ライフサイエンスコーパス: CLL

1 ies, including chronic lymphocytic leukemia (CLL).

2 c biomarker of chronic lymphocytic leukemia (CLL).

3 5 mutations in chronic lymphocytic leukemia (CLL).

4 patients with chronic lymphocytic leukemia (CLL).

5 or refractory chronic lymphocytic leukemia (CLL).

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

7 landscape for chronic lymphocytic leukemia (CLL).

8 patients with chronic lymphocytic leukemia (CLL).

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

10 disposition to chronic lymphocytic leukemia (CLL).

11 cer, including chronic lymphocytic leukemia (CLL).

12 s disturbed in chronic lymphocytic leukemia (CLL).

13 er adults with chronic lymphocytic leukemia (CLL).

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

15 ine and treatment of relapsed and refractory CLL.

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

17 sion-free survival in patients with relapsed CLL.

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

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

20 th rituximab alone in patients with relapsed CLL.

21 ncogenic and/or tumor suppressor function in CLL.

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

23 nd ROR1 might be beneficial to patients with CLL.

24 gulation of the expression of mature tRFs in CLL.

25 Similar results were obtained for indolent CLL.

26 on and the regulatory chromatin landscape of CLL.

27 ated in patients with relapsed or refractory CLL.

28 ssociations and the clinical impact of CK in CLL.

29 are encouraging for relapsed and refractory CLL.

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

31 cells from healthy donors and patients with CLL.

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

33 nd has emerged as a breakthrough therapy for CLL.

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

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

36 ed noncoding variants in the pathogenesis of CLL.

37 mice to explore the role of phosphatases in CLL.

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

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

40 e the prognostic impact of this biomarker in CLL.

41 transformation component but had persistent CLL.

42 wnstream targets compared with nonregressing CLL.

43 butes to CLL pathogenesis in mouse and human CLL.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 unctional consequences of these mutations in CLL are unknown.

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

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

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

78 ant advances have been made in understanding CLL biology.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 CLL cells from an idelalisib-treated patient showed decr

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

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

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

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

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

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

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

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

109 CLL cells rely on oxidative phosphorylation for their bi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 ib blocked cytokine-induced proliferation of CLL cells.

125 e highly synergistic in restoring killing of CLL cells.

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

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

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

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

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

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

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

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

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

135 We found that CLL commonly demonstrates not only exponential expansion

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

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

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

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

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

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

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

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

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

145 Spontaneously regressed CLL displayed a transcriptome profile characterized by d

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

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

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

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

150 Thus, CLL epigenetic diversification leads to decreased coordi

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

152 ted coherence across different layers of the CLL epigenome.

153 poorly characterized intermediate-programmed CLL epitype.

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

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

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

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

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

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

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

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

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

163 Notably, human CLLs harboring SF3B1 mutations exhibit altered response

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 CLL is an incurable disease with a heterogeneous clinica

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

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

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

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

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

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

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

187 These CLL-like cells show genome instability and dysregulation

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

189 The CLL lineage tree shape revealed earlier branching and lo

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

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

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

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

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

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

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

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

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

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

200 CLL patients diagnosed with symptomatic COVID-19 across

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

202 0% of positive CLL cells is able to separate CLL patients into 2 subgroups with different prognoses,

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

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

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

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

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

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

209 Nineteen CLL patients were included.

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

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

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

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

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

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

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

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

218 predicted TTFT and OS among newly diagnosed CLL patients.

219 nded with significantly worse survival among CLL patients.

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

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

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

223 iously treated chronic lymphocytic leukemia (CLL) patients.

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

225 ble to determine whether epimutations affect CLL populations homogeneously.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

242 variants as the probable functional basis of CLL risk.

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

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

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

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

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

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

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

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

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

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

253 eviously untreated and treated patients with CLL/SLL.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 aneous CLL regression, with implications for CLL treatment.

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

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

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

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

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

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

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

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

287 016, 42 patients with relapsed or refractory CLL were enrolled in this study and 38 were infused with

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

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

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

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

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

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

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

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

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

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

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

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

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