ライフサイエンスコーパス: MCL

1 MCL (57% [4 of 7]), DLBCL (56% [5 of 9]), and MF (88% [7

2 MCL is an aggressive B-cell lymphoma that overexpresses

3 MCL patients typically live for years but experience mul

4 MCL reduced IL-6 secretion through down-regulating NF-ka

5 MCL showed large interpatient variability in basal level

6 MCL, an uncommon B-cell lymphoma driven by dysregulated

7 MCL-1 association with genomic DNA increased postirradia

8 MCL-1 is an antiapoptotic member of the BCL-2 protein fa

9 CL-2 family members myeloid cell leukemia 1 (MCL-1) and BCL-XL in lymphoma cells.

10 Myeloid cell leukemia 1 (MCL-1) is a prosurvival BCL-2 protein family member high

11 i-apoptotic protein myeloid cell leukemia 1 (MCL-1) is exploited by the intra-macrophage parasite Lei

12 related protein A1, myeloid cell leukemia 1 (MCL-1), and BCL2 interacting mediator of cell death.

13 rrant expression of myeloid cell leukemia-1 (MCL-1) is a major cause of drug resistance in triple-neg

14 BCL-2 and myeloid cell leukemia sequence 1 (MCL-1) promote multiple myeloma (MM) cell survival.

15 for violations of the 10 mg nitrate-N L(-1) MCL in the conterminous U.S.

16 genes identified in the exome cohort in 191 MCL tumors, each having clinical follow-up data.

17 ting responders from non-responders to BCL-2/MCL-1 targeted therapy.

18 nodal (n = 28), and primary splenic (n = 27) MCL cases.

19 Overall response rate was 44% (MCL, 75%; FL, 38%; DLBCL, 18%).

20 DNA methylation profiles in the context of 5 MCL reference epigenomes.

21 -five patients were included; ocular adnexal MCL was found to be most common in older individuals (me

22 vel combination therapeutic strategy against MCL and other B-cell malignancies.

23 ed chemotherapy refractoriness in aggressive MCL.

24 logic inhibition induced cytotoxicity in all MCL models.

25 aining why in vivo combinations of BCL-2 and MCL-1 antagonists are more effective when concurrent rat

26 ty, suggesting that cotargeting of BCL-2 and MCL-1 could be an effective treatment strategy in myelom

27 lcineurin blockade synergized with BCL-2 and MCL-1 inhibitors in killing ABC DLBCL cells.

28 ance to BH3 mimetic antagonists of BCL-2 and MCL-1 is an important clinical problem.

29 ib resistance in primary human MCL cells and MCL cell lines expressing wild-type Bruton's tyrosine ki

30 DLBCL and MCL had a poor prognosis (5-year DSS, 21% and 50%, respe

31 of 92% and 71%, respectively) than DLBCL and MCL patients (10-year disease-specific survival of 41% a

32 RT), whereas high-grade lymphomas (DLBCL and MCL) were treated with chemotherapy in combination with

33 High-grade DLBCL and MCL, as well as MF, are frequently secondary eyelid lymp

34 g a markedly better prognosis than DLBCL and MCL.

35 with orbital lymphoma: EMZL, DLBCL, FL, and MCL.

36 widespread lymphoma (stage IIIE or IVE) and MCL of any stage were managed with chemotherapy with or

37 oth C-type lectin receptors (CLR) Mincle and MCL in Msg protein presence alone but to even greater am

38 inhibitors through repression of p-STAT3 and MCL-1 induction, known resistance mechanisms of MEK inhi

39 cquired resistance to BCL-2 (venetoclax) and MCL-1 (S63845) antagonists, we identify common principle

40 eavage of PARP-1, downregulation of XIAP and MCL-1, and activation of caspases, which collectively co

41 ib was primarily mediated through BCL-xL and MCL-1-dependent mechanisms that might complement BCL-2 b

42 high levels of BCL-2 relative to BCL-XL and MCL-1.

43 TOR or the antiapoptotic proteins BCL-XL and MCL-1.

44 S63845, the targeting of BCL-2, BCL-XL, and MCL-1 is now possible in vivo, but optimal clinical use

45 eversal of drug resistance and enhanced anti-MCL activity in MCL patient samples and patient-derived

46 n with ABT-199, downregulated anti-apoptotic MCL-1 and BCL-XL levels, which likely contribute to the

47 ore likely to continue exceeding the arsenic MCL, raising environmental justice concerns.

48 st for routine diagnostic practice to assess MCL prognosis.

49 processes driven by dynamic feedback between MCL cells and TME, leading to kinome adaptive reprogramm

50 ed by recombination-activating genes in both MCL subtypes, whereas in 8% of cases the translocation o

51 beta-cells, a process partially prevented by MCL-1 overexpression.

52 In RNA-seq data from 103 of these cases, MCL tumors with these mutations had a distinct imbalance

53 x in murine xenograft models of mantle cell (MCL), germinal-center diffuse large B-cell (GCB-DLBCL),

54 We therefore cocultured primary circulating MCL cells from 21 patients several weeks ex vivo with st

55 ist of GO terms using the Markov Clustering (MCL) algorithm, based on the overlap of gene members bet

56 In conclusion, MCL can help maintain immune equilibrium and decrease PG

57 This contrasted MCL tumors, where alpha-BCR-induced signaling was variab

58 ment with 2 molecular subtypes, conventional MCL (cMCL) and leukemic non-nodal MCL (nnMCL), that diff

59 CL-2 and functionally redundant counterpart, MCL-1, are frequently over-expressed in high-risk diffus

60 We assigned CWSs and counties MCL compliance categories (High if above the MCL; Low if

61 ses were indistinguishable from cyclin D1(+) MCL.

62 A minor subset of 4 cyclin D1(-) MCL cases lacked cyclin D rearrangements and showed upre

63 and gene-expression profiles of cyclin D1(-) MCL cases were indistinguishable from cyclin D1(+) MCL.

64 However, a small subset of cyclin D1(-) MCL has been recognized, and approximately one-half of t

65 identification and diagnosis of cyclin D1(-) MCL.

66 hile the primary event in cyclin D1(-)/D2(-) MCL remains elusive.

67 A subset of cyclin D1(-)/D2(-)/D3(-) MCL with aggressive features has cyclin E dysregulation.

68 Importantly, decreased MCL-1 expression was observed in islets from patients wi

69 e results identify NOXA mRNA destabilization/MCL-1 adaptation as a non-genomic mechanism that limits

70 combining these agents with newly developed MCL-1 inhibitors in the clinic.

71 ectedly, decreased BACH2 levels in dispersed MCL cells were due to direct transcriptional repression

72 DLBCL, MCL, and disseminated EMZL and FL were primarily treated

73 ly of the lymphoma subtypes EMZL, FL, DLBCL, MCL, and MF.

74 ernal beam radiation therapy, whereas DLBCL, MCL, and high Ann Arbor stage EMZL and FL were frequentl

75 identify other potential mechanisms driving MCL pathogenesis, we investigated 56 cyclin D1(-)/SOX11(

76 However, SOX11 oncogenic pathways driving MCL tumor progression are poorly understood.

77 AK and PI3K inhibitors reduce SOX11-enhanced MCL cell migration and stromal interactions and revert c

78 K and CXCR4 inhibitors impair SOX11-enhanced MCL engraftment in bone marrow.

79 reated in prospective trials of the European MCL Network.

80 prove the poor outcomes of ibrutinib-exposed MCL patients.

81 arget genes encoding anti-apoptosis factors (MCL-1, PTTG1, and survivin) and cell-cycle regulators (c

82 es of B-cell non-Hodgkin lymphoma: EMZL, FL, MCL, and DLBCL.

83 pathway and an increased response following MCL/MINCLE stimulation in peripheral blood mononuclear c

84 rves as an independent prognostic factor for MCL outcome.

85 UMI-77 is an established BH3-mimetic for MCL-1 and was developed to induce apoptosis in cancer ce

86 provides a valuable new treatment option for MCL patients and is now being tested upfront.

87 hypothesis of multiple cellular origins for MCL.

88 9 or their downstream signaling pathways for MCL-expressing ROR1.

89 MYC itself is pivotal for MCL survival because its downregulation and pharmacologi

90 ctopic expression of CCND1 in multiple human MCL cell lines resulted in increased SOX11 transcription

91 cells, and 2 distinct murine models of human MCL.

92 ercome ibrutinib resistance in primary human MCL cells and MCL cell lines expressing wild-type Bruton

93 e targeted to induce mitophagy, and identify MCL-1 as a drug target for therapeutic intervention in A

94 read in human colorectal cancer and identify MCL-1 as a novel downstream effector of oxygen sensing.

95 Our results identify MCL-1 as a critical prosurvival protein for preventing b

96 7 treatment increased histone acetylation in MCL cells.

97 7 treatment increased histone acetylation in MCL cells.

98 resistance and enhanced anti-MCL activity in MCL patient samples and patient-derived xenograft models

99 sed proliferation and increased apoptosis in MCL in vitro and in vivo MCL models.

100 efficacy of targeting the MALT1-MYC axis in MCL patients.

101 ns to CCND3 (6 cases) and CCND2 (4 cases) in MCL that overexpressed, respectively, these cyclins.

102 tinib were cytotoxic, triggered a decline in MCL-1 levels, and inhibited mTORC1 signaling.

103 re, the activity of CUDC-907 was examined in MCL cell lines and patient primary cells, including ibru

104 horylated Y705 STAT3 and SOX11 expression in MCL cell lines, primary tumors, and patient-derived xeno

105 HU induction of stalled replication forks in MCL-1-depleted cells, there was a decreased ability to s

106 in regulatory elements marked by H3K27ac in MCL primary cases, including a distant enhancer showing

107 new insights and therapeutic implications in MCL.

108 itinib treatment suggested that increases in MCL-1 levels and mTORC1 activity correlate with resistan

109 tyrosine kinase (BTK) and SYK inhibitors in MCL.

110 e as a relevant early oncogenic mechanism in MCL, targeting key driver genes.

111 PH1 was associated with inferior outcomes in MCL and showed a significant increase in protein express

112 3K/AKT and ERK1/2 FAK-downstream pathways in MCL.

113 nt regulation of messenger RNA processing in MCL pathobiology.

114 to consistently achieve durable response in MCL.

115 t and suggests UBR5 mutations play a role in MCL transformation.

116 e the distribution of Salmonella serovars in MCL and their products, a total of 1287 pre-harvest samp

117 stance to inhibition of BCR/BTK signaling in MCL.

118 Although targeting genetic variants in MCL is not yet feasible in the clinical setting, the ide

119 ninfected B cells (BCL-2) to early-infected (MCL-1/BCL-2) and immortalized cells (BFL-1).

120 inhibitor; bortezomib can indirectly inhibit MCL-1.

121 In intravenous MCL xenograft models, SOX11(+) MCL cells display higher

122 that depletion of MCL-1 but not its isoform MCL-1S increases genomic instability and cell sensitivit

123 inhibitor of MCL-1 with efficacy in killing MCL-1-dependent cancer cells in vitro and in vivo.

124 the microcapsules cross-linked with laccase (MCL), the second group was the microcapsules cross-linke

125 beta-catenin was detected in all leukemic MCL samples and its level of expression rapidly increase

126 the EPA for HAA5 [maximum contaminant level (MCL) 60 mug L(-1)] and the limits currently being review

127 ns were above the maximum contaminant level (MCL) along segments of the PRB exhibiting upward trendin

128 ter, reducing the maximum contaminant level (MCL) from 50 to 10 mug/L.

129 10 mug/L arsenic maximum contaminant level (MCL).

130 Drinking water maximum contaminant levels (MCL) are established by the U.S. EPA to protect human he

131 er than the EC-maximum contamination levels (MCL).

132 n, which induces anti-apoptotic factors like MCL-1.

133 Major concern in the Mixed Crop-Livestock (MCL) farms, in which livestock and vegetables grown clos

134 ) (16.3% [43 of 263]), mantle cell lymphoma (MCL) (6.8% [18 of 263]), and diffuse large B-cell lympho

135 (DLBCL) (10% [n = 9]), mantle cell lymphoma (MCL) (8% [n = 7]), and mycosis fungoides (MF) (9% [n = 8

136 FL) (11%, n = 91), and mantle cell lymphoma (MCL) (8%, n = 66).

137 CL) (n = 25, 10%), and mantle cell lymphoma (MCL) (n = 17, 7%).

138 oliferative effects on mantle cell lymphoma (MCL) cells in vitro by degrading BTK, IKFZ1, and IKFZ3 a

139 nvironment account for mantle cell lymphoma (MCL) cells survival in lymphoid organs.

140 antagonist of eIF4E in mantle cell lymphoma (MCL) cells.

141 el, phase III European Mantle Cell Lymphoma (MCL) Elderly trial (ClinicalTrials.gov identifier: NCT00

142 OX11 overexpression in mantle cell lymphoma (MCL) has been associated with more aggressive behavior a

143 Mantle cell lymphoma (MCL) is a B-cell lymphoma characterized by cyclin D1 exp

144 Mantle cell lymphoma (MCL) is a mature B-cell lymphoma characterized by poor c

145 Mantle cell lymphoma (MCL) is a mature B-cell neoplasm initially driven by CCN

146 Mantle cell lymphoma (MCL) is a unique type of non-Hodgkin lymphoma characteri

147 Mantle cell lymphoma (MCL) is an aggressive B cell lymphoma that is largely ch

148 Mantle cell lymphoma (MCL) is an uncommon B-cell non-Hodgkin lymphoma (NHL) th

149 erall survival (OS) in mantle cell lymphoma (MCL) is based on the clinical factors included in the Ma

150 Mantle cell lymphoma (MCL) is characterized by an aggressive clinical course a

151 Mantle cell lymphoma (MCL) is characterized by the t(11;14)(q13;q32) transloca

152 Mantle cell lymphoma (MCL) may be 1 of the few cancers for which multiple chem

153 of novel mutations in mantle cell lymphoma (MCL) patients including mutations in the ubiquitin E3 li

154 ctivity in a subset of mantle cell lymphoma (MCL) patients, but the drug resistance remains a conside

155 in lymphoma treatment, mantle cell lymphoma (MCL) remains incurable, and we are still unable to ident

156 tic leukemia (CLL) and mantle cell lymphoma (MCL) tumors.

157 ples from persons with mantle cell lymphoma (MCL) undergoing frontline treatment, providing evidence

158 y expressed in typical mantle cell lymphoma (MCL), but it is absent in the more indolent form of MCL.

159 t into the ontogeny of mantle cell lymphoma (MCL), we assessed 206 patients from a morphological, imm

160 relapsed or refractory mantle cell lymphoma (MCL), with manageable tolerability.

161 elapsed and refractory mantle cell lymphoma (MCL).

162 mphocytic leukemia and mantle cell lymphoma (MCL).

163 ith previously treated mantle cell lymphoma (MCL); however, nearly half of all patients experience tr

164 ted drug resistance in mantle cell lymphoma (MCL); however, the biological functions of BACH2 and its

165 NHL subtypes included mantle cell lymphoma (MCL; n = 28), follicular lymphoma (FL; n = 29), diffuse

166 tion signatures of 82 mantle cell lymphomas (MCL) in comparison with cell subpopulations spanning the

167 cell receptor (BCR) signaling in maintaining MCL survival.

168 biquitinase USP9x regulate cytokine-mediated MCL-1 protein turnover in rodent beta-cells.

169 Micheliolide (MCL) was demonstrated to provide a therapeutic role in r

170 The C-type lectin receptors (CLR) MINCLE, MCL, and DECTIN-2 are expressed on myeloid cells and sen

171 that TNF is sufficient to upregulate MINCLE, MCL, and DECTIN-2 in macrophages.

172 In MRSA infection mouse model, MCL down-regulated the expression of IL-6, TNF-alpha, MC

173 Consistent with this model, MCL-1-depleted cells had a reduced frequency of IR-induc

174 ally, we determined that sunitinib modulates MCL-1 stability by affecting its proteasomal degradation

175 dian progression-free survival was 6 months (MCL, 14 months; FL, 11 months; DLBCL, 1 month).

176 idea that antigen drive is relevant for most MCL cases, although the specific antigens and the precis

177 nventional MCL (cMCL) and leukemic non-nodal MCL (nnMCL), that differ in their clinicobiological beha

178 athway-activating genetic screen to nominate MCL-1 and BCL-XL as potential nodes of resistance.

179 -263 target BCL-2, BCL-XL and BCL-w, but not MCL-1.

180 Ss in the High/High compliance category (not MCL compliant) were more likely in the Southwest (61.1%)

181 s of ocular adnexal mantle-cell lymphoma (OA-MCL) have not previously been evaluated in a large multi

182 suggest that the distinctive features of OA-MCL are its appearance in older male individuals, advanc

183 To characterize the clinical features of OA-MCL.

184 Patients with OA-MCL frequently presented with disseminated lymphoma (n =

185 The prognosis of patients with OA-MCL might be improved by addition of rituximab to chemot

186 Medical records of 55 patients with OA-MCL were reviewed; the median length of follow-up was 33

187 Approximately 18% of MCL patients were found to have mutations in UBR5, with

188 performed a large-scale genomic analysis of MCL using data from 51 exomes and 34 genomes alongside p

189 e NF-kappaB pathway, plays in the biology of MCL.

190 MCE was diagnosed when MCL or combination of MCL was present.

191 Here we report that depletion of MCL-1 but not its isoform MCL-1S increases genomic insta

192 one marrow and gastrointestinal dispersal of MCL and blastoid subtypes of MCL.

193 gized with ABT-263 through downregulation of MCL-1.

194 inversely correlated with the expression of MCL-1.

195 cally distinct and highly aggressive form of MCL with poor or no response to regimens including cytar

196 ut it is absent in the more indolent form of MCL.

197 We identify gains of MCL-1 at high frequency in multiple independent NSCLC co

198 ificantly associated with subclonal gains of MCL-1.

199 BCR/BTK-independent signaling and growth of MCL cells.

200 ignaling to promote activation and growth of MCL cells.

201 cacy is limited by compensatory induction of MCL-1.

202 Inhibition of MCL-1 or mTORC1 signaling sensitized cells to clinically

203 upon pharmacologic or genetic inhibition of MCL-1.

204 reports a novel small molecule inhibitor of MCL-1 with efficacy in killing MCL-1-dependent cancer ce

205 Dual modulation of MCL-1 stability at different dose ranges of sunitinib wa

206 ape of acquired resistance via modulation of MCL-1/BCL-XL and (2) appropriate selection of initial th

207 D8-activating enzyme inhibitor in a panel of MCL cell lines, primary MCL tumor cells, and 2 distinct

208 standing of the molecular pathophysiology of MCL has resulted in an explosion of specifically targete

209 ecisive, negative factor in the prognosis of MCL.

210 ll transcription factor in the regulation of MCL dispersal.

211 s-infected cells and relies on regulation of MCL-1 mitochondrial localization and BFL-1 transcription

212 locks CDK9, the transcriptional regulator of MCL-1.

213 g and PI3K-AKT-mTOR axis leads to release of MCL cells from TME, reversal of drug resistance and enha

214 ys account for the anti-inflammatory role of MCL after PGN stimulation.

215 tic responses, suggesting that sequencing of MCL-1 inhibitors with targeted therapies could overcome

216 The silencing of MCL and Mincle resulted in TNF-alpha secretions similar

217 rphan receptor 1), seen in a large subset of MCL, results in BCR/BTK-independent signaling and growth

218 al dispersal of MCL and blastoid subtypes of MCL.

219 We finally combined venetoclax treatment of MCL and ABC-DLBCL xenografts with a pretargeted RIT (PRI

220 ssing a major unmet need in the treatment of MCL and other B-cell lymphomas.

221 ith or without rituximab in the treatment of MCL.

222 ance is indeed driven by the upregulation of MCL-1 and BCL-XL.

223 e the rationality for the potential usage of MCL in sepsis caused by G(+) bacteria (e.g., S. aureus)

224 layer through which BCR signaling impacts on MCL cell survival.

225 ing hypoxia and normoxia coordinate not only MCL tumor dispersal but also drug resistance, including

226 cer cells to anti-apoptotic BCL-2, BCL-XL or MCL-1, which correlated with the respective protein expr

227 In parallel, MCL cells as compared with normal B cells expressed elev

228 Postirradiation, MCL-1-depleted cells exhibited decreased gamma-H2AX foci

229 Development of strategies to prevent MCL-1 loss in the early stages of T1D may enhance beta-c

230 reover, SOX11(+) xenograft and human primary MCL tumors overexpress cell migration and stromal stimul

231 F-kappaB DNA recruitment and induced primary MCL cells apoptosis.

232 ibitor in a panel of MCL cell lines, primary MCL tumor cells, and 2 distinct murine models of human M

233 Patients with highly proliferative MCL and those with TP53 mutations tend to respond poorly

234 all, our results suggest that SOX11 promotes MCL homing and invasion and increases CAM-DR through the

235 g the stability of the antiapoptotic protein MCL-1 and inducing mTORC1 signaling, thus evoking little

236 mal degradation of the antiapoptotic protein MCL-1.

237 critical role for the anti-apoptotic protein MCL-1 as a driver of adaptive survival in tumor cells tr

238 g a dependence on the anti-apoptotic protein MCL-1.

239 eased expression of the pro-survival protein MCL-1, an induction of apoptosis, and an enhanced reduct

240 We identified novel recurrent MCL drivers, including CDKN1B, SAMHD1, BCOR, SYNE1, HNRN

241 val for patients with relapsed or refractory MCL receiving BR.

242 Adult patients with relapsed or refractory MCL underwent (18)F-FDG PET at screening and after 6 cyc

243 US Food and Drug Administration for relapsed MCL based on a clinical trial demonstrating an overall r

244 5, U.S. public water suppliers have reported MCL violations to the national Safe Drinking Water Infor

245 re, we demonstrate that voruciclib represses MCL-1 protein expression in preclinical models of DLBCL.

246 ity (BIM, caspase-3, BCL-XL) and resistance (MCL-1, XIAP).

247 G2 in triggering autophagy in drug-resistant MCL cells through induction of IL6.

248 in inducing lethality in ibrutinib-resistant MCL cells.

249 primary cells, including ibrutinib-resistant MCL cells.

250 s further examined in an ibrutinib-resistant MCL patient-derived xenograft (PDX) mouse model.

251 therapeutic option for relapsed or resistant MCL.

252 Our results provide a rationale to screen MCL patients for ROR1 expression and to consider new the

253 In several MCL cases, the WNT/beta-catenin canonical pathway is act

254 Concordantly, SOX11(+) MCL cells have higher cell migration, transmigration thr

255 is, we investigated 56 cyclin D1(-)/SOX11(+) MCL by fluorescence in situ hybridization (FISH), whole-

256 IL-21 treatment induced toxicity in SOX11(+) MCL cells.

257 n intravenous MCL xenograft models, SOX11(+) MCL cells display higher cell migration, invasion, and g

258 ance (CAM-DR) to the same levels as SOX11(-) MCL cells.

259 tional drug therapies compared with SOX11(-) MCL cells.

260 c profile was identified for primary splenic MCL, which was enriched for DBA.44-positive cases (P < 0

261 etaMcl-1KO), we observed that, surprisingly, MCL-1 ablation does not affect islet development and fun

262 By targeting MCL-1 and BCL-XL, resistant AML cell lines could be rese

263 MF had a significantly better prognosis than MCL and DLBCL.

264 We demonstrate that MCL cells develop ibrutinib resistance through evolution

265 It was demonstrated that MCL obtained by microfluidics are more physicochemically

266 Our mechanistic studies discovered that MCL-1 is a mitophagy receptor and directly binds to LC3A

267 We proved here that MCL played an anti-inflammatory role in Staphylococcus a

268 We report here that MCL-1 downregulation is associated with cytokine-mediate

269 These findings reveal that MCL-1 gains occur with high frequency in lung adenocarci

270 on the mechanisms of mitophagy, reveal that MCL-1 is a mitophagy receptor that can be targeted to in

271 Ochratoxin A (OTA) concentrations above the MCL (3 ug/kg), but OTA levels were no affected by wheat

272 MCL compliance categories (High if above the MCL; Low if below) for each 3-y period.

273 oxins, but not OTA concentrations, below the MCL.

274 Violations exceeding the MCL and the population served by violating systems were

275 e for CLRs in autoimmunity and implicate the MCL/MINCLE pathway as a potential therapeutic target in

276 and we further found an upregulation of the MCL/MINCLE signaling pathway and an increased response f

277 tant enhancer showing de novo looping to the MCL oncogene SOX11.

278 drives sequestered pro-apoptotic proteins to MCL-1 and vice versa, explaining why in vivo combination

279 c quantiles indicate declines are related to MCL implementation.

280 -induced MYC regulation is not restricted to MCL, but represents a common mechanism.

281 fully understand malignant transformation to MCL.

282 effective therapeutic approach for treating MCL and overcoming ibrutinib resistance, thereby address

283 We identified two MCL subgroups, respectively carrying epigenetic imprints

284 Consistent with this, we uncovered MCL- and MINCLE-expressing cells in brain lesions of MS

285 Patients >65 years with untreated MCL, stages II-IV were eligible for inclusion.

286 reased apoptosis in MCL in vitro and in vivo MCL models.

287 MCE was diagnosed when MCL or combination of MCL was present.

288 emale predilection (69% [22 of 32]), whereas MCL (71% [5 of 7]) and MF (88% [7 of 8]) had a male pred

289 re, the present data support a model whereby MCL-1 depletion increases 53BP1 and RIF1 colocalization

290 Health Organization's recommended level (WHO-MCL = 1.5 mg F(-)/L).

291 in bringing arsenic levels to less than WHO-MCL of 10 mug/L.

292 BM) specimens from 183 younger patients with MCL from the Nordic MCL2 and MCL3 trials, which represen

293 ce until progression for older patients with MCL persisted in a mature follow-up.

294 We suggest patients with MCL should be stratified according to TP53 status, and t

295 vely poor ultimate outcomes of patients with MCL treated in the real world.

296 rospective cohort study of all patients with MCL who experienced disease progression while receiving

297 nger, transplantation-eligible patients with MCL, AHCT consolidation after induction was associated w

298 mproving clinical outcomes for patients with MCL.

299 to reach durable remission in patients with MCL.

300 proved the overall survival of patients with MCL; however, resistance to ibrutinib has emerged as a d