ライフサイエンスコーパス: CLL

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

2 management of chronic lymphocytic leukemia (CLL).

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

4 ced stages of chronic lymphocytic leukaemia (CLL).

5 e treatment of chronic lymphocytic leukemia (CLL).

6 terogeneity of chronic lymphocytic leukemia (CLL).

7 ymphocytes in chronic lymphocytic leukaemia (CLL).

8 ors, including chronic lymphocytic leukemia (CLL).

9 patients with chronic lymphocytic leukemia (CLL).

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

11 prognosis in chronic lymphocytic leukaemia (CLL).

12 athogenesis of chronic lymphocytic leukemia (CLL).

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

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

15 rtant regulator for the anergic phenotype of CLL.

16 nosis and management of ibrutinib-refractory CLL.

17 mg every 3 weeks in relapsed and transformed CLL.

18 dulators of response to kinase inhibitors in CLL.

19 hly active in the treatment of patients with CLL.

20 ve disease-related symptoms in patients with CLL.

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

22 zed clinical trials of chemoimmunotherapy in CLL.

23 lar mediators promoting tumor progression in CLL.

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

25 ight into the regulation of BCR signaling in CLL.

26 strategy for potential clinical treatment of CLL.

27 outcomes in patients with previously treated CLL.

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

29 cell subset and, ultimately, progression to CLL.

30 s critical to inhibit immune surveillance in CLL.

31 criptome sequencing for 61 ibrutinib-treated CLLs.

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

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

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

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

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

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

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

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

40 41 patients (25 previously untreated for CLL and 16 previously treated) were enrolled.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

55 10.7%), in 8 of 10 patients with progressive CLL, and in 1 patient with prolymphocytic transformation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 3B1, BIRC3, NOTCH1, and ATM in 406 untreated CLL cases by ultra-deep next-generation sequencing, whic

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

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

80 2, but low-to-negligible miR-15/16 Moreover, CLL cases with high-level ROR1 have deletion(s) at the c

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

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

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

84 CLL cell proliferation in vitro correlated with RANK exp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 1-mediated CD19 and CD20 trogocytosis from B-CLL cells is associated with its ability to induce homot

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 olism for their ability to eliminate primary CLL cells.

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

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

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

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

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

149 elements, thus implicating this oncogene in CLL development.

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

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

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

153 1 B cells bearing restricted BCRs can become CLL during aging.

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

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

156 40/IL-4 stimulation prevented the ability of CLL-EVs to induce increased synapse signaling and confer

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 Signals from the CLL microenvironment promote progression of the disease

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

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

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

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

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

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

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

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

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

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

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

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

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

207 s hence fundamental for our understanding of CLL pathogenesis.

208 ional evidence demonstrating their impact on CLL pathways.

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

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

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

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

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

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

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

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

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

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

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

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

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

222 embrolizumab exhibited selective efficacy in CLL patients with RT.

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

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

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

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

227 were examined in longitudinal samples of 48 CLL patients.

228 tcome after first-line chemoimmunotherapy of CLL patients.

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

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

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

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

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

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

235 sed refractory chronic lymphocytic leukemia (CLL) patients.

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

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

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

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

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

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

242 3 trial, we enrolled patients with relapsed CLL progressing less than 24 months from last therapy.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 CLL tumors had elevated basal levels for the phosphoryla

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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