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 experience frequent relapses resulting in m

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

5 MCL showed large interpatient variability in basal level

6 MCL(-/-) mice showed impaired vaccine resistance against

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

8 MCL-1 association with genomic DNA increased postirradia

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

10 MCL-1 protein expression was likewise enhanced in human

11 mily member, myeloid cell leukemic factor 1 (MCL-1).

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

13 Myeloid cell leukemia 1 (MCL-1) is a BCL-2 family protein that has been implicate

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

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

16 f the antiapoptotic myeloid cell leukemia 1 (MCL-1).

17 rosurvival proteins myeloid cell leukemia-1 (MCL-1) and B-cell lymphoma-extra large (BCL-XL) in stem/

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

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

20 er, member myeloid cell leukemia sequence 1 (MCL-1), and could be reversed by simultaneous inhibition

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

22 cell responses to antigen triggering, in 133 MCL cases; assessed the functionality of AID by evaluati

23 loring intraclonal diversification within 14 MCL cases.

24 Transfection of 2 MCL cell lines with miR-18b decreased their proliferatio

25 nt, pevonedistat prolonged the survival of 2 MCL-bearing mouse models when compared with controls.

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

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

28 Here we report the clinical observation of 3 MCL patients with symptomatic CNS relapse treated with s

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

30 ing in vivo class switch recombination in 52 MCL cases; and sought for indications of ongoing antigen

31 In a tissue microarray of 62 MCL samples, BCL2 expression positively correlated with

32 In a MCL-1 dependent human tumor cell line, administration of

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

34 based combinations with these agents against MCL, including ibrutinib-resistant MCL.

35 IL-21 possesses potent cytotoxicity against MCL cell lines and primary tumors.

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

37 ed chemotherapy refractoriness in aggressive MCL.

38 logic inhibition induced cytotoxicity in all MCL models.

39 A proteome-wide analysis in MCL lines and an MCL patient-derived xenograft identified a restricted se

40 female predilection (57.8% [104 of 180]) and MCL having a marked male predominance (77.8% [14 of 18])

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

42 was 23.81% versus 4.55% in conventional and MCL farms (P = 0.004) and 66.67% versus 7.76% in convent

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

44 Unlike EMZL and FL, DLBCL and MCL were frequently secondary diseases (41.7% [5 of 12]

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

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

47 Diffuse large B-cell lymphoma and MCL had a poor prognosis, with 5-year disease-specific s

48 n monocytes and macrophages, with MINCLE and MCL proteins localized intracellularly under resting con

49 mRNA expression of MINCLE and MCL was high in monocytes and macrophages, with MINCLE a

50 tested the contribution of SYK, MINCLE, and MCL by small interfering RNA knockdown and genetic compl

51 ation limits the interaction between p53 and MCL-1/BAK.

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

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

54 the cohort from the European MCL Younger and MCL Elderly trials, we aimed to evaluate the additional

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

56 AID+ immature B cells lacked anti-apoptotic MCL-1 and were deleted by apoptosis.

57 st for routine diagnostic practice to assess MCL prognosis.

58 e tumor ecosystem, few studies have assessed MCL microenvironment.

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

60 Differences in immunopathogenesis between MCL and LCL may result from an imbalance between prostag

61 ll-cycle progression, which was amplified by MCL-specific cytokines (insulin-like growth factor-1, B-

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

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

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

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

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

67 n levels and compared with infected control, MCL-1-silenced infected macrophages documented enhanced

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

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

70 K --> AKT pathways, and in turn destabilizes MCL-1.

71 ed to assess the efficacy of SE in detecting MCL in dyspeptic patients with GERD compared with patien

72 miRNA microarray profiling of 74 diagnostic MCL samples from the Nordic MCL2 trial (screening cohort

73 ognostic miRNAs were validated in diagnostic MCL samples from 94 patients of the independent Nordic M

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

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

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

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

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

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

80 -dose cytarabine, in the randomized European MCL Younger trial.

81 reated in prospective trials of the European MCL Network.

82 By using the cohort from the European MCL Younger and MCL Elderly trials, we aimed to evaluate

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

84 Whether adjusted for MCL International Prognostic Index (MIPI) or not, deleti

85 rves as an independent prognostic factor for MCL outcome.

86 hypothesis of multiple cellular origins for MCL.

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

88 were recovered, with 17.44% and 5.88%, from MCL and conventional farms samples (P < 0.001).

89 Human MCL-5 cells (metabolically competent) were exposed to Ba

90 dies that are specifically taken up by human MCL cells in the bone marrow of xenografted mice.

91 and antagonistic mutation responses of human MCL-5 cells to mixtures of benzo[a]pyrene and 2-amino-1-

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

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

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

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

96 hat pevonedistat has significant activity in MCL preclinical models, possibly related to effects on N

97 demonstrated important clinical activity in MCL.

98 tion of both BTK and IkappaB kinase alpha in MCL lines and CD40-dependent B cells, with downstream lo

99 A proteome-wide analysis in MCL lines and an MCL patient-derived xenograft identifie

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

101 y histology, the OR rate was 94% (76% CR) in MCL, 37% (31% CR) in DLCL, and 90% (50% CR) in FL.

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

103 and growth pattern as prognostic factors in MCL.

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

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

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

107 y for the resistance-associated increases in MCL-1 levels.

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

109 tion has promising efficacy, particularly in MCL and FL.

110 by targeting multiple oncogenic pathways in MCL.

111 ranscription activities in these pathways in MCL.

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

113 dings define the HSP90-dependent proteome in MCL.

114 STAT3 signaling with autophagy regulation in MCL cells, the disruption of which may offer a promising

115 ort for proliferation and drug resistance in MCL, our results highlight a selective approach to targe

116 to consistently achieve durable response in MCL.

117 the data reveals higher Salmonella risks in MCL farms' environment and their products sold in farmer

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

119 CD38-targeted LNPs induced gene silencing in MCL cells and prolonged survival of tumor-bearing mice w

120 anonical NF-kappaB signaling specifically in MCL cells in the lymph node.

121 TK and BCL2 as a new therapeutic strategy in MCL, especially for patients with primary resistance to

122 herapeutic potential of cyclin D1 therapy in MCL and present a novel RNAi delivery system that opens

123 ages, suggesting the active role of TOM70 in MCL-1 transport.

124 IP assay demonstrated that infection-induced MCL-1 expression was regulated by transcription factor C

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

126 During infection, MCL-1 was found to be localized in mitochondria and this

127 inhibitor; bortezomib can indirectly inhibit MCL-1.

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

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

130 y, multiple HSP90 inhibitors potently killed MCL lines in vitro, and the clinical agent AUY922 was ac

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

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

133 n patients with mucocutaneous leishmaniasis (MCL) or localized cutaneous leishmaniasis (LCL).

134 ages that may improve minimal change lesion (MCL) detection.

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

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

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

138 ) (16.3% [43 of 263]), mantle cell lymphoma (MCL) (6.8% [18 of 263]), and diffuse large B-cell lympho

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

140 Mantle cell lymphoma (MCL) accumulates in lymphoid organs, but disseminates ea

141 We used mantle cell lymphoma (MCL) as a prototypic blood cancer for validating a novel

142 Mantle cell lymphoma (MCL) cells exhibit increased B-cell receptor and nuclear

143 otherapy resistance in mantle cell lymphoma (MCL) cells.

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

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

146 d has activity against mantle cell lymphoma (MCL) in the central nervous system (CNS).

147 pathways activated in mantle cell lymphoma (MCL) in vivo, we contrasted gene expression profiles of

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

149 Mantle cell lymphoma (MCL) is a rare and aggressive form of non-Hodgkin's lymp

150 Mantle-cell lymphoma (MCL) is a rather aggressive B-cell malignancy whose cons

151 Mantle cell lymphoma (MCL) is an uncommon subtype of non-Hodgkin lymphoma prev

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

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

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

155 alterations (CNAs) in mantle cell lymphoma (MCL) patients treated first line with immunochemotherapy

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

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

158 oved for patients with mantle cell lymphoma (MCL) who have received one prior therapy.

159 d clinical activity in mantle cell lymphoma (MCL), primary and acquired resistance to ibrutinib is co

160 erleukin-21 (IL-21) in mantle cell lymphoma (MCL), providing a preclinical rationale for IL-21 therap

161 elderly patients with mantle cell lymphoma (MCL), there is no defined standard therapy.

162 antigen involvement in mantle cell lymphoma (MCL), we analyzed the expression levels of activation-in

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

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

165 elapsed and refractory mantle cell lymphoma (MCL).

166 th relapsed/refractory mantle cell lymphoma (MCL).

167 fractory patients with mantle cell lymphoma (MCL).

168 ma (DLCL), and 17 with mantle cell lymphoma (MCL).

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

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

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

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

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

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

175 In the mitochondria, MCL-1 interacts with the major pro-apoptotic protein BAK

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

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

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

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

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

181 In addition to lymph nodes, MCL often involves blood, bone marrow, and spleen and is

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

183 -263 target BCL-2, BCL-XL and BCL-w, but not MCL-1.

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

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

186 To characterize the clinical features of OA-MCL.

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

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

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

190 We also found that conditional ablation of MCL-1 significantly reduced the size of both DC populati

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

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

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

194 erentially expressed in patients who died of MCL in both cohorts.

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

196 GO-203 is associated with downregulation of MCL-1 levels.

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

198 ng of CREB resulted in reduced expression of MCL-1 and increased apoptosis.

199 on preferentially up-regulated expression of MCL-1 at both the mRNA and protein levels and compared w

200 utamine were found to maintain expression of MCL-1 but importantly induce pro-apoptotic BIM expressio

201 es with BCL-2 and BCL-XL, high expression of MCL-1 sequestered BIM released from BCL-2 and BCL-XL, th

202 inversely correlated with the expression of MCL-1.

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

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

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

206 ld be reversed by simultaneous inhibition of MCL-1.

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

208 on of BCL-2, lower A1, and similar levels of MCL-1 and BCL-XL.

209 signaling pathways in the lymphomagenesis of MCL and the biologic basis for ibrutinib sensitivity of

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

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

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

213 w will explore the molecular pathogenesis of MCL and the current and evolving therapeutic strategies

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

215 ll transcription factor in the regulation of MCL dispersal.

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

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

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

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

220 lator of apoptosis (PUMA) as the key role of MCL-1 in both settings, with Mcl-1(+/-);Puma(-/-) mice c

221 Herein we report a series of MCL-1 inhibitors that emanated from a high throughput sc

222 Silencing of MCL-1 in the spleen of infected mice showed decreased pa

223 al dispersal of MCL and blastoid subtypes of MCL.

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

225 ith or without rituximab in the treatment of MCL.

226 view recent advances in the understanding of MCL biology and outline our recommended approach to ther

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

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

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

230 Small interfering RNA-mediated MINCLE or MCL knockdown caused on average reduced TDB- or TDM-indu

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

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

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

234 ndent lethality against cultured and primary MCL cells.

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

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

237 We further demonstrated that proliferating MCL harbored an imbalance in Bcl-2 family expression, le

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

239 iate enhanced autophagy formation to promote MCL cell survival.

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

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

242 nst melanoma, with the antiapoptotic protein MCL-1 as the main contributor to resistance.

243 loited the macrophage anti-apoptotic protein MCL-1 to prevent BAK-mediated mitochondria-dependent apo

244 via TORC1/2 inhibition, which led to reduced MCL-1 protein levels, thereby facilitating BIM-mediated

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

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

247 and favorable safety in relapsed/refractory MCL.

248 Among novel drugs used to treat relapsing MCL patients, ibrutinib, an oral inhibitor of Bruton tyr

249 poptosis, suggesting that miR-18b may render MCL cells resistant to chemotherapy by decelerating cell

250 5, U.S. public water suppliers have reported MCL violations to the national Safe Drinking Water Infor

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

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

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

254 f the in vitro isolated, ibrutinib-resistant MCL cells, which overexpress CDK6, BCL2, Bcl-xL, XIAP, a

255 induced apoptosis of the ibrutinib-resistant MCL cells.

256 s against MCL, including ibrutinib-resistant MCL.

257 MUC1-C is a potential strategy for reversing MCL-1-mediated resistance in TNBC.

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

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

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

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

262 c compounds, identifying potent and specific MCL-1 inhibitors.

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

264 roteasome maturation protein), CERS6, STMN1, MCL-1 and ROCK2, among others.

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

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

267 Further, preemptively targeting MCL-1 and/or BCL-XL alongside administration of ABT-199

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

269 We demonstrate that MCL cells develop ibrutinib resistance through evolution

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

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

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

273 Taken together, our data indicate that MCL regulates the development of vaccine-induced Th17 ce

274 The MCL-002 (SPRINT) study was a randomised, phase 2 study o

275 ified combination to MIPI and MIPI-b for the MCL Younger/MCL Elderly cohort.

276 Of interest, in the MCL cell lines with lower half-maximal inhibitory concen

277 -dependent cell death in the majority of the MCL cell lines and primary tumor cells tested.

278 , we showed that our model recapitulated the MCL in situ molecular signatures (ie, proliferation, NF-

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

280 e median survival of mice engrafted with the MCL cells.

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

282 s new therapeutic opportunities for treating MCL and other B-cell malignancies.

283 We identified two MCL subgroups, respectively carrying epigenetic imprints

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

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

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

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

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

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

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

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

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

293 ns will increasingly encounter patients with MCL who require therapy after ibrutinib.

294 s in other contexts, trials in patients with MCL will be essential for defining the efficacy of and m

295 added from the second cycle in patients with MCL, and was associated with a high rate of CR and molec

296 rst-line treatment for elderly patients with MCL.

297 subtype is the main outcome predictor, with MCL and DLBCL having a markedly poorer prognosis than EM

298 2] and 88.9% [16 of 18], respectively), with MCL showing a frequent occurrence of stage IVE lymphoma

299 apy, high-dose cytarabine, and ASCT, younger MCL patients with deletions of CDKN2A (p16) and TP53 sho

300 ation to MIPI and MIPI-b for the MCL Younger/MCL Elderly cohort.