ライフサイエンスコーパス: bortezomib

1 2 and 6 days, respectively); and protocol 7 (bortezomib).

2 ects suggested a possible positive effect of bortezomib.

3 ed from fibrosis by the proteasome inhibitor bortezomib.

4 reduction in the risk of death compared with bortezomib.

5 overcomes resistance to proteasome inhibitor bortezomib.

6 treatment with the 20S proteasome inhibitor bortezomib.

7 nd were not significantly improved by adding bortezomib.

8 rgin, tunicamycin or the myeloma therapeutic bortezomib.

9 uropathy, the main dose-limiting toxicity of bortezomib.

10 the mouse tissue samples administrated with bortezomib.

11 nated AGR2 clearance in response to MG132 or bortezomib.

12 stance in FGbeta(3) cells more potently than bortezomib.

13 followed by dose-attenuated RVd maintenance (bortezomib 1 mg/m(2) subcutaneously on days 1, 8, and 15

14 cles of standard R-CHOP alone or R-CHOP plus bortezomib 1.3 mg/m(2) intravenously on days 1 and 4 (VR

15 ); tacrolimus, methotrexate, and bortezomib (bortezomib 1.3 mg/m(2) intravenously on days 1, 4, and 7

16 d allocated patients to receive subcutaneous bortezomib 1.3 mg/m(2), and oral thalidomide 100 mg, dex

17 y mouth on days 1 to 21), IV or subcutaneous bortezomib (1.0 mg/m(2) on days 1, 8, 15, and 22), and d

18 d and refractory multiple myeloma to receive bortezomib (1.3 mg per square meter of body-surface area

19 ved up to nine 6-week cycles of subcutaneous bortezomib (1.3 mg/m(2) of body surface area on days 1,

20 to receive selinexor (100 mg once per week), bortezomib (1.3 mg/m(2) once per week), and dexamethason

21 e (25 mg orally on days 1-14 every 21 days), bortezomib (1.3 mg/m(2) subcutaneously on days 1, 4, 8,

22 (500 mg daily orally on days 1, 8, and 15), bortezomib (1.3 mg/m(2) subcutaneously or intravenously

23 clax (800 mg per day orally) or placebo with bortezomib (1.3 mg/m(2) subcutaneously or intravenously

24 and dexamethasone (20 mg twice per week), or bortezomib (1.3 mg/m(2) twice per week for the first 24

25 Bortezomib (1.3 mg/m(2)) was administered intravenously

26 ays 1, 2, 8, 9, 15, and 16 of 28-day cycles; bortezomib (1.3 mg/m(2)) was given as an intravenous bol

27 sone (20 mg oral or intravenous infusion) or bortezomib (1.3 mg/m(2); intravenous bolus or subcutaneo

28 days 1, 4, 8, and 11), followed by weekly IV bortezomib (1.6 mg/m(2) on days 1, 8, 15, and 22) for 4

29 dy arms: 89 to tacrolimus, methotrexate, and bortezomib; 92 to tacrolimus, methotrexate, and maraviro

30 tudy, the combination of oral selinexor with bortezomib (a proteasome inhibitor) and dexamethasone in

31 Bortezomib, a proteasome inhibitor used in the managemen

32 d Src, was reversible, and was stabilized by bortezomib, a proteasome inhibitor.

33 In preclinical studies, venetoclax enhanced bortezomib activity, suggesting that cotargeting of BCL-

34 L amyloidosis who were previously exposed to bortezomib, alkylators, and other immunomodulatory drugs

35 BDR consisted of a single 21-day cycle of bortezomib alone (1.3 mg/m(2) IV on days 1, 4, 8, and 11

36 d enhanced antitumor efficacy as compared to bortezomib alone, delaying disease progression, but with

37 psed myeloma who had received treatment with bortezomib, an immunomodulatory drug, or both, or who we

38 However, treatment with bortezomib, an inhibitor of the 20S proteasome, caused a

39 ge, 1-13); 26 (39%) were refractory to prior bortezomib and 35 (53%) to lenalidomide; 39 (59%) had pr

40 se phenotypes in Axin mutants by identifying bortezomib and additional peptide boronic acids.

41 ter 1 to 3 prior lines of therapy, including bortezomib and an immunomodulatory drug; lenalidomide-re

42 The synergistic effect in combination with bortezomib and anthracyclines highlights the potential o

43 915 newly diagnosed AL patients treated with bortezomib and assessed at our center were included.

44 nefits of low doses of ABBV-075 coupled with bortezomib and azacitidine treatment, despite the lack o

45 Bortezomib and carfilzomib are two Food and Drug Adminis

46 We showed that bortezomib and carfilzomib extremely increased the ubiqu

47 In this study, we unveiled a new role of bortezomib and carfilzomib in enhancing OAT1 expression

48 We therefore investigate the roles of bortezomib and carfilzomib in reversing the ubiquitinati

49 nd unveiled a novel role of anticancer drugs bortezomib and carfilzomib in their regulation of OAT1 e

50 transport activity after the treatment with bortezomib and carfilzomib resulted from a reduced rate

51 Anticancer drugs bortezomib and carfilzomib target the ubiquitin-proteaso

52 trast, two well-known proteasome inhibitors, bortezomib and carfilzomib, do not effectively downregul

53 somal activity in cells that were exposed to bortezomib and carfilzomib.

54 lationship between initial administration of bortezomib and chalazia onset, and the positive dechalle

55 dard therapy responded to the combination of bortezomib and cytarabine, concomitant with the re-estab

56 dexamethasone (41 [21%] patients) than with bortezomib and dexamethasone (70 [34%] patients; odds ra

57 b with bortezomib and dexamethasone (EBd) or bortezomib and dexamethasone (Bd) until disease progress

58 mib and dexamethasone (carfilzomib group) or bortezomib and dexamethasone (bortezomib group) through

59 iple myeloma (RRMM) received elotuzumab with bortezomib and dexamethasone (EBd) or bortezomib and dex

60 amethasone and 9.46 months (8.11-10.78) with bortezomib and dexamethasone (hazard ratio 0.70 [95% CI

61 oved progression-free survival compared with bortezomib and dexamethasone (median 11.20 months [95% C

62 (1%) were reported in patients who received bortezomib and dexamethasone (pneumonia [n=1], hepatic e

63 longer progression-free survival (PFS) over bortezomib and dexamethasone (Vd) in patients with relap

64 e inhibitor) is approved in combination with bortezomib and dexamethasone for patients with relapsed

65 and dexamethasone group and 62 (30%) in the bortezomib and dexamethasone group died.

66 examethasone group vs 35 [17%] of 204 in the bortezomib and dexamethasone group), fatigue (26 [13%] v

67 and dexamethasone group and 207 (51%) to the bortezomib and dexamethasone group-and the first dose of

68 one group and 16.5 months [9.4-19.8] for the bortezomib and dexamethasone group.

69 This novel combination of venetoclax with bortezomib and dexamethasone has an acceptable safety pr

70 Venetoclax plus bortezomib and dexamethasone has shown encouraging clini

71 in combination with dexamethasone than with bortezomib and dexamethasone in an interim analysis.

72 ortezomib, and dexamethasone versus standard bortezomib and dexamethasone in patients with previously

73 f this study was to evaluate venetoclax plus bortezomib and dexamethasone in patients with relapsed o

74 ion-free survival compared with placebo plus bortezomib and dexamethasone in the phase 3 PANORAMA 1 t

75 Panobinostat plus bortezomib and dexamethasone significantly increased med

76 benefit with panobinostat over placebo with bortezomib and dexamethasone was modest.

77 We randomly assigned patients (1:1) to bortezomib and dexamethasone with or without pomalidomid

78 d 270 patients received at least one dose of bortezomib and dexamethasone, and these patients were in

79 bortezomib, and dexamethasone compared with bortezomib and dexamethasone.

80 ib, and dexamethasone and 278 were allocated bortezomib and dexamethasone.

81 ts received the same chemotherapy regimen of bortezomib and dexamethasone.

82 mg in safety expansion) in combination with bortezomib and dexamethasone.

83 anobinostat (n=387) or placebo (n=381), plus bortezomib and dexamethasone.

84 survival with venetoclax versus placebo plus bortezomib and dexamethasone.

85 free drugs and their combinations, including bortezomib and Doxil.

86 ecreased toxicity and efficient intratumoral bortezomib and doxorubicin delivery by nanoformulation.

87 tifunctional nanoparticles for codelivery of bortezomib and doxorubicin to synchronize their pharmaco

88 Synergistic anticancer effects of combined bortezomib and doxorubicin were observed in vitro agains

89 n the largest AL cohort treated with upfront bortezomib and explore the impact of posttreatment dFLC

90 re, we report that the proteasome inhibitors bortezomib and ixazomib markedly increased protein level

91 of 5 prior therapies (range, 1-15); 61% were bortezomib and lenalidomide double refractory, and 46% h

92 the retrospective studies reported to date, bortezomib and lenalidomide seem to improve survival.

93 e for patients with multiple myeloma in whom bortezomib and lenalidomide treatment has failed.

94 wo established frontline antimyeloma agents, bortezomib and lenalidomide.

95 We found that the combination of bortezomib and leucovorin enhanced caspase activation an

96 ials at the NCI to evaluate clofarabine with bortezomib and nilotinib with paclitaxel in patients wit

97 anobinostat in combination with subcutaneous bortezomib and oral dexamethasone for this indication.

98 10 mg three times weekly, plus subcutaneous bortezomib and oral dexamethasone.

99 al, -4.8 to 5.8) difference detected between bortezomib and placebo in eGFR slope (primary end point)

100 eucovorin enhances the anti-cancer effect of bortezomib and present this novel combinatorial treatmen

101 Bortezomib and recombinant ADAMTS13 are under investigat

102 The combination of bortezomib and SP1017 augments accumulation of ubiquitin

103 human MM/SCID mice model, the combination of bortezomib and SP1017 exerted enhanced antitumor efficac

104 Notably, co-treatment of bortezomib and SP1017 intensifies SP1017-induced disorga

105 was administered orally on the same days as bortezomib and the day after.

106 7; p=0.92) for tacrolimus, methotrexate, and bortezomib, and 1.10 (0.86-1.41; p=0.49) for tacrolimus,

107 dose thalidomide, using sub-cutaneous weekly bortezomib, and determining the maximum tolerated dose o

108 2 or above was less frequent with selinexor, bortezomib, and dexamethasone (41 [21%] patients) than w

109 nsification treatment with cyclophosphamide, bortezomib, and dexamethasone (CVD) versus no intensific

110 ht chain (AL) amyloidosis, cyclophosphamide, bortezomib, and dexamethasone (CyBorD) is considered sta

111 orded in patients who received pomalidomide, bortezomib, and dexamethasone (pneumonia [n=2], unknown

112 doses, safety, and efficacy of pomalidomide, bortezomib, and dexamethasone (PVD) combination in patie

113 Lenalidomide, bortezomib, and dexamethasone (RVd) followed by autologo

114 se of combination therapy with lenalidomide, bortezomib, and dexamethasone (RVD) in this population h

115 The combination of lenalidomide, bortezomib, and dexamethasone (RVD) is a highly effectiv

116 ents received a combination of lenalidomide, bortezomib, and dexamethasone (RVD) with or without auto

117 and AHCT and four subsequent cycles of len, bortezomib, and dexamethasone (RVD; AHCT + RVD), all fol

118 received at least one dose of pomalidomide, bortezomib, and dexamethasone and 270 patients received

119 281 patients were assigned pomalidomide, bortezomib, and dexamethasone and 278 were allocated bor

120 (95% CI 11.73-not evaluable) with selinexor, bortezomib, and dexamethasone and 9.46 months (8.11-10.7

121 This study supports use of pomalidomide, bortezomib, and dexamethasone as a treatment option in p

122 ree survival when treated with pomalidomide, bortezomib, and dexamethasone compared with bortezomib a

123 3.2 months [IQR 6.2-19.8] for the selinexor, bortezomib, and dexamethasone group and 16.5 months [9.4

124 ndomly allocated-195 (49%) to the selinexor, bortezomib, and dexamethasone group and 207 (51%) to the

125 47 (24%) patients in the selinexor, bortezomib, and dexamethasone group and 62 (30%) in the

126 (77 [39%] of 195 patients in the selinexor, bortezomib, and dexamethasone group vs 35 [17%] of 204 i

127 The combination of pomalidomide, bortezomib, and dexamethasone has shown promising result

128 A once-per-week regimen of selinexor, bortezomib, and dexamethasone is a novel, effective, and

129 Pomalidomide, bortezomib, and dexamethasone significantly improved pro

130 te the clinical benefit of weekly selinexor, bortezomib, and dexamethasone versus standard bortezomib

131 ith the individual profiles of pomalidomide, bortezomib, and dexamethasone.

132 with novel agents (NA) such as thalidomide, bortezomib, and lenalidomide may be associated with incr

133 RI31277 was as effective as dexamethasone or bortezomib, and SRI31277 combined with bortezomib showed

134 detected no significant differences between bortezomib- and placebo-treated groups in median measure

135 4 events with tacrolimus, methotrexate, and bortezomib; and 18 (20%) had grade 3 and 63 (68%) had gr

136 ; 73 [82%] for tacrolimus, methotrexate, and bortezomib; and 78 [85%] for tacrolimus, methotrexate, a

137 First, lenalidomide and bortezomib are currently used in frontline treatment and

138 utaneous bortezomib has replaced intravenous bortezomib as it is associated with a more favourable to

139 our knowledge, there have been 24 reports of bortezomib-associated chalazia.

140 tly suppressed by proteasome inhibitor MG132/bortezomib at mRNA and protein levels in lung cancer cel

141 s for acute kidney injury and who received a bortezomib-based chemotherapy regimen relative to those

142 with myeloma cast nephropathy treated with a bortezomib-based chemotherapy regimen, the use of high-c

143 ose chemotherapy and stem cell transplant or bortezomib-based chemotherapy.

144 antation can be considered up front or after bortezomib-based conditioning.

145 mong 169 patients who received chemotherapy (bortezomib-based in 58%), 67% achieved serum free light

146 tolerance profile of doublet versus triplet bortezomib-based regimens in patients with initial myelo

147 Bortezomib-based regimens remain the cornerstone of the

148 d with 65% of patients in 2010-2014 received bortezomib-based therapy, 79% of patients in 2005-2009 r

149 ve either orally administered or parenteral (bortezomib-based) therapy.

150 Sensitized animals were treated with bortezomib, belatacept, and anti-CD40 mAb twice weekly f

151 safety of MDex and MDex with the addition of bortezomib (BMDex).

152 S) ), or inhibiting proteasome activity with bortezomib (BORT), could suppress experimental AAD.

153 5 to day 35); tacrolimus, methotrexate, and bortezomib (bortezomib 1.3 mg/m(2) intravenously on days

154 myeloma (MM) tumor cells with two MM drugs (bortezomib (BTZ) and carfilzomib (CFZ)) in devices fabri

155 Although bortezomib (BTZ) is one of the most potent proteasome in

156 We previously showed that bortezomib (BTZ) partially depletes plasma cells, yet ha

157 de assemblies sequestrates IAPs and releases bortezomib (BTZ), a proteasome inhibitor, in the cytosol

158 Proteasome inhibitors, such as bortezomib (BTZ), are highly effective and widely used t

159 Finally, a bortezomib (BTZ)/MEK inhibitor combination showed enhanc

160 synchronizing the delivery of chemotherapy (bortezomib; BTZ) and BMME-disrupting agents (ROCK inhibi

161 Inhibition of the proteasome (bortezomib), but not macroautophagy (3-methyladenine), m

162 ggested efficacy of the proteasome inhibitor bortezomib, but no systematic trial has been undertaken

163 an-HSPA inhibition sensitized NSCLC cells to bortezomib, but not to platinum derivates.

164 Administration of bortezomib (Bzb) reversed the loss of trabecular bone st

165 Bortezomib can improve the depth of response after trans

166 bioavailable small-molecule BCL-2 inhibitor; bortezomib can indirectly inhibit MCL-1.

167 cyclophosphamide) and proteasome inhibitors (bortezomib, carfilzomib, ixazomib), both in combination

168 ts with myeloma who had previous exposure to bortezomib, carfilzomib, lenalidomide, pomalidomide, dar

169 The daratumumab+bortezomib combination is emerging as a novel standard o

170 Upfront bortezomib confers durable hematologic responses.

171 Bortezomib-conjugated telodendrimers, together with doxo

172 : a hydrophilic polyethylene glycol (PEG), a bortezomib-conjugating intermediate, and a dendritic dox

173 mmalian target of rapamycin and enhanced the bortezomib cytotoxicity.

174 some inhibitor therapy, and planned route of bortezomib delivery if assigned to the bortezomib group.

175 The pan-proteasome inhibitor bortezomib demonstrated clinical efficacy in off-label t

176 atic germinal center (GC) response may limit bortezomib desensitization therapy.

177 evaluated the efficacy of the combination of bortezomib, dexamethasone, and rituximab (BDR) in 59 pre

178 en either lenalidomide-dexamethasone (RD) or bortezomib-dexamethasone (VD) but it is changing rapidly

179 b/dexamethasone (DD, n = 106) or daratumumab/bortezomib/dexamethasone (DVD, n = 62).

180 The proteasome inhibitor bortezomib did not block the 48-kDa beta-catenin, instea

181 The addition of bortezomib did not improve progression-free survival.

182 Bortezomib did not increase PNPLA3 levels in Pnpla3(148M

183 Using data from completed bortezomib dose-finding trials, we explore its toxicity

184 Patients received bortezomib, doxorubicin, and dexamethasone chemotherapy,

185 s (HMM) species after treatment with DPTA or bortezomib + DPTA, in contrast to the WT enzyme.

186 rial), we investigated whether two cycles of bortezomib (each cycle: 1.3 mg/m(2) intravenously on day

187 Weekly administration of bortezomib enhanced tolerability and convenience.

188 e EFS was 5.7 months for patients with prior bortezomib exposure and 11.0 months for bortezomib-naive

189 Average time from bortezomib exposure to onset of first eyelid complicatio

190 asma cells (PC) with a proteasome inhibitor, bortezomib, followed by the sustained inhibition of PC g

191 ks post-NBPI by treating mice with saline or bortezomib for varying durations between P8 and P32.

192 Lenalidomide and bortezomib frontline exposure has raised a growing need

193 [n=1]) and two (<1%) of 456 patients in the bortezomib group (cardiac arrest [n=1] and pneumonia [n=

194 group versus 40.0 months (32.6-42.3) in the bortezomib group (hazard ratio 0.791 [95% CI 0.648-0.964

195 ib group versus 9.4 months (8.4-10.4) in the bortezomib group at a preplanned interim analysis (hazar

196 omib group) or bortezomib and dexamethasone (bortezomib group) through a blocked randomisation scheme

197 mib group vs 46 [10%] of 456 patients in the bortezomib group), hypertension (67 [15%] vs 15 [3%]), p

198 (464 to the carfilzomib group and 465 to the bortezomib group).

199 b group and 324 (71%) of 456 patients in the bortezomib group, and serious adverse events in 273 (59%

200 n the carfilzomib group and 182 (40%) in the bortezomib group.

201 on days 1, 2, 4, 5, 8, 9, 11, and 12 in the bortezomib group.

202 te of bortezomib delivery if assigned to the bortezomib group.

203 roup and in 162 (36%) of 456 patients in the bortezomib group.

204 group and in 16 (3%) of 465 patients in the bortezomib group.

205 In the past decade, bortezomib has been increasingly used in combination wit

206 Subcutaneous bortezomib has replaced intravenous bortezomib as it is

207 Bortezomib, however, associated with gastrointestinal an

208 ous bortezomib, suggesting that subcutaneous bortezomib improves the tolerability of the panobinostat

209 ne patients received chemotherapy (including bortezomib in 22), whereas 8 and 13 patients received va

210 e combination of costimulation blockade with bortezomib in a sensitized non-human primate kidney tran

211 ich may explain the overall poor response to bortezomib in clinical trials of patients with advanced

212 ptosis induction of the proteasome inhibitor bortezomib in combination experiments significantly.

213 is randomized, placebo-controlled trial (the Bortezomib in Late Antibody-Mediated Kidney Transplant R

214 h improved efficacy and safety profiles over bortezomib in multiple myeloma patients.

215 peutic effects are primarily associated with bortezomib-induced attenuation of 20S proteasome beta1 s

216 s to identifying SNPs associated with severe bortezomib-induced peripheral neuropathy (BiPN) in patie

217 there was an increase in the use of pre-ASCT bortezomib induction and of unattenuated melphalan condi

218 Proteasome inhibitor bortezomib is a novel therapeutic agent for focal radiat

219 Bortezomib is a standard therapy in light-chain amyloido

220 However, bortezomib is cytotoxic against nonimmune cells, which l

221 ting the ubiquitin-proteasome machinery with bortezomib is effective in GIST cells through a dual mec

222 ts who become refractory to lenalidomide and bortezomib is very poor, indicating the need for new the

223 Bortezomib, lenalidomide, and dexamethasone (VRd) is a s

224 NF-kappaB (IkappaBalpha), despite efficient bortezomib-mediated inhibition of proteasome activity.

225 reatment and frontline therapy with combined bortezomib, melphalan, and dexamethasone independently p

226 longer with daratumumab in combination with bortezomib, melphalan, and prednisone (D-VMP) versus bor

227 ib, melphalan, and prednisone (D-VMP) versus bortezomib, melphalan, and prednisone (VMP) alone in pat

228 rk, two treatment options were combined: (1) bortezomib monotherapy and bortezomib plus dexamethasone

229 ious modalities including sirolimus (n = 5), bortezomib (n = 3), mycophenolate mofetil (n = 2), splen

230 patients, were randomly assigned to receive bortezomib (n=21) or placebo (n=23).

231 rior bortezomib exposure and 11.0 months for bortezomib-naive patients.

232 uation of ocular therapy in combination with bortezomib omission if eyelid signs persist.

233 eries, the combination of ocular therapy and bortezomib omission led to complete resolution of eyelid

234 n average of 1.8 months before proceeding to bortezomib omission.

235 alone was 1.8 months versus 3.1 months after bortezomib omission.

236 1 or more prior lines of therapy (including bortezomib) on days 1, 8, and 15 of 28-day cycles, for u

237 he clinically approved proteasome inhibitor, bortezomib, or inhibition of glucosylceramide synthesis

238 to evaluate regimens using either maraviroc, bortezomib, or post-transplantation cyclophosphamide for

239 nt of either a proteasome inhibitor MG132 or bortezomib, or with a p-ERK/MEK inhibitor U0126 attenuat

240 th carfilzomib and 17% of those treated with bortezomib (P = .002).

241 , patients were randomly assigned to receive bortezomib plus dexamethasone (BD), or BD plus cyclophos

242 es the tolerability of the panobinostat plus bortezomib plus dexamethasone regimen.

243 ere combined: (1) bortezomib monotherapy and bortezomib plus dexamethasone, and (2) thalidomide monot

244 eath by 87% versus dexamethasone, 81% versus bortezomib plus dexamethasone, and 63% versus lenalidomi

245 his issue of Blood, Mateos et al report that bortezomib plus melphalan and prednisone (VMP) and lenal

246 In conclusion, our trial failed to show that bortezomib prevents GFR loss, improves histologic or mol

247 use model that the 20S proteasome inhibitor, bortezomib, prevents contractures after NBPI.

248 -CHOP alone (R-CHOP group; control), or with bortezomib (RB-CHOP group; experimental; 1.3 mg/m(2) int

249 New drugs including N-acetylcysteine, bortezomib, recombinant ADAMTS13, and caplacizumab show

250 number of prior regimens was 1; and 52% were bortezomib-refractory.

251 Bortezomib release was accelerated significantly by acid

252 erapy for diffuse large B-cell lymphoma with bortezomib (REMoDL-B), an open-label, adaptive, randomis

253 al NF-kappaB activation and thereby promotes bortezomib resistance in MM cells.

254 tly activates STAT3 target genes, leading to bortezomib resistance in multiple myeloma.

255 of salvage regimen is based on lenalidomide/bortezomib resistance, daratumumab availability, and cos

256 ispersal but also drug resistance, including bortezomib resistance, via plasmacytic differentiation.

257 We found that this pathway involves bortezomib-resistant degradation of the inhibitor of NF-

258 These findings were confirmed on bortezomib-resistant multiple myeloma cells as well as o

259 fraction of freshly isolated MM cells harbor bortezomib-resistant NF-kappaB activity.

260 marrow plasma, and can activate an atypical bortezomib-resistant NF-kappaB pathway in MM cells.

261 Moreover, HAPLN1 can also confer bortezomib-resistant survival of MM cells.

262 inically applicable inhibitors (safingol and bortezomib, respectively) significantly inhibited aggres

263 apeutic strategy for NKTL patients with poor bortezomib response.

264 ects and effects of the proteasome inhibitor bortezomib revealed stabilization of multiple targets of

265 In the absence of neuropathy, a bortezomib-rituximab-based option is reasonable for rela

266 ne or bortezomib, and SRI31277 combined with bortezomib showed greater tumor reduction than either ag

267 nts aged <=65 years with NDMM, is evaluating bortezomib (subcutaneous) + lenalidomide + dexamethasone

268 nts in the VRd group received 1.3 mg/m(2) of bortezomib subcutaneously or intravenously on days 1, 4,

269 n was mitigated by the proteasome inhibitor, bortezomib, suggesting that cisplatin induced proteasome

270 ious trials of this regimen with intravenous bortezomib, suggesting that subcutaneous bortezomib impr

271 transplantation (HSCT) with daratumumab plus bortezomib, thalidomide, and dexamethasone (D-VTd) signi

272 esponse and progression-free survival versus bortezomib, thalidomide, and dexamethasone (VTd) in pati

273 Bortezomib, thalidomide, and dexamethasone (VTd) plus au

274 all patients who received a trial drug (ie, bortezomib, thalidomide, dexamethasone, or panobinostat)

275 ith newly diagnosed myeloma, the addition of bortezomib to lenalidomide and dexamethasone resulted in

276 ith newly diagnosed myeloma, the addition of bortezomib to lenalidomide and dexamethasone resulted in

277 We aimed to study whether the addition of bortezomib to lenalidomide and dexamethasone would impro

278 se To evaluate the impact of the addition of bortezomib to rituximab, cyclophosphamide, doxorubicin,

279 We aimed to investigate whether adding bortezomib to standard therapy could improve outcomes in

280 erexpression led to decreased sensitivity to bortezomib treatment in NKTL based on deprivation of EZH

281 esis, either by restoring miR-29b levels via bortezomib treatment or by directly inhibiting BRD4 bind

282 , and Thr residues was nearly insensitive to bortezomib treatment.

283 ased levels, which were also restored by the bortezomib treatment.

284 at MTI-101 is synergistic when combined with bortezomib, using both myeloma cell lines and primary my

285 ve FDA-approved proteasome-inhibiting drugs, bortezomib (Velcade(R)), carfilzomib (Kyprolis(R)), and

286 The effect of bortezomib was attenuated in the receptor variants that

287 a improved or resolved in most patients when bortezomib was discontinued, the temporal relationship b

288 Bortezomib was given at 1.3 mg/m(2) intravenously on day

289 Bortezomib was increased to 1.3 mg/m(2) for dose level 2

290 the first-in-class proteasome inhibitor (PI) bortezomib, we purified and investigated patient-derived

291 mporary treatment regiments using NA (mainly bortezomib) were associated with a lower risk for a SPM

292 lines of therapy (including lenalidomide and bortezomib), were refractory to their last line of thera

293 the acquired resistance of myeloma cells to bortezomib, which could be overcome by PRL-3 silencing.

294 73% were seen in patients not refractory to bortezomib who had 1 to 3 prior therapies.

295 directed therapies using lenalidomide and/or bortezomib with dexamethasone and HDIVig led to a signif

296 Bortezomib with dexamethasone is a standard treatment op

297 ts to receive either an initial treatment of bortezomib with lenalidomide and dexamethasone (VRd grou

298 The combination of the proteasome inhibitor bortezomib with lenalidomide and dexamethasone has shown

299 led, 65 received carfilzomib and 30 received bortezomib, with median 25 months of follow-up.

300 talizations compared with patients receiving bortezomib (without IMiDs), but 1-year overall survival