 Whether this phenomenon also occurs in early CLL phases and its underlying mechanisms have yet to be

54 ata suggest that an appropriately engineered CLL-1 TDB could be effective in the treatment of AML.

55 l targeted therapies is projected to enhance CLL survivorship but can impose a substantial financial

56 ted from thousands of single cells from five CLL samples.

57 -arm phase 2 clinical trial of ibrutinib for CLL between March 2014 and October 2015 at the National

58 tor of BCL2 currently in clinical trials for CLL and other malignancies.

59 41 patients (25 previously untreated for CLL and 16 previously treated) were enrolled.

60 vitro cytotoxic activity of venetoclcax for CLL cells with high-level expression of ROR1, indicating

61 CLL models and characterising biopsies from CLL patients, that NFAT2 is an important regulator for t

62 as accompanied by loss of membrane CD20 from CLL B cells, which was evident with rituximab but not ob

63 T cells from CLL patients in various stages of the disease, modified

64 of PMNs had taken a fraction of the dye from CLL B cells at 3 and 20 hours, respectively, with no sig

65 nts from two randomized trials of the German CLL Study Group (CLL8: fludarabine and cyclophosphamide

66 tudy (CLLM1; CLL Maintenance 1 of the German CLL Study Group), patients older than 18 years and diagn

67 cohort (41 [14%], of whom two [5%] also had CLL-phenotype MBL) than in the UK cohort (six [2%], of w

68 cohort (six [2%], of whom two [33%] also had CLL-phenotype MBL; p<0.0001), but the median absolute B-

69 iNKT cells indeed hinder CLL survival in vitro by restraining CD1d-expressing nur

70 use of PARP inhibitors in ATM-affected human CLL.ATM and TP53 mutations are associated with poor prog

71 In CLL, no data exist exploring the specific changes in the

72 cts of miR-26a, miR-130an and antimiR-155 in CLL therapy.

73 Knockdown of miR-363 in CLL cells prior to CD40/IL-4 stimulation prevented the a

74 se a new pathway for NF-kappaB activation in CLL and highlight the importance of exosomes as extracel

75 utcomes of IgM and IgD isotype activation in CLL cells, providing novel insight into the regulation o

76 g mechanisms leading to BCR over-activity in CLL are not fully understood.

77 y isolated peripheral blood CLL cells and in CLL cells cultured with nurselike cells, a model that mi

78 aluated in primary CLL cells in vitro and in CLL patients.

79 induced dose and time-dependent apoptosis in CLL cells, sparing normal B lymphocytes.

80 demonstrate the benefit of PD-1 blockade in CLL patients with RT, and could change the landscape of

81 zed clinical trials of chemoimmunotherapy in CLL.

82 a signature molecule of p66Shc deficiency in CLL and indicate that ILT3 may functionally contribute t

83 miR-15/16, which may target other drivers in CLL.

84 le for transcription factor dysregulation in CLL, where excess programming by EGR and NFAT with reduc

85 embrolizumab exhibited selective efficacy in CLL patients with RT.

86 eads to increased activity of Syk and Erk in CLL cells.

87 r T-cell kinase whose aberrant expression in CLL cells also associates with BCR signalling capacity,

88 However, unlike ZAP70 whose expression in CLL cells predicts prognosis, we find Lck expression and

89 robust method of measuring Lck expression in CLL cells using flow cytometry.

90 the major driver of PKCbetaII expression in CLL cells where enhanced association of this transcripti

91 the up regulation of PKCbetaII expression in CLL cells, and the first to link SP1 with the pathogenes

92 ILT3 expression in CLL was found to be driven by Deltex1, a suppressor of a

93 (VEGF) regulates PRKCB promoter function in CLL cells, stimulating PKCbeta gene transcription via in

94 ocytic leukaemia (CLL), but its functions in CLL manifestation are still unclear.

95 c management is now becoming a major goal in CLL so that patients can best benefit from the increasin

96 lie inter- and intratumor heterogeneities in CLL affecting disease progression and resistance.

97 n immunotherapy approaches with ibrutinib in CLL and other cancers.

98 The ectopic expression of ILT3 in CLL was a distinctive feature of neoplastic B cells and

99 clinical development of MALT1 inhibitors in CLL, in particular for ibrutinib-resistant forms of this

100 dulators of response to kinase inhibitors in CLL.

101 ion of the B-cell receptor activates JAK2 in CLL cells and the JAK2 inhibitor ruxolitinib improves sy

102 ILT3 as a selective marker of malignancy in CLL and the first example of phenotypic continuity betwe

103 Epigenetic maturation in CLL was associated with an indolent gene expression patt

104 s significantly extend the role of NOTCH1 in CLL pathogenesis, and have direct implications for speci

105 ly increased CD4+ and CD8+ T cell numbers in CLL patients.

106 ings are highly similar to those observed in CLL patients and identify EBI2 as a promoter of B-cell m

107 The results obtained for OBZ in CLL provide new arguments for FcgammaRIIIA-mediated mech

108 elements, thus implicating this oncogene in CLL development.

109 e find Lck expression and disease outcome in CLL are unrelated despite observations that its inhibiti

110 ved molecular chaperone, is overexpressed in CLL compared with resting B cells.

111 eficiency in the signaling adaptor p66Shc in CLL cells, we undertook to identify unique phenotypic tr

112 rucial regulator of the anergic phenotype in CLL.NFAT2 is a transcription factor that has been linked

113 of the gene coding for PKCbetaII, PRKCB, in CLL cells remain poorly described, but could be importan

114 lar mediators promoting tumor progression in CLL.

115 in mechanisms of translational regulation in CLL and normal B cells may provide opportunities for sel

116 c clone, given recent reports on its role in CLL progression.

117 t the therapeutic efficacy of ruxolitinib in CLL are warranted.

118 s showed inhibition of phospho-AKT (S473) in CLL tumor cells following a single dose and near-complet

119 to the over-activity of the BCR signaling in CLL and inhibition of HSP90 has the potential to achieve

120 ight into the regulation of BCR signaling in CLL.

121 s a targetable mediator of BCR signalling in CLL cells, and that variance in Lck expression associate

122 tify a "NOTCH1 gene-expression signature" in CLL cells, and show that this signature is significantly

123 s critical to inhibit immune surveillance in CLL.

124 rated that Lyn in macrophages rather than in CLL cells is critical for the malignancy.

125 Acquired resistance to therapy in CLL is often caused by mutations in the response network

126 nary dynamics induced by targeted therapy in CLL, we perform serial exome and transcriptome sequencin

127 We demonstrate that USP7 is upregulated in CLL cells, and its loss or inhibition disrupts homologou

128 utologous patient CD4(+) T cells internalize CLL-EVs containing miR-363 that targets the immunomodula

129 technologies has provided new insights into CLL complexity, identifying a growing list of putative d

130 Improved delivery of miRNA molecules into CLL cells was obtained by developing a novel system base

131 nhibits CPT, was highly effective in killing CLL cells in stromal microenvironment at clinically achi

132 ey feature of chronic lymphocytic leukaemia (CLL) cells is overexpressed protein kinase CbetaII (PKCb

133 with relapsed chronic lymphocytic leukaemia (CLL) in combination with rituximab.

134 Chronic lymphocytic leukaemia (CLL) is a clonal disorder of mature B cells.

135 thogenesis of chronic lymphocytic leukaemia (CLL) is contingent upon antigen receptor (BCR) expressed

136 Chronic lymphocytic leukaemia (CLL) is the most common clonal B-cell disorder character

137 Several chronic lymphocytic leukaemia (CLL) susceptibility loci have been reported; however, mu

138 patients with chronic lymphocytic leukaemia (CLL) who do not require systemic therapy.

139 n linked with chronic lymphocytic leukaemia (CLL), but its functions in CLL manifestation are still u

140 of cases with chronic lymphocytic leukaemia (CLL)-phenotype MBL and CD5-negative MBL, as well as diff

141 ced stages of chronic lymphocytic leukaemia (CLL).

142 ymphocytes in chronic lymphocytic leukaemia (CLL).

143 prognosis in chronic lymphocytic leukaemia (CLL).

144 on studies of chronic lymphocytic leukaemia (CLL, N = 1,842), Hodgkin lymphoma (HL, N = 1,465) and mu

145 ntrast between chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL) tumors.

146 vival (PFS) in chronic lymphocytic leukemia (CLL) based on 3 randomized, phase 3 clinical trials.

147 ral history of chronic lymphocytic leukemia (CLL) by David Galton in 1966, the considerable heterogen

148 ately 4-13% of chronic lymphocytic leukemia (CLL) cases, where they are associated with disease progr

149 d migration of chronic lymphocytic leukemia (CLL) cells and that these effects were blocked by the hu

150 uman and mouse chronic lymphocytic leukemia (CLL) develops from CD5(+) B cells that in mice and macaq

151 y ibrutinib in chronic lymphocytic leukemia (CLL) has been challenged by the frequent emergence of re

152 loid cells, in chronic lymphocytic leukemia (CLL) has not been well characterized.

153 Treatment of chronic lymphocytic leukemia (CLL) has shifted from chemo-immunotherapy to targeted ag

154 Chronic lymphocytic leukemia (CLL) is a common B-cell malignancy with a remarkably het

155 Chronic lymphocytic leukemia (CLL) is a malignant disease of small mature lymphocytes.

156 Chronic lymphocytic leukemia (CLL) is an incurable disease characterized by accumulati

157 Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of B cells in

158 Chronic lymphocytic leukemia (CLL) is characterized by the expansion of malignant CD5(

159 B-cell chronic lymphocytic leukemia (CLL) is the most common adult human leukemia.

160 al data from a chronic lymphocytic leukemia (CLL) patient, we show that a simple linear phylogeny bet

161 ear cells from chronic lymphocytic leukemia (CLL) patients on clinical trials of ibrutinib (BTK/ITK i

162 Chronic lymphocytic leukemia (CLL) patients progressed early on ibrutinib often develo

163 gressors among chronic lymphocytic leukemia (CLL) patients suggests the existence of a regulatory net

164 In chronic lymphocytic leukemia (CLL) patients with mutated IGHV, 3 recent studies have d

165 management of Chronic Lymphocytic Leukemia (CLL) patients, this common B cell malignancy still remai

166 sed refractory chronic lymphocytic leukemia (CLL) patients.

167 patients with chronic lymphocytic leukemia (CLL) received 8 cycles of either 1000 mg (the current st

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

169 patients with chronic lymphocytic leukemia (CLL) treated with ibrutinib has been attributed to histo

170 inhibition in chronic lymphocytic leukemia (CLL) where the ataxia telangiectasia mutated (ATM)-p53 p

171 patients with chronic lymphocytic leukemia (CLL) who had previously received ibrutinib.

172 ell therapy of chronic lymphocytic leukemia (CLL) with chimeric antigen receptor (CAR)-modified T cel

173 sed/refractory chronic lymphocytic leukemia (CLL) with prolongation of progression-free and overall s

174 emia (ALL) and chronic lymphocytic leukemia (CLL), including the expansion and persistence of CTL019

175 e treatment of chronic lymphocytic leukemia (CLL), mantle cell lymphoma, and Waldenstrom macroglobuli

176 mphoma (iNHL), chronic lymphocytic leukemia (CLL), or T-cell lymphoma (TCL) were treated with 25 or 7

177 etic lesion in chronic lymphocytic leukemia (CLL), promoting overexpression of BCL2, which factors in

178 Within chronic lymphocytic leukemia (CLL), responses to 62% of drugs were associated with 2 o

179 In chronic lymphocytic leukemia (CLL), the increment in PBLs is slower than the expected

180 In human chronic lymphocytic leukemia (CLL), tumor B cells lodge in lymph nodes where interacti

181 management of chronic lymphocytic leukemia (CLL).

182 ories: AML and chronic lymphocytic leukemia (CLL).

183 e treatment of chronic lymphocytic leukemia (CLL).

184 terogeneity of chronic lymphocytic leukemia (CLL).

185 ors, including chronic lymphocytic leukemia (CLL).

186 patients with chronic lymphocytic leukemia (CLL).

187 athogenesis of chronic lymphocytic leukemia (CLL).

188 patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) that was maintaine

189 patients with chronic lymphocytic leukemia (CLL); however, their high cost has raised concerns about

190 ly approved in chronic lymphocytic leukemia (CLL; B-cell CLL) and follicular lymphoma (FL).

191 b (GA101) has been implemented as first-line CLL therapy.

192 ymphomas, 4 CLL/small lymphocytic lymphomas (CLL/SLLs), and 1 low-grade NHL not otherwise specified.

193 In M-CLL, there were fewer genetic lesions, although the meth

194 mple of phenotypic continuity between mature CLL cells and their progenitors in the bone marrow.

195 2, but low-to-negligible miR-15/16 Moreover, CLL cases with high-level ROR1 have deletion(s) at the c

196 Here the authors show, by analysing mouse CLL models and characterising biopsies from CLL patients

197 survivals close to 25 years, and Ig-mutated CLL, where have more aggressive disease with median surv

198 we uncovered mutated LCP1 and WNK1 as novel CLL drivers, supported by functional evidence demonstrat

199 Up to 10% of CLL patients transform from an indolent subtype to an ag

200 40/IL-4 stimulation prevented the ability of CLL-EVs to induce increased synapse signaling and confer

201 structural basis of autonomous activation of CLL B cells, showing that BcR immunoglobulins initiate i

202 id, gammacnull (NSG) mice, administration of CLL cells caused an appreciable compact bone erosion tha

203 ized the BCR kinases and caused apoptosis of CLL cells through the mitochondrial apoptotic pathway.

204 ect the future prevalence and cost burden of CLL in the era of oral targeted therapies in the United

205 tcome after first-line chemoimmunotherapy of CLL patients.

206 oved survival; meanwhile, the annual cost of CLL management will increase from $0.74 billion to $5.13

207 The per-patient lifetime cost of CLL treatment will increase from $147,000 to $604,000 (3

208 ical pathways influencing the development of CLL, HL and MM.

209 athway to trisomy 12, an important driver of CLL.

210 the biological and clinical heterogeneity of CLL and offers opportunities for innovative treatment st

211 single dose and near-complete inhibition of CLL proliferation (Ki-67) by cycle 2.

212 vitro and in vivo disrupt the interaction of CLL cells with their microenvironment, resulting in indu

213 el that evaluated the evolving management of CLL from 2011 to 2025: chemoimmunotherapy (CIT) as the s

214 In the Emu-Tcl1 murine model of CLL, we identified gene expression signatures indicative

215 This SnapShot provides an overview of CLL biology and therapy, with a focus on genetics and mi

216 ngs provide insight into the pathobiology of CLL to suggest a more complex relationship between expre

217 rtant regulator for the anergic phenotype of CLL.

218 the frequency of B1 cells, the precursors of CLL cells in rodents.

219 p66Shc shapes the transcriptional profile of CLL cells and leads to an upregulation of the surface re

220 inished the immune-suppressive properties of CLL cells through BTK-dependent and -independent mechani

221 edian PFS was not reached in the subgroup of CLL patients with mutated IGHV.

222 une response can further promote survival of CLL cells and may contribute to the unfavorable prognosi

223 s a target for a more selective treatment of CLL by CAR T cells.

224 Treatment of CLL cells in vitro with MI-2 inhibited MALT1 proteolytic

225 Treatment of CLL patients with RTX is associated with CD20 loss via a

226 strategy for potential clinical treatment of CLL.

227 s hence fundamental for our understanding of CLL pathogenesis.

228 Fourteen percent of CLLs were driven by mTOR signaling in a non-BCR-dependen

229 s and signal capacity have all linked BCR on CLL cells to disease prognosis.

230 in vitro results show that CD84 expressed on CLL cells interact with CD84 expressed on cells in their

231 sion correlates with high CD1d expression on CLL cells and impaired iNKT cells.

232 ates with negative or low CD1d expression on CLL cells and normal iNKT cells, suggesting indirect leu

233 ional evidence demonstrating their impact on CLL pathways.

234 We report on CLL patients treated with single-agent ibrutinib on an i

235 e selection of CD38 as a molecular target on CLL cells, both consenting efficient and specific intrac

236 the 2008 Modified International Workshop on CLL guidelines) or small lymphocytic lymphoma were eligi

237 her than phagocytosis of anti-CD20-opsonized CLL B cells, and we discuss the implications of this fin

238 osis by purified PMNs of anti-CD20-opsonized CLL B cells, but could detect only the repeated close co

239 the unfavorable prognosis of ZAP-70-positive CLL.

240 olism for their ability to eliminate primary CLL cells.

241 gnature is significantly enriched in primary CLL cases expressing ICN1, independent of NOTCH1 mutatio

242 in kinase (DNA-PK), was evaluated in primary CLL cells in vitro and in CLL patients.

243 cantly increased mRNA translation in primary CLL cells, measured using bulk metabolic labeling and a

244 kinase inhibitors were active in progressive CLL, but outcomes were mixed.

245 earlier (median 7.9 months) than progressive CLL (median 23.4 months) (P = .003).

246 und exclusively in patients with progressive CLL after disease progression.

247 10.7%), in 8 of 10 patients with progressive CLL, and in 1 patient with prolymphocytic transformation

248 r transformation (RT) and 8 with progressive CLL/SLL.

249 somes, both between indolent and progressive CLLs as well as within the individual patients at the on

250 riptional activities of p53 in proliferating CLL cells may offer a possible therapeutic strategy.

251 P90 and its client AKT, but not BTK, reduced CLL viability.

252 nosis and management of ibrutinib-refractory CLL.

253 omplete responses (CRs); relapsed/refractory CLL, 56% (n = 55) with 1 CR; peripheral TCL, 50% (n = 16

254 Twenty-five patients including 16 relapsed CLL and 9 RT (all proven diffuse large cell lymphoma) pa

255 pies for patients with del(17p) and relapsed CLL from 2014, and for first-line treatment from 2016 on

256 3 trial, we enrolled patients with relapsed CLL progressing less than 24 months from last therapy.

257 h ofatumumab alone in patients with relapsed CLL, including in those with high-risk disease, and thus

258 itized p53-defective, chemotherapy-resistant CLL cells to clinically achievable doses of HRR-inducing

259 of MI-2 against CLL and ibrutinib-resistant CLL.

260 ytic leukemia/small lymphocytic lymphoma (RR-CLL/SLL), irrespective of risk factors associated with p

261 polymorphism microarray analyses of a single CLL patient over 29 years of observation and treatment,

262 th human IgG1 therapeutic antibody targeting CLL-1 that could potentially be used in humans to treat

263 istory of the disease in the Emu-Tcl1 (Tcl1) CLL mouse model and 68 CLL patients.

264 We found that Tcl1-CLL cells express CD1d and that iNKT cells critically de

265 Based on previous observations that CLL cells exhibit mitochondrial dysfunction and altered

266 We observed that CLL cells that have recently exited the lymph node micro

267 Signals from the CLL microenvironment promote progression of the disease

268 o-embryonic surface protein expressed on the CLL cells of over 90% of patients, but not on virtually

269 Neonatal B1 B cells and their CLL progeny in aged mice continued to express moderately

270 Thus, even in the era of targeted therapies, CLL with alterations in the ATM/p53 pathway remains a cl

271 ts support the contribution of iNKT cells to CLL immune surveillance and highlight iNKT cell frequenc

272 In contrast, progression due to CLL in 10 patients (11.9%) occurred later, diagnosed at

273 ng the relevance of HIF-1alpha expression to CLL pathogenesis.

274 cell subset and, ultimately, progression to CLL.

275 gnificant decrease in absolute live or total CLL B-cell numbers, confirming that trogocytosis occurs,

276 mg every 3 weeks in relapsed and transformed CLL.

277 outcomes in patients with previously treated CLL.

278 criptome sequencing for 61 ibrutinib-treated CLLs.

279 In U-CLL, increased levels/signaling associated with +12, del

280 aturation status, generally higher than in U-CLL, varied and was increased in cases with lower sIgM l

281 stinguish between patients with Ig-unmutated CLL, where typically have more indolent disease with med

282 3B1, BIRC3, NOTCH1, and ATM in 406 untreated CLL cases by ultra-deep next-generation sequencing, whic

283 ized phase 2 study in symptomatic, untreated CLL patients to evaluate if an obinutuzumab dose respons

284 Similarly, in flow cytometry assays using CLL B-cell targets labeled with the membrane dye PKH67 a

285 BCL6 downregulation were also observed when CLL cells were cocultured with nurselike cells.

286 Results The number of people living with CLL in the United States is projected to increase from 1

287 highly effective in high-risk patients with CLL after they experience treatment failure with ibrutin

288 in the clinical management of patients with CLL and heralded a new era in the clinical treatment of

289 assess the benefit of FCR for patients with CLL and identified 5 randomized trials that met our incl

290 Prospective study of 66 patients with CLL enrolled in a single-arm phase 2 clinical trial of i

291 spective cohort study of older patients with CLL or MM identified from the Surveillance, Epidemiology

292 Methods Twenty-four patients with CLL received lymphodepleting chemotherapy and anti-CD19

293 mplications of this finding in patients with CLL treated with rituximab or obinutuzumab in vivo.

294 Symptomatic patients with CLL who did not require systemic therapy were enrolled a

295 lignant IGH clone in marrow of patients with CLL who responded by IWCLL criteria was associated with

296 INTERPRETATION: In patients with CLL, ruxolitinib was associated with significant improve

297 hly active in the treatment of patients with CLL.

298 ve disease-related symptoms in patients with CLL.

299 e targeted agents, patients progressing with CLL were continued on ibrutinib for up to 3 months, with

300 ssenger RNA levels vary significantly within CLL patients and correlate with the expression of HIF-1a