ライフサイエンスコーパス: CLL

1 CLL cells from an idelalisib-treated patient showed decr

2 CLL cells rely on oxidative phosphorylation for their bi

3 CLL is an incurable disease with a heterogeneous clinica

4 CLL patients diagnosed with symptomatic COVID-19 across

5 CLL relies on the concomitant cooperation of B-cell rece

6 CLL-directed treatment with BTKi's at COVID-19 diagnosis

7 CLL-TIM is an ensemble algorithm composed of 28 machine

8 watch and wait"), while 61% had received >=1 CLL-directed therapy (median, 2; range, 1-8).

9 We examined the impact of epitype in 1286 CLL patients from 4 independent cohorts representing a c

10 present study, we analyzed a cohort of 1630 CLL samples and identified the presence of ~20% of CLL c

11 hose with high-risk disease such as del(17p) CLL.

12 Coculture of T cells with CTLA-4(+) CLL cells decreased IL-2 production.

13 Coculture of CTLA-4(+) CLL cells with CD80-GFP(+) cell lines revealed transfer

14 Thirty patients had a CLL clone >=0.5 x 10(9)/L, enabling next-generation sequ

15 ough ibrutinib increases AID expression in a CLL cell line, it is unable to do so in primary CLL samp

16 ing, we analyzed AID expression and PFs in a CLL cohort before and during ibrutinib treatment.

17 Ninety patients (45%) were receiving active CLL therapy at COVID-19 diagnosis, most commonly Bruton

18 In patients with advanced CLL, a 5 x 10(8) dose of CART-19 may be more effective t

19 ble to determine whether epimutations affect CLL populations homogeneously.

20 on in the microenvironment protected against CLL and acute myeloid leukemia.

21 nded with significantly worse survival among CLL patients.

22 eal carcinoma, an EBV-associated cancer, and CLL/SLL forms of non-Hodgkin lymphomas; these cancers we

23 ning effects of baseline characteristics and CLL-directed therapy, is critical to optimally manage CL

24 significant increase of myeloid leukemia and CLL incidences was strongly correlated with the U.S. pop

25 ever, the incidences of myeloid leukemia and CLL significantly outpaced that of all cancers.

26 Interestingly, archetypal CLL genomic aberrations including HIST1H1B and TP53 muta

27 ight be an effective modality for blocking B-CLL growth in patients.

28 y boosts in vitro cycling of blood-derived B-CLL cells following CpG DNA priming.

29 Using CpG DNA-primed human B-CLL clones and approaches involving both immunofluoresce

30 for selective introduction of miR-29b into B-CLL cells for therapeutic benefit.

31 ined for continued cycling of CFSE-labeled B-CLL cells.

32 ne found within spleens and lymph nodes of B-CLL patients, significantly boosts in vitro cycling of b

33 The CD49d+ subpopulation from CD49d bimodal CLL displayed higher levels of proliferation compared wi

34 s pattern of CD49d expression, CD49d bimodal CLL showed a higher level of variability in sequential s

35 ditionally, transfection of peripheral blood CLL cells with STAT3 short hairpin RNA downregulated Wnt

36 erienced clinical behavior similar to CD49d+ CLL, both in chemoimmunotherapy (n = 1522) and in ibruti

37 rosurvival circuit that provides circulating CLL cells with a microenvironment-independent survival a

38 Me-iPLEX was used to classify CLL samples into 1 of 3 known epigenetic subtypes (epity

39 ms in the clinic, for each patient with CLL, CLL-TIM provides explainable predictions through uncerta

40 , epitype predicted TTP and OS with 2 common CLL therapies: chemoimmunotherapy and ibrutinib.

41 CLL) due to immune dysfunction and cytotoxic CLL treatment.

42 inib with venetoclax to eradicate detectable CLL with the intention of stopping therapy.

43 d IgH.TEmu mice, which spontaneously develop CLL, and stable EMC CLL cell lines derived from these mi

44 ms IGLV3-21*01-expressing B cells to develop CLL.

45 predicted TTFT and OS among newly diagnosed CLL patients.

46 dicate that BTKi therapy can provide durable CLL control after disease progression on venetoclax.

47 ch spontaneously develop CLL, and stable EMC CLL cell lines derived from these mice to explore the ro

48 L by including all IGLV3-21(R110)-expressing CLL cases regardless of IGHV mutational status.

49 10)), we show that IGLV3-21(R110)-expressing CLL represents a distinct subset with poor prognosis ind

50 ve ability (area under the curve = 0.80) for CLL, in particular among older, male participants.

51 e lymphoma, and 50% (95% CI, 16% to 84%) for CLL.

52 re were limited therapeutic alternatives for CLL, which often resulted in treating through the advers

53 er of therapeutic alternatives available for CLL, discussion of efficacy and potential adverse effect

54 aneous CLL regression, with implications for CLL treatment.

55 Robust analysis of outcomes for CLL patients, particularly examining effects of baseline

56 nd has emerged as a breakthrough therapy for CLL.

57 shared with other kinase inhibitors used for CLL treatment, such as the BTK inhibitor ibrutinib and t

58 Because ibrutinib forces CLL cells out of the LN, we hypothesized that ibrutinib

59 nanopore sequencing of full-length cDNA from CLL samples with and without SF3B1 mutation, as well as

60 y data as well as our own ChIP-seq data from CLL patients, we identified six candidate functional var

61 T cells derived from CLL patients or murine CLL models are skewed to an antig

62 Phenotyping Tregs from CLL patients treated with idelalisib supported our in vi

63 hibit GLI1, was highly cytotoxic for GLI1(+) CLL cells relative to that of CLL cells without GLI1.

64 ions also were GLI1(+) Patients with GLI1(+) CLL cells had a shorter median treatment-free survival t

65 Eligible patients had CLL, were previously treated, were aged 18 years or olde

66 ows that a large proportion of patients have CLL cells with activated Hh signaling, which is associat

67 (CLL) identified 89 (11%) patients as having CLL cells with mutations in genes encoding proteins that

68 butes to CLL pathogenesis in mouse and human CLL.

69 signaling, which we also identified in human CLL cases.

70 n and enhanced basal calcium levels in human CLL cells.

71 Importantly, also in human CLL, we found overexpression of many phosphatases includ

72 Notably, human CLLs harboring SF3B1 mutations exhibit altered response

73 e the prognostic impact of this biomarker in CLL.

74 re(4,5), and growing populations of cells in CLL diversify by stochastic changes in DNA methylation k

75 have previously shown that CD8(+) T cells in CLL exhibit impaired activation and reduced glucose upta

76 CD8(+) T cells in CLL patients are chronically exposed to leukemic B cells

77 ssociations and the clinical impact of CK in CLL.

78 d epigenetic-transcriptional coordination in CLL is also reflected in the dysregulation of the transc

79 ed drug-induced DNA damage and cell death in CLL primary cells.

80 BXW7 in CLL, we truncated the WD40 domain in CLL cell line HG-3 via clustered regularly interspaced s

81 To identify target proteins of FBXW7 in CLL, we truncated the WD40 domain in CLL cell line HG-3

82 re tRFs were up-regulated at least 2-fold in CLL, while 701 fragments were down-regulated at least 2-

83 ncogenic and/or tumor suppressor function in CLL.

84 al fitness of CD8(+) T cells are impaired in CLL.

85 gnition of B cells carrying this mutation in CLL patients or healthy donors.

86 unctional consequences of these mutations in CLL are unknown.

87 e highly stable CD49d expression observed in CLL patients with a homogeneous pattern of CD49d express

88 that genome-wide DNA methylation patterns in CLL are strongly associated with phenotypic differentiat

89 Profiling by BH3 mimetics was performed in CLL cells fully resistant to venetoclax due to CD40-medi

90 mice to explore the role of phosphatases in CLL.

91 that CD49d can drive disease progression in CLL, and that the pattern of CD49d expression should als

92 of pre-tRNA(His), and are down-regulated in CLL 3- to 5-fold vs. normal B cells.

93 preinfusion products forecasted response in CLL successfully in discovery and validation cohorts and

94 network that are known to play key roles in CLL.

95 ed an anergic response to BCR stimulation in CLL cells.

96 failure of immune-therapeutic strategies in CLL and may lead to improved targeting in the future.

97 emains current standard-of-care treatment in CLL.

98 gulation of the expression of mature tRFs in CLL.

99 t be axiomatically considered unfavorable in CLL, representing a heterogeneous group with variable cl

100 moter and induces the expression of Wnt5a in CLL cells.

101 tigated the expression of all mature tRFs in CLLs vs. normal controls.

102 R) activation, which may occur in individual CLL patients, catalytically-inactive BTK restored the ab

103 Similar results were obtained for indolent CLL.

104 ell lines revealed transfer of CD80-GFP into CLL tumor cells, similar to CTLA-4(+) T cells able to tr

105 Chronic lymphocytic leukaemia (CLL) is a highly informative model for cancer evolution

106 h dynamics of chronic lymphocytic leukaemia (CLL) to analyse the growth rates and corresponding genom

107 or refractory chronic lymphocytic leukaemia (CLL) who are on targeted therapies.

108 Chronic lymphocytic leukaemia (CLL), the most frequent type of leukaemia in adults, is

109 we focused on chronic lymphocytic leukaemia (CLL), where MIM showed high overall expression, however,

110 e effective in chronic lymphocytic leukemia (CLL) after previous progression on venetoclax.

111 myeloma (MM), chronic lymphocytic leukemia (CLL) and acute myeloid leukemia, we compare the performa

112 DNA damage in chronic lymphocytic leukemia (CLL) and lymphoma patient-derived primary cells as well

113 r treatment of chronic lymphocytic leukemia (CLL) and non-Hodgkin lymphoma, but the mechanisms confer

114 y activated by chronic lymphocytic leukemia (CLL) B-cell targets opsonized with glycoengineered anti-

115 phenomenon in chronic lymphocytic leukemia (CLL) but its biological basis remains unknown.

116 Chronic lymphocytic leukemia (CLL) cells cycle between lymph node (LN) and peripheral

117 e prognosis of chronic lymphocytic leukemia (CLL) depends on different markers, including cytogenetic

118 patients with chronic lymphocytic leukemia (CLL) due to immune dysfunction and cytotoxic CLL treatme

119 e treatment of chronic lymphocytic leukemia (CLL) has been revolutionized by targeted therapies that

120 management of chronic lymphocytic leukemia (CLL) has undergone dramatic changes over the previous 2

121 usly untreated chronic lymphocytic leukemia (CLL) have been limited.

122 patients with chronic lymphocytic leukemia (CLL) identified 89 (11%) patients as having CLL cells wi

123 then, and the chronic lymphocytic leukemia (CLL) incidence has increased continuously since 1998.

124 therapies for chronic lymphocytic leukemia (CLL) include venetoclax, the oral inhibitor of B-cell ly

125 Chronic lymphocytic leukemia (CLL) is a malignancy of mature B cells driven by B-cell

126 landscape for chronic lymphocytic leukemia (CLL) is rapidly evolving.

127 Chronic lymphocytic leukemia (CLL) is the most common adult leukemia in Western countr

128 mu-TCL1 murine chronic lymphocytic leukemia (CLL) model impaired B cell receptor signaling and B cell

129 Chronic lymphocytic leukemia (CLL) occurs in 2 major forms: aggressive and indolent.

130 ated in 10% of chronic lymphocytic leukemia (CLL) patients and is associated with poor outcome.

131 e dysfunction, chronic lymphocytic leukemia (CLL) patients may be at particularly high risk of infect

132 fractory (R/R) chronic lymphocytic leukemia (CLL) patients treated with CD19-targeted chimeric antige

133 iously treated chronic lymphocytic leukemia (CLL) patients.

134 B-cell chronic lymphocytic leukemia (CLL) results from accumulation of leukemic cells that ar

135 Chronic lymphocytic leukemia (CLL) risk stratification studies typically focus on time

136 Chronic lymphocytic leukemia (CLL) therapy has changed dramatically with the introduct

137 tic factors in chronic lymphocytic leukemia (CLL) treated with chemoimmunotherapy, but are less well

138 with relapsed chronic lymphocytic leukemia (CLL) was terminated early because of superior efficacy o

139 patients with chronic lymphocytic leukemia (CLL) with inhibitors of Bruton's tyrosine kinase (BTK),

140 In chronic lymphocytic leukemia (CLL), acquired T-cell dysfunction impedes development of

141 In chronic lymphocytic leukemia (CLL), AID is overexpressed in the proliferative fraction

142 patients with chronic lymphocytic leukemia (CLL), but its efficacy in combination with other agents

143 tly mutated in chronic lymphocytic leukemia (CLL), but its role in the pathogenesis of CLL remains el

144 effective for chronic lymphocytic leukemia (CLL), focusing attention on improving efficacy.

145 reased risk of chronic lymphocytic leukemia (CLL), follicular lymphoma (FL), and diffuse large B-cell

146 In chronic lymphocytic leukemia (CLL), intra-tumoral DNA methylation (DNAme) heterogeneit

147 In chronic lymphocytic leukemia (CLL), signaling through several prosurvival B cell surfa

148 ies, including chronic lymphocytic leukemia (CLL).

149 c biomarker of chronic lymphocytic leukemia (CLL).

150 5 mutations in chronic lymphocytic leukemia (CLL).

151 patients with chronic lymphocytic leukemia (CLL).

152 or refractory chronic lymphocytic leukemia (CLL).

153 rst line [1L]) chronic lymphocytic leukemia (CLL).

154 landscape for chronic lymphocytic leukemia (CLL).

155 patients with chronic lymphocytic leukemia (CLL).

156 sion-making in chronic lymphocytic leukemia (CLL).

157 disposition to chronic lymphocytic leukemia (CLL).

158 cer, including chronic lymphocytic leukemia (CLL).

159 s disturbed in chronic lymphocytic leukemia (CLL).

160 er adults with chronic lymphocytic leukemia (CLL).

161 ly it to study chronic lymphocytic leukemia (CLL).

162 patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL).

163 ma (n = 8), or chronic lymphocytic leukemia (CLL; n = 7).

164 's lymphoma or chronic lymphocytic leukemia [CLL]).

165 e been approved for B-cell malignancies like CLL, small lymphocytic lymphoma, and so forth.

166 of IGHV mutations distinguishes mutated (M) CLL with a markedly superior prognosis from unmutated (U

167 PI3Kdelta inhibitor idelalisib on malignant CLL cells but also on healthy human T, B, and NK lymphoc

168 ted therapy, is critical to optimally manage CLL patients through this evolving pandemic.

169 uximab was given intravenously (NHL, 900 mg; CLL, 600 or 900 mg) for 12 cycles.

170 e develop the CLL Treatment-Infection Model (CLL-TIM) that identifies patients at risk of infection o

171 me instability and dysregulation of multiple CLL-associated cellular processes, including deregulated

172 in Tcl-1 transgenic mice developing a murine CLL highly similar to the human disease.

173 T cells derived from CLL patients or murine CLL models are skewed to an antigen-experienced T-cell s

174 Patients with RP-mutant CLL also demonstrated a higher mutational burden, enrich

175 psed/refractory or high-risk treatment-naive CLL.

176 This allows us to successfully predict new CLL-related DNA elements.

177 Nineteen CLL patients were included.

178 shortened telomeres similar to nonregressing CLL, indicating prior proliferation.

179 wnstream targets compared with nonregressing CLL.

180 mples and identified the presence of ~20% of CLL cases (n = 313) characterized by a bimodal expressio

181 -determining regions (CDRs) classify ~30% of CLL cases into prognostically important subsets.

182 gulator of NOTCH1, is mutated in 2% to 6% of CLL patients.

183 variants as the probable functional basis of CLL risk.

184 Conversely, a single case of CLL relapse following spontaneous regression was associa

185 tter understanding of the characteristics of CLL tumors and to elucidate the relationship between clo

186 gnatures, including robust classification of CLL epitypes that independently stratify patient risk at

187 hat dynamic changes in the disease course of CLL were shaped by the genetic events that were already

188 ose to expand the conventional definition of CLL subset 2 to subset 2L by including all IGLV3-21(R110

189 f cellular senescence and the development of CLL-like disease in elderly mice.

190 Examinations of CLL patients with late relapses while on ibrutinib, whic

191 nd progression to highly aggressive forms of CLL, and the advent of new therapies targeting crucial b

192 n is identified in approximately one-half of CLL cases even in the absence of NOTCH1 mutations.

193 formation thus charts the lineage history of CLL and its evolution with therapy.

194 e highly synergistic in restoring killing of CLL cells.

195 on and the regulatory chromatin landscape of CLL.

196 We found that a significant majority of CLL patients appear to have multiple clones distinguishe

197 Here we describe a novel mechanism of CLL tumor immune evasion that is independent of T-cell e

198 iring patterns not only in the CS network of CLL cells, but also of healthy cells.

199 We observed that the common clonal origin of CLL results in a consistently increased epimutation rate

200 etic lesions involved in the pathogenesis of CLL and how these genetic insights influence clinical ma

201 a (CLL), but its role in the pathogenesis of CLL remains elusive.

202 ed noncoding variants in the pathogenesis of CLL.

203 ib blocked cytokine-induced proliferation of CLL cells.

204 protein levels, implying that, regardless of CLL cells' ROR1 levels, blocking the interaction between

205 ed sensitivity or even primary resistance of CLL to these drugs.

206 basis, showing a ~ 8-fold increased risk of CLL in first-degree relatives.

207 These data suggest that the subgroup of CLL patients admitted with COVID-19, regardless of disea

208 eptor ROR1 are coexpressed on the surface of CLL cells, and Western immunoblotting showed an inverse

209 ic for GLI1(+) CLL cells relative to that of CLL cells without GLI1.

210 otherapy has revolutionized the treatment of CLL, residual disease, acquired resistance, suboptimal d

211 cohorts representing a comprehensive view of CLL disease course and therapies.

212 CTLA-4 on CLL-derived human cell lines decreased CD80 expression o

213 se rate using 2018 International Workshop on CLL (iwCLL) criteria was 83%, and 61% achieved a minimal

214 eatment as per the international workshop on CLL 2008 criteria.

215 s were response by International Workshop on CLL criteria, safety, and progression-free and overall s

216 contrast, trogocytosis of antibody-opsonized CLL B cells by PMNs was mediated primarily by FcgammaRII

217 identifies patients at risk of infection or CLL treatment within 2 years of diagnosis as validated o

218 mpared with peripheral blood (PB), and in PB CLL subsets expressing the CXCR4dim/CD5bright phenotype,

219 transformation component but had persistent CLL.

220 or the extensively validated 30% of positive CLL cells is able to separate CLL patients into 2 subgro

221 es of RNA expression and DNAme in 22 primary CLL and 13 healthy donor B lymphocyte samples.

222 sed p21 expression in cell lines and primary CLL cells in vitro.

223 cell line, it is unable to do so in primary CLL samples.

224 rs in this contemporary cohort include prior CLL for squamous cell carcinoma and basal cell carcinoma

225 poorly characterized intermediate-programmed CLL epitype.

226 AR T cells with concurrent ibrutinib for R/R CLL were well tolerated, with low CRS severity, and led

227 s close homolog Ship1, significantly reduced CLL formation in IgH.TEmu mice.

228 ine and treatment of relapsed and refractory CLL.

229 are encouraging for relapsed and refractory CLL.

230 thout bulky lymphadenopathy, BCRi-refractory CLL, or an adverse mutation profile had the most durable

231 ival in patients with relapsed or refractory CLL treated with targeted therapy.

232 016, 42 patients with relapsed or refractory CLL were enrolled in this study and 38 were infused with

233 ated in patients with relapsed or refractory CLL.

234 d safety of ibrutinib in relapsed/refractory CLL and consideration of study provisions that allow cro

235 c inhibitor effective in relapsed/refractory CLL and follicular lymphoma.

236 study, 134 patients with relapsed/refractory CLL or SLL (median age, 66 years [range, 42-85 years]; m

237 onsecutive patients with relapsed/refractory CLL who received a BTKi (ibrutinib, n = 21; zanubrutinib

238 st-line and treatment of relapsed/refractory CLL.

239 Spontaneously regressed CLL displayed a transcriptome profile characterized by d

240 tions indicate that spontaneously regressing CLL appear to undergo a period of proliferation before e

241 therapy options for first-line and relapsed CLL, it is ever more important to develop sound rational

242 , approved in the United States for relapsed CLL/SLL and FL.

243 led 208 patients with CLL, 181 with relapsed CLL and 27 treatment-naive patients with high-risk disea

244 sion-free survival in patients with relapsed CLL.

245 th rituximab alone in patients with relapsed CLL.

246 paB, STAT1, and STAT3 in lymph node-resident CLL cells and in cells stimulated with CpG oligonucleoti

247 tion is overexpressed in lymph node-resident CLL cells compared with cells in the blood.

248 ribe targeted delivery of miR-29b to ROR1(+) CLL cells leading to downregulation of DNMT1 and DNMT3A,

249 expression of Bcl-XL and Mcl-1 and sensitize CLL cells to venetoclax.

250 0% of positive CLL cells is able to separate CLL patients into 2 subgroups with different prognoses,

251 was associated with increased BCR signaling, CLL proliferation, and clonal evolution.

252 ical and clinical features of 20 spontaneous CLL regression cases incorporating phenotypic, functiona

253 iological processes underpinning spontaneous CLL regression, with implications for CLL treatment.

254 From a clinical standpoint, CLL patients with CD49d bimodal expression, regardless o

255 Surprisingly, CLL driver genes are characterized by specific local wir

256 d that other signaling pathways that sustain CLL cell survival are only partially inhibited by ibruti

257 wide expression profiling comparing IgH.TEmu CLL cells with wild-type splenic B cells identified 96 d

258 in both EMC cell lines and primary IgH.TEmu CLL cells.

259 We found that CLL commonly demonstrates not only exponential expansion

260 The CLL epigenome is also an important disease-defining feat

261 The CLL lineage tree shape revealed earlier branching and lo

262 onse to ibrutinib between cell lines and the CLL clone and imply that ibrutinib could differ from ide

263 nt of a number of prognostic factors and the CLL International Prognostic Index, which is helpful in

264 any correlated (r2 >= 0.5) variants, at the CLL risk loci located outside of gene promoters.

265 We found that ibrutinib decreases the CLL PFs and, interestingly, also reduces AID expression,

266 In this work, we develop the CLL Treatment-Infection Model (CLL-TIM) that identifies

267 ted coherence across different layers of the CLL epigenome.

268 These CLL-like cells show genome instability and dysregulation

269 Thus, CLL epigenetic diversification leads to decreased coordi

270 e provide evidence that SHIP2 contributes to CLL pathogenesis in mouse and human CLL.

271 d, in day 28 samples, reported responders to CLL therapy with high accuracy.

272 kedly superior prognosis from unmutated (UM) CLL cases.

273 ant advances have been made in understanding CLL biology.

274 uzumab in patients with previously untreated CLL and coexisting conditions.

275 ata from samples of 258 previously untreated CLL patients to gain a better understanding of the chara

276 Among patients with untreated CLL and coexisting conditions, venetoclax-obinutuzumab w

277 alcium ([Ca(2+)] (i) ), we show that various CLL-specific PLCgamma(2) variants such as PLCgamma(2)S70

278 Our results indicate that, while CLL cells are in the process of building their survival

279 hese patients, 7 (4 with lymphoma and 3 with CLL) had a complete remission, and 1 had remission of th

280 e ibrutinib for unselected older adults with CLL is unlikely to be cost-effective under current prici

281 ithin the host TET2 gene was associated with CLL remission.

282 Compared with CLL patients treated with CAR T cells without ibrutinib,

283 orithms in the clinic, for each patient with CLL, CLL-TIM provides explainable predictions through un

284 mbination with other agents in patients with CLL and coexisting conditions is not known.

285 n treatment-free survival than patients with CLL cells lacking expression of GLI1 independent of IGHV

286 BTK resynthesis was faster in patients with CLL than in healthy volunteers.

287 Delaying ibrutinib for most patients with CLL until later lines of therapy may be a reasonable str

288 Patients with CLL were randomly assigned to 2 years of venetoclax (Ven

289 d cohort of previously treated patients with CLL who are at high risk of death, and could be used in

290 We enrolled 208 patients with CLL, 181 with relapsed CLL and 27 treatment-naive patien

291 eep remission for most treated patients with CLL, including those with high-risk disease such as del(

292 tumumab in high-risk, relapsed patients with CLL, provided support for approval of ibrutinib in the U

293 ns of leukaemia cells from 107 patients with CLL, spanning decades-long disease courses.

294 ithms based on data from 4,149 patients with CLL.

295 egimen for high-risk and older patients with CLL.

296 nd ROR1 might be beneficial to patients with CLL.

297 cells from healthy donors and patients with CLL.

298 eviously untreated and treated patients with CLL/SLL.

299 The associations of sCD23 with CLL and DLBCL and CXCL13 with DLBCL persisted among case

300 , we provide strategies we use in real-world CLL clinical practice to address common adverse events a