ライフサイエンスコーパス: bortezomib

1 treatment with the 20S proteasome inhibitor bortezomib.

2 rgin, tunicamycin or the myeloma therapeutic bortezomib.

3 itive to the proteasome inhibitors MG132 and bortezomib.

4 the first-line multiple myeloma therapeutic bortezomib.

5 t, resulted in resistance to temozolomide or bortezomib.

6 at of the classical 20S proteasome inhibitor bortezomib.

7 ent with the antimyeloma drugs melphalan and bortezomib.

8 ells, including those that were resistant to bortezomib.

9 nges upon drug treatment with the example of bortezomib.

10 hat is sensitive to the proteasome inhibitor bortezomib.

11 cell resistance to the proteasome inhibitor bortezomib.

12 onal basis for the antithrombotic effects of bortezomib.

13 reduction in the risk of death compared with bortezomib.

14 nd were not significantly improved by adding bortezomib.

15 overcomes resistance to proteasome inhibitor bortezomib.

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

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

18 omib-dexamethasone (VD; n = 168; intravenous bortezomib 1.3 mg/m(2), days 1, 4, 8, and 11 plus oral d

19 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

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

21 panobinostat (20 mg orally) or placebo, with bortezomib (1.3 mg/m(2) intravenously) and dexamethasone

22 evious ASCT were re-induced with intravenous bortezomib (1.3 mg/m(2) on days 1, 4, 8, 11), intravenou

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

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

25 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

26 t therapy, including 19 (27%) retreated with bortezomib, 11 (58%) of whom achieved complete or partia

27 nts were refractory to both lenalidomide and bortezomib (80.2%).

28 Bortezomib, a proteasome inhibitor used in the managemen

29 Here we report that bortezomib, a proteasome inhibitor with anticancer and a

30 combined with ER stress inducers, especially bortezomib, a remarkable synergistic cytotoxicity ensued

31 how that the proteasome inhibitors MG132 and bortezomib activate the RIPK3-MLKL necroptotic pathway i

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

33 l Staging System stage, and planned route of bortezomib administration if randomly assigned to bortez

34 asone was given on the days of and following bortezomib administration.

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

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

37 1 overexpression or the proteasome inhibitor bortezomib also reduced 3BP2 and MITF expression.

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

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

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

41 ificantly higher likelihood of responding to bortezomib and a longer response duration, supporting th

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

43 ved at least two previous regimens including bortezomib and an immunomodulatory drug, median overall

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

45 re sensitivity to therapeutic agents such as bortezomib and can also inhibit tumor growth induced by

46 Based on data available today, bortezomib and carfilzomib treatment appear to improve c

47 nd cyclophosphamide), proteasome inhibitors (bortezomib and carfilzomib), nucleoside analogs (fludara

48 0S proteasome with specificity distinct from bortezomib and carfilzomib.

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

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

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

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

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

54 cantly longer progression-free survival than bortezomib and dexamethasone alone and was associated wi

55 tes of thrombocytopenia and neutropenia than bortezomib and dexamethasone alone.

56 mib-thalidomide-dexamethasone (VTD; n = 167; bortezomib and dexamethasone as before plus oral thalido

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

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

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

60 nation of carfilzomib and dexamethasone with bortezomib and dexamethasone in patients with relapsed o

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

62 ple myeloma, daratumumab in combination with bortezomib and dexamethasone resulted in significantly l

63 Panobinostat plus bortezomib and dexamethasone significantly increased med

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

65 The patient was treated with bortezomib and dexamethasone, which resulted in improvem

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

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

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

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

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

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

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

73 Combined treatments with bortezomib and inhibitor of STAT3 abrogated proteasome a

74 Patients who failed treatment with bortezomib and lenalidomide and had adequate prior alkyl

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

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

77 tory drugs and 64% had disease refractory to bortezomib and lenalidomide), and 76% had received autol

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

79 s platform, we predicted chemosensitivity to bortezomib and melphalan, two clinical multiple myeloma

80 dose-dependently increased by UPS inhibitors bortezomib and MG132.

81 Established anti-flaviviral drugs (e.g., bortezomib and mycophenolic acid) and others that had no

82 w recent evidence for the potential roles of bortezomib and N-acetylcysteine, and explore new therape

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

84 The bortezomib and PC regimens significantly reduced Ab leve

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

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

87 Similarly, a combination regimen of bortezomib and the histone deacetylase inhibitor trichos

88 n combination with rituximab, dexamethasone, bortezomib, and B-cell receptor signaling inhibitors, co

89 New agents such as nelarabine, bortezomib, and clofarabine may be effective in preventi

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

91 s (29.0-40.6) in those who received placebo, bortezomib, and dexamethasone (hazard ratio [HR] 0.94, 9

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

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

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

95 3) in 73 patients who received panobinostat, bortezomib, and dexamethasone versus 19.5 months (14.1-3

96 .0-44.8) in those who received panobinostat, bortezomib, and dexamethasone versus 35.8 months (29.0-4

97 corporation of the novel agents thalidomide, bortezomib, and lenalidomide in the front-line therapy h

98 e introduction of novel agents, thalidomide, bortezomib, and lenalidomide, as part of frontline treat

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

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

101 plasma exchange-Rituximab; group II (n = 8), Bortezomib; and group III (n = 10), optimization of main

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

103 rtezomib-melphalan-prednisone (VMP; n = 167; bortezomib as before plus oral melphalan 9 mg/m(2) and o

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

105 In this study, we demonstrate that bortezomib at 10 nM or higher concentrations killed long

106 CHOP regimen, but replacing vincristine with bortezomib at a dose of 1.3 mg per square meter of body-

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

108 population of 855 patients who had received bortezomib-based induction therapy in the four trials, t

109 rial was designed to compare three frontline bortezomib-based regimens in transplantation-ineligible

110 Bortezomib-based regimens remain the cornerstone of the

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

112 Bortezomib-based treatment resulted in a strong decrease

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

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

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

116 The proteosome inhibitor bortezomib (BTZ) induces endoplasmic reticulum and oxida

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

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

119 BM microenvironment play a critical role in bortezomib (BTZ) resistance.

120 eloma efficacy of cyclophosphamide (CTX) and bortezomib (Btz), which are both standardly used to mana

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

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

123 is regulated by NF-kappaB and suppressed by bortezomib (BZ), which has shown promising results in th

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

125 me has not improved with the introduction of bortezomib (Bzb).

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

127 nd exaggerated after-discharges in rats with bortezomib CIPN.

128 Bortezomib-conjugated telodendrimers, together with doxo

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

130 Although all bortezomib-containing regimens produced good outcomes, V

131 tezomib-thalidomide-dexamethasone (VTD) with bortezomib-cyclophosphamide-dexamethasone (VCD) as induc

132 mmalian target of rapamycin and enhanced the bortezomib cytotoxicity.

133 interferon-alpha, alemtuzumab, bendamustine, bortezomib, dasatinib, imatinib, lenalidomide, rituximab

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

135 ve trial in patients with pPCL, we show that bortezomib, dexamethasone plus doxorubicin or cyclophosp

136 Three-drug therapy with bortezomib, dexamethasone, and an alkylating agent (BDex

137 nsecutive series of 32 patients treated with bortezomib, dexamethasone, and cyclophosphamide.

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

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

140 eeks (eight 21-day cycles) of induction with bortezomib-dexamethasone (VD; n = 168; intravenous borte

141 Lenalidomide-bortezomib-dexamethasone appears effective and tolerable

142 ophosphamide-dexamethasone, bendamustine, or bortezomib-dexamethasone provide durable responses and a

143 1q21 conferred no adverse prognosis in this bortezomib-dexamethasone-treated group.

144 ab is added to lenalidomide-dexamethasone or bortezomib-dexamethasone.

145 The combination of cyclophosphamide/bortezomib/dexamethasone (CyBorD) showed early promise o

146 ophosphamide/dexamethasone, bendamustine, or bortezomib/dexamethasone provided durable responses and

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

148 Recommendations for the bortezomib dosages were within the package insert.

149 the entire course of treatment, the approved bortezomib dose exceeds the conventional ceiling DLT rat

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

151 d treated with a single rituximab dose and 4 bortezomib doses preceded by plasmapheresis.

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

153 Weekly administration of bortezomib enhanced tolerability and convenience.

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

155 Use of bortezomib for induction therapy in at-risk patients is

156 We investigated whether substituting bortezomib for vincristine in frontline therapy with R-C

157 Bortezomib frequently produces severe treatment-related

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

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

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

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

162 mib group vs 45 [10%] of 456 patients in the bortezomib group), hypertension (41 [9%] vs 12 [3%]), th

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

164 ed (464 to the carfilzomib group; 465 to the bortezomib group).

165 mib group) or bortezomib with dexamethasone (bortezomib group).

166 (464 to the carfilzomib group and 465 to the bortezomib group).

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

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

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

170 omib group and 11.1 months (8.2-14.3) in the bortezomib group.

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

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

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

174 Bortezomib has become a cornerstone in the treatment of

175 Bortezomib has been used to reduce HLA antibody in patie

176 Bortezomib, however, associated with gastrointestinal an

177 hat of the FDA-approved proteasome inhibitor bortezomib; (ii) CuPT potently inhibits proteasome-speci

178 inistration include the proteasome inhibitor bortezomib, immunomodulator lenalidomide, and Bruton's t

179 Bortezomib improved several histological hallmarks of di

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

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

182 iple myeloma, as well as in combination with bortezomib in patients with newly diagnosed multiple mye

183 nical trials of proteasome inhibitor PS-341 (bortezomib) in solid tumors led to the invention of MLN9

184 hagy induction while significantly enhancing bortezomib-induced apoptosis in HNSCC cells.

185 ze paclitaxel-, cisplatin-, vincristine- and bortezomib-induced neuropathy in C57BL/6 mice with a com

186 Bortezomib induces AIRAP expression at the transcription

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

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

189 Bortezomib is an U.S. Food and Drug Administration-appro

190 The proteasome inhibitor bortezomib is effective in hematologic malignancies such

191 elphalan and dexamethasone standard therapy, bortezomib is less beneficial to patients harboring t(11

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

193 PS341 (Bortezomib) is the first proteasome inhibitor drug which

194 went a second HDM/ASCT followed by 1 year of bortezomib, lenalidomide, dexamethasone.

195 owed by either allogeneic transplantation or bortezomib/lenalidomide maintenance.

196 followed by 25 weeks (five 35-day cycles) of bortezomib maintenance (1.6 mg/m(2), days 1, 8, 15, and

197 Bortezomib maintenance was feasible without producing cu

198 , A23187, brefeldin A, DTT, geldanamycin, or bortezomib manifested reduced activation of the mitochon

199 We hypothesized that bortezomib may abrogate neutralizing Ab levels, making d

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

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

202 RSK2 inhibition also sensitized MM cells to bortezomib, melphalan, and dexamethasone, but did not do

203 s oral thalidomide 100 mg, days 1 to 21), or bortezomib-melphalan-prednisone (VMP; n = 167; bortezomi

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

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

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

207 We observed a differential effect of bortezomib on class I versus class II antibody and hypot

208 Treatment was given during a 21-day cycle (bortezomib on days 1 and 8; thalidomide every day; dexam

209 t or placebo on days 1, 3, 5, 8, 10, and 12; bortezomib on days 1, 4, 8, and 11; and dexamethasone on

210 In fact, the effect of bortezomib on IL-8 production was higher than that exert

211 1 or more prior lines of therapy (including bortezomib) on days 1, 8, and 15 of 28-day cycles, for u

212 by combination with the proteasome inhibitor bortezomib or a second mitochondrial-derived activator o

213 ination, also not when further combined with bortezomib or a SMAC mimetic.

214 was not negatively impacted by resistance to bortezomib or carfilzomib.

215 KRAS mutation did not reduce sensitivity to bortezomib or dexamethasone.

216 poptosis induced by the proteasome inhibitor bortezomib or the alkylating agent temozolomide.

217 double autologous stem cell transplant plus bortezomib, or combination of immunotherapy with lenalid

218 ivo application of the proteasome inhibitor, bortezomib, partially restored expression of these prote

219 The relatively recent clinical success of bortezomib, particularly in multiple myeloma, has establ

220 statin/cyclophosphamide (PC) regimen, or the bortezomib/PC (BPC) combination regimen.

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

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

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

224 Bortezomib plus melphalan and prednisone (VMP) and lenal

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

226 ls are treated with the proteasome inhibitor bortezomib, proposed as an alternative chemotherapeutic

227 mutate the target of the cancer therapeutic bortezomib, PSMB5, and identify known and novel mutation

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

229 These data indicate that bortezomib reduces HLA class I antibody more effectively

230 ingly, inclusion of the proteasome inhibitor bortezomib reduces thrombotic risk, yet the molecular ba

231 he subset of patients with lenalidomide- and bortezomib-refractory disease as well as in patients wit

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

233 Bortezomib release was accelerated significantly by acid

234 Knockdown of LDHA can restore sensitivity of bortezomib resistance cell lines while gain-of-function

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

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

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

238 entify known and novel mutations that confer bortezomib resistance.

239 is optimized method in a case study of drug (bortezomib) resistant and drug-sensitive multiple myelom

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

241 veral genetically diverse MM cells including Bortezomib-resistant MM cells are addicted to RelB-p52 f

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

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

244 nosporamide A (IC50 = 5.1 nM), whereas their bortezomib-resistant sublines were 9- and 17-fold cross-

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

246 Food and Drug Administration-approved for bortezomib-resistant, relapsed/refractory mantle-cell ly

247 Mdr2(-/-) mice with the proteasome inhibitor bortezomib restored PC2 expression and significantly red

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

249 es using LDHA or HIF1A induced resistance in bortezomib-sensitive cell lines.

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

251 In xenograft mice models, bortezomib stimulated the conversion of LC3-I to LC3-II,

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

253 Panobinostat 20 mg in combination with bortezomib, thalidomide, and dexamethasone is an efficac

254 MM, and 53%, 75%, and 6% had received prior bortezomib, thalidomide, and lenalidomide, respectively.

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

256 lome conducted a randomized trial to compare bortezomib-thalidomide-dexamethasone (VTD) with bortezom

257 1 to 4], or 1, 2, 4, and 5 [cycles 5 to 8]), bortezomib-thalidomide-dexamethasone (VTD; n = 167; bort

258 ere separated into groups to receive saline, bortezomib, the pentostatin/cyclophosphamide (PC) regime

259 was unknown in 5), and the mean duration of bortezomib therapy before the onset of chalazia was slig

260 view of the reduced response of t(11;14) to bortezomib, this highlights the impact of therapy on the

261 truncated HC that sensitizes plasma cells to bortezomib through an elevated unfolded protein response

262 for establishing the future credentials for bortezomib to gain initial FDA approval in 2003.

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

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

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

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

267 ved fewer plasma cells in the bone marrow of bortezomib-treated mice but not in PC-treated mice.

268 ential strategy to treat thrombocytopenia in bortezomib-treated multiple myeloma patients.

269 nostic impact of cytogenetic aberrations for bortezomib-treated patients.

270 resistant to the original therapy, including bortezomib treatment and high-dose melphalan in stem cel

271 Bortezomib treatment elevated HNF1alpha and PCSK9 cellul

272 were detectable within autophagosomes after bortezomib treatment indicating that autophagy induction

273 In vitro bortezomib treatment of lymphocytes resulted in a mean d

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

275 After bortezomib treatment, they showed ultrastructural change

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

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

278 erse drug reactions, the association between bortezomib use and chalazia is classified as possible.

279 he literature suggest an association between bortezomib use and chalazia.

280 VMP consisted of one 6-week cycle of bortezomib using a biweekly schedule, followed by eight

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

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

283 ednisone, and either vincristine (R-CHOP) or bortezomib (VR-CAP).

284 roved chymotrypsin-like proteasome inhibitor bortezomib, VR23 produced a synergistic effect in killin

285 tat or placebo was given three times a week, bortezomib was administered once a week, and dexamethaso

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 proteasome inhibitor bortezomib was initially approved for the treatment of r

291 Notably, PSMB5, a molecular target of bortezomib, was shown to be a target of STAT3.

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

293 73% were seen in patients not refractory to bortezomib who had 1 to 3 prior therapies.

294 ib with dexamethasone (carfilzomib group) or bortezomib with dexamethasone (bortezomib group).

295 hasone could be considered in cases in which bortezomib with dexamethasone is a potential treatment o

296 Bortezomib with dexamethasone is a standard treatment op

297 zomib administration if randomly assigned to bortezomib with dexamethasone.

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

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

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