ライフサイエンスコーパス: thalidomide

1 es were 8.9 months (placebo) and 8.5 months (thalidomide).

2 mide, rituximab alone or in combination, and thalidomide).

3 be associated with the clinical efficacy of thalidomide.

4 rite outgrowth, known detrimental effects of Thalidomide.

5 thasone, and 1 patient subsequently required thalidomide.

6 bogenic conditions, such as those induced by thalidomide.

7 apy, including bortezomib, lenalidomide, and thalidomide.

8 h combined chemoradiotherapy with or without thalidomide.

9 grade 3 toxicities in patients treated with thalidomide.

10 zziness, and malaise were more frequent with thalidomide.

11 re higher than with repeat administration of thalidomide.

12 reated with lenalidomide, bortezomib, and/or thalidomide.

13 Thalidomide, 1.5 to 2.5 mg/kg per day, or placebo once d

14 randomly assigned to bortezomib 1.3 mg/m(2), thalidomide 100 mg, and dexamethasone 40 mg, with (n = 4

15 ezomib and dexamethasone as before plus oral thalidomide 100 mg, days 1 to 21), or bortezomib-melphal

16 ubcutaneous bortezomib 1.3 mg/m(2), and oral thalidomide 100 mg, dexamethasone 20 mg, and panobinosta

17 ell lines such as MM1.S, OPM2, and U266 with thalidomide (100 muM) and its structural analog lenalido

18 nonresponders to placebo who began receiving thalidomide, 11 of 21 (52.4%) subsequently reached remis

19 by significantly more children treated with thalidomide (13/28 [46.4%] vs 3/26 [11.5%]; risk ratio [

20 rapy produced higher efficacy (34%-38%) than thalidomide (16%; P = .06).

21 ys 1, 2, 8, 9, 15, and 16 of a 28-day cycle; thalidomide 200 mg on days 1 to 28; and dexamethasone 20

22 o bortezomib for 1 year, in combination with thalidomide (200 mg per day orally) and dexamethasone (4

23 -old APP23 mice with short-term treatment of thalidomide (3 days).

24 of multiple myeloma followed by repeat IMiD (thalidomide [34; 24%] or lenalidomide [106; 76%]) as one

25 ive phase 2 trials: 44 received single-agent thalidomide, 41 single-agent lenalidomide, and 40 a comb

26 autologous stem cell transplantation (78%), thalidomide (44%), and lenalidomide (34%); 22% of patien

27 Maintenance consisted of thalidomide 50 mg (VAD) once per day or bortezomib 1.3 m

28 45 mg/m(2), or 56 mg/m(2), respectively, and thalidomide 50 mg.

29 cation treatment in 1 arm consisted of daily thalidomide (50 mg) for 2 years.

30 Overall, 31 of 49 children treated with thalidomide (63.3%) achieved clinical remission, and 32

31 and isotype-selective Sirt2 inhibitors with thalidomide, a bona fide cereblon ligand.

32 Lenalidomide and thalidomide abrogated this stimulatory effect of BMSCs a

33 We conclude that thalidomide added to MP improves OS and PFS in previousl

34 In the 1950s, the drug thalidomide, administered as a sedative to pregnant wome

35 These results suggest that chronic thalidomide administration is an alternative approach fo

36 ases, and the immunomodulators imiquimod and thalidomide allowed 5 patients to reach sustained comple

37 Thalidomide also significantly improved scores on the vi

38 unomodulatory drugs (IMiDs; lenalidomide and thalidomide) among beneficiaries with myeloma, who can r

39 Thalidomide, an effective treatment for ENL, inhibited t

40 The administration of thalidomide, an immunomodulatory drug with antiangiogeni

41 We hypothesized that thalidomide, an oral antiangiogenic agent, when combined

42 rate degradation and key differences between thalidomide analog activity in vitro and in vivo.

43 verse effects of a reference anti-angiogenic thalidomide analog, 5HPP-33, on in vitro angiogenesis wi

44 rtunity to characterize the class effects of thalidomide analogs and improve on the therapeutic promi

45 Thalidomide analogs bind the CRL4(CRBN) ubiquitin ligase

46 ation antimalarials that include quinacrine, thalidomide analogs, and Mycophenalate Mofetil may also

47 nd testing of individual enantiomers for two thalidomide analogs, including CC-122, a compound curren

48 The clinical success of thalidomide analogues demonstrates the therapeutic effic

49 This engenders interest in evaluating thalidomide analogues such as lenalidomide with better t

50 This unique specific interaction between (S)-thalidomide and (R)-NDI derivative counterparts, evident

51 s were reported in 74% of patients receiving thalidomide and 22% receiving placebo; constipation, diz

52 Twenty-eight children were randomized to thalidomide and 26 to placebo.

53 domly assigning 323 patients with myeloma to thalidomide and 345 to a control arm, no difference was

54 ties, kinetics, and cell-type specificity of thalidomide and 4 analogs, all but 1 of which are in cli

55 trate that minor side chain modifications in thalidomide and a novel analogue, CC-122, can modulate t

56 The 2 TT3 trials used thalidomide and bortezomib during induction, before and

57 the tumor cells to the apoptotic effects of thalidomide and bortezomib.

58 To date, such effectors are derived from thalidomide and confer a broad substrate spectrum that i

59 GEP) of purified plasma cells 48 hours after thalidomide and dexamethasone test doses showed these ag

60 ith any evidence of clinical improvement, so thalidomide and dexamethasone were administered as repla

61 long-term plasmapheresis in conjunction with thalidomide and dexamethasone.

62 intravenous immunoglobulin, anti TNF agents, thalidomide and haematopoietic stem cell transplantation

63 lated skin IgG4-RD successfully treated with thalidomide and investigated their phenotypic characteri

64 Thalidomide and its analog, Lenalidomide, are in current

65 Through inhibition of CRBN ubiquitination, thalidomide and its analogs allow CRBN to accumulate, le

66 ur results reveal a novel mechanism by which thalidomide and its analogs modulate the CRBN function i

67 Here, we examine the effect of thalidomide and its analogs on CRBN ubiquitination and i

68 Despite the teratogenicity of thalidomide and its derivatives lenalidomide and pomalid

69 Thalidomide and its derivatives lenalidomide and pomalid

70 Thalidomide and its immunomodulatory drug (IMiD) analogs

71 The immunomodulatory drug (IMiD) thalidomide and its structural analogs lenalidomide and

72 Thalidomide and lenalidomide are immunomodulatory drugs

73 Thalidomide and lenalidomide constitute an important par

74 sus criteria, we re-assessed the efficacy of thalidomide and lenalidomide in 125 patients with myelof

75 rimary malignancies in patients treated with thalidomide and lenalidomide in the Arkansas total thera

76 r Pomalidomide as a treatment for conditions Thalidomide and Lenalidomide treat currently.

77 se agents include the immunomodulatory drugs thalidomide and lenalidomide, the proteasome inhibitor b

78 This is in marked contrast to Thalidomide and Lenalidomide, which had detrimental effe

79 as found to be essential for the activity of thalidomide and lenalidomide.

80 omalidomide is a potent structural analog of thalidomide and member of a new class of immunomodulator

81 estion by comparing VMP with bortezomib plus thalidomide and prednisone (VTP) as induction.

82 omib plus either melphalan and prednisone or thalidomide and prednisone.

83 ravenous docetaxel and bevacizumab plus oral thalidomide and prednisone.

84 Thalidomide and related drugs are key drugs for the trea

85 echanism of action and targets through which thalidomide and related immunomodulatory drugs (IMiDs) e

86 well in case reports, including bortezomib, thalidomide and stem cell transplantation.

87 so correctly classify species-specific drug (Thalidomide) and false negative drug (D-penicillamine) i

88 Total therapy trials (TT; TT2(-/+) thalidomide) and TT3 (TT3a with bortezomib, thalidomide;

89 lines of therapy; bortezomib, lenalidomide, thalidomide, and carfilzomib/marizomib in 88%, 88%, 62%,

90 with patients treated with cyclophosphamide, thalidomide, and dexamethasone (CTD) (22.5% [n = 121 of

91 examethasone (CVAD) versus cyclophosphamide, thalidomide, and dexamethasone (CTD; intensive) or melph

92 d an attenuated regimen of cyclophosphamide, thalidomide, and dexamethasone (CTDa; n = 426) with melp

93 ion (HSCT) with daratumumab plus bortezomib, thalidomide, and dexamethasone (D-VTd) significantly imp

94 investigated the combination of carfilzomib, thalidomide, and dexamethasone (KTd) as induction/consol

95 progression-free survival versus bortezomib, thalidomide, and dexamethasone (VTd) in patients with ne

96 Bortezomib, thalidomide, and dexamethasone (VTd) plus autologous ste

97 e maintenance for 3 years versus bortezomib, thalidomide, and dexamethasone in year 1 and thalidomide

98 nostat 20 mg in combination with bortezomib, thalidomide, and dexamethasone is an efficacious and wel

99 n therapy as per protocol (cyclophosphamide, thalidomide, and dexamethasone or cyclophosphamide, lena

100 With the introduction of bortezomib, thalidomide, and lenalidomide, higher rates of CR are be

101 , 75%, and 6% had received prior bortezomib, thalidomide, and lenalidomide, respectively.

102 ation or regimens incorporating bortezomide, thalidomide, and lenalidomide--substantially increase th

103 Thalidomide- and IMiD-induced SALL4 degradation can be a

104 PURPOSE We previously demonstrated that thalidomide appears to add to the activity of docetaxel

105 e in BACE1 level and activity with long-term thalidomide application.

106 IMiDs, including lenalidamide and thalidomide, are also in active development in castratio

107 in TT2's control arm to 25.1%/35.6% in TT2's thalidomide arm and to 32.9%/48.8% in TT3a.

108 h at 72 months, survival was superior on the thalidomide arm in the one third exhibiting cytogenetic

109 ival rate was 16% and 12% in the placebo and thalidomide arms, respectively.

110 mized trials establish a definitive role for thalidomide as induction therapy in conjunction with dex

111 al (ISRCTNG8454111) examined traditional and thalidomide-based induction and maintenance regimens and

112 D-positive patients who received maintenance thalidomide became MRD negative.

113 oxicity (MPT-T) and the same MP regimen with thalidomide being replaced by lenalidomide (MPR-R).

114 Thalidomide binding to CRBN elicits subsequent ubiquitin

115 degron peptides to CRBN depends on an intact thalidomide-binding pocket but is not competitive with I

116 Thalidomide binds readily to TBX5 through amino acids R8

117 Thalidomide binds to cereblon (CRBN), a substrate recept

118 des K48-linked polyubiquitin chains and that thalidomide blocks the formation of CRBN-ubiquitin conju

119 Prototypic drugs thalidomide, bortezomib, and lenalidomide have each been

120 though the incorporation of the novel agents thalidomide, bortezomib, and lenalidomide in the front-l

121 ter treatment with novel agents (NA) such as thalidomide, bortezomib, and lenalidomide may be associa

122 a has been the introduction of novel agents, thalidomide, bortezomib, and lenalidomide, as part of fr

123 vincristine, and doxorubicin), novel agents (thalidomide, bortezomib, or lenalidomide), or hematopoie

124 N-Arylphthalimides (1-10P) derived from thalidomide by insertion of hydrophobic groups were eval

125 d with either cyclophosphamide (BD group) or thalidomide (C-BD group).

126 uated, and our data suggest that maintenance thalidomide can eradicate MRD in some patients.

127 osyncrasies in FAERS, for example reports of thalidomide causing a deadly ADR when used against myelo

128 tudy that was originally designed to examine thalidomide combined with intensive therapy.

129 d adolescents with refractory Crohn disease, thalidomide compared with placebo resulted in improved c

130 Thalidomide-containing regimens had better efficacy than

131 Thalidomide could be considered as a therapeutic option

132 ally selected from bortezomib, lenalidomide, thalidomide, cyclophosphamide, and corticosteriods) whic

133 munoglobulins, cyclosporine, plasmapheresis, thalidomide, cyclophosphamide, hemoperfusion, tumor necr

134 Thalidomide-dependent degradation of the embryonic trans

135 This thalidomide-derived azide as well as the highly versatil

136 PROTAC by Cu(I)-catalyzed cycloaddition of a thalidomide-derived azide to an alkynylated inhibitor.

137 g modes of hydrolyzed metabolites of several thalidomide-derived effectors, which we elucidated via c

138 ansplantation; TT3A applied VTD (bortezomib, thalidomide, dexamethasone) in the first year of mainten

139 s who received a trial drug (ie, bortezomib, thalidomide, dexamethasone, or panobinostat).

140 We studied 140 patients who received either thalidomide-dexamethasone (81; 58%) or lenalidomide-dexa

141 zomib-thalidomide-dexamethasone (VTD) versus thalidomide-dexamethasone (TD) as induction therapy befo

142 PURPOSE Thalidomide-dexamethasone (THAL-DEX) is standard inducti

143 Bortezomib-thalidomide-dexamethasone (VTD) is an effective inductio

144 e survival were demonstrated with bortezomib-thalidomide-dexamethasone (VTD) versus thalidomide-dexam

145 ted a randomized trial to compare bortezomib-thalidomide-dexamethasone (VTD) with bortezomib-cyclopho

146 1, 2, 4, and 5 [cycles 5 to 8]), bortezomib-thalidomide-dexamethasone (VTD; n = 167; bortezomib and

147 amethasone [VTD]) versus a dual combination (thalidomide-dexamethasone [TD]) in patients with multipl

148 d safety of a triple combination (bortezomib-thalidomide-dexamethasone [VTD]) versus a dual combinati

149 from the GIMEMA MM-BO2005 study (bortezomib-thalidomide-dexamethasone v thalidomide-dexamethasone) s

150 v VAD), and PETHEMA GEM05MENOS65 (bortezomib-thalidomide-dexamethasone v thalidomide-dexamethasone) s

151 OS65 (bortezomib-thalidomide-dexamethasone v thalidomide-dexamethasone) studies were pooled in an int

152 tudy (bortezomib-thalidomide-dexamethasone v thalidomide-dexamethasone) supplemented the integrated p

153 zomib/thalidomide/dexamethasone (VTD) versus thalidomide/dexamethasone (TD) versus vincristine, BCNU,

154 roup conducted a trial to compare bortezomib/thalidomide/dexamethasone (VTD) versus thalidomide/dexam

155 b or thalidomide/dexamethasone or bortezomib/thalidomide/dexamethasone followed by HDT/ASCT; n = 276)

156 thalidomide, and dexamethasone in year 1 and thalidomide/dexamethasone in years 2 and 3 in the 2003-3

157 ized induction with VBMCP/VBAD/bortezomib or thalidomide/dexamethasone or bortezomib/thalidomide/dexa

158 lthough 80% of patients randomly assigned to thalidomide discontinued study drug after 2 years becaus

159 Vascular remodeling was induced with thalidomide dissolved in dimethyl sulfoxide and sterile

160 The protocol allowed an increase in thalidomide dose up to 1,000 mg daily based on patient t

161 Exposure to thalidomide during a critical window of development resu

162 /L vs >2.5 mg/L), previous use or non-use of thalidomide during induction therapy, and previous use o

163 ed trial designed to evaluate the effects of thalidomide during induction treatment and as maintenanc

164 o thalidomide) or to the experimental group (thalidomide during induction, between transplantations,

165 prominent in individuals who were exposed to thalidomide early in the sensitive period (days 20 to 26

166 tion between the chiral NDI receptor and the thalidomide enantiomer of the opposite configuration.

167 a 21-day cycle (bortezomib on days 1 and 8; thalidomide every day; dexamethasone on days 1, 2, 8, an

168 extension, nonresponders to placebo received thalidomide for an additional 8 weeks.

169 All responders continued to receive thalidomide for an additional minimum 52 weeks.

170 The role of thalidomide for previously untreated elderly patients wi

171 intenance with interferon for the VAD arm or thalidomide for the TAD arm.(1) This study together with

172 r improvement was observed at 8 weeks in the thalidomide group (75% response, 13/28 [46.4%] vs 3/26 [

173 The thalidomide group included significantly more untreated

174 Mean duration of clinical remission in the thalidomide group was 181.1 weeks (95% CI, 144.53-217.76

175 slight excess of rash and neuropathy in the thalidomide group.

176 This demonstrated that thalidomide had a teratogenic effect between approximate

177 However, whether thalidomide has any therapeutic effects on neurodegenera

178 Immunomodulatory derivatives of thalidomide (IMiD compounds), such as pomalidomide and l

179 Immunomodulatory derivatives of thalidomide (IMiDs) have been used for the treatment of

180 Thalidomide improved cough and respiratory quality of li

181 In this large trial of patients with NSCLC, thalidomide in combination with chemotherapy did not imp

182 induction and maintenance), the TT3b trial (thalidomide in induction and lenalidomide in maintenance

183 lenalidomide in maintenance), the TT6 trial (thalidomide in induction and lenalidomide in maintenance

184 ssion-free survival in patients who received thalidomide in induction and maintenance therapy in the

185 f IMiD combination regimens: the TT3a trial (thalidomide in induction and maintenance), the TT3b tria

186 e (VAD) group of the HOVON65/GMMG-HD4 trial (thalidomide in maintenance).

187 ntiated the apoptotic effects of Velcade and thalidomide in MM cells.

188 nvestigated whether the clinical efficacy of thalidomide in multiple myeloma is associated with CRBN

189 e show the beneficial therapeutic effects of thalidomide in patients with low XBP1s/u ratios.

190 of accuracy towards the determination of (S)-thalidomide in the blood samples, so it can be successfu

191 the limb defects seen in children exposed to thalidomide in utero.

192 blon (CRBN), a primary teratogenic target of thalidomide, in the antimyeloma activity of IMiDs.

193 Herein, thalidomide-induced degradation of SALL4 was examined in

194 tion factor of which polymorphisms phenocopy thalidomide-induced limb defects in humans.

195 Both X-irradiation and thalidomide-induced phocomelia have been interpreted as

196 Thalidomide-induced teratogenicity is dependent on its b

197 Similarly, thalidomide inhibited the TBX5/HAND2 physical interactio

198 ation therapy of docetaxel, bevacizumab, and thalidomide inhibited tumor growth most effectively.

199 While the anti-angiogenic drug thalidomide inhibits HIF-1-dependent VEGF transcription

200 However, the mechanism of thalidomide involving in the mitigation of AD neuropatho

201 Thalidomide is a tumor necrosis factor alpha (TNFalpha)

202 known as immunomodulatory drugs derived from thalidomide is developed and sold as racemates because o

203 Thalidomide is effective in patients with myeloma with R

204 Long-term treatment with thalidomide is hampered by neurotoxicity.

205 maintenance after melphalan, prednisone, and thalidomide is not well established.

206 structures of the DDB1-CRBN complex bound to thalidomide, lenalidomide and pomalidomide.

207 The introduction of thalidomide, lenalidomide, and bortezomib has dramatical

208 The data here show that thalidomide, lenalidomide, and pomalidomide affect stem

209 ere insensitive to the inhibitory effects of thalidomide, lenalidomide, and pomalidomide on LPM diffe

210 activities of immunomodulatory drugs such as thalidomide, lenalidomide, and pomalidomide, recognizes

211 ue therapies (high-dose statins, octreotide, thalidomide, lenalidomide, and tamoxifen) were described

212 agents with angiogenic inhibitory capacity (thalidomide, lenalidomide, bevacizumab, sunitinib, soraf

213 the antitumor and teratogenic activities of thalidomide-like drugs are dissociable.

214 Thalidomide-like drugs such as lenalidomide are clinical

215 The thalidomide-like molecules (collectively called the IMiD

216 mb malformations are well established in the thalidomide literature, correlation with associated eye

217 Median PFS was significantly longer with thalidomide maintenance (log-rank P < .001).

218 mide (VMPT) induction followed by bortezomib-thalidomide maintenance (VMPT-VT) with VMP in patients w

219 The role of thalidomide maintenance after melphalan, prednisone, and

220 This trial compared the effect of thalidomide maintenance and no maintenance on progressio

221 a lower incidence of hematologic SPMs in the thalidomide maintenance arm (hazard ratio = 0.38; P = .0

222 n associated with improved survival, whereas thalidomide maintenance has sometimes been associated wi

223 Thalidomide maintenance has the potential to modulate re

224 Thalidomide maintenance significantly improves PFS and c

225 Thalidomide maintenance therapy after autologous stem ce

226 apy compared with conventional induction and thalidomide maintenance treatment.

227 etween nine 4-week cycles of MPT followed by thalidomide maintenance until disease progression or una

228 ed MM patients were randomized to open-label thalidomide maintenance until progression, or no mainten

229 ith clinically significant neuropathy during thalidomide maintenance vs myelosuppression with MPR.

230 Overview analysis demonstrated that thalidomide maintenance was associated with a significan

231 l, was available for 96 patients who started thalidomide maintenance.

232 CQLQ scores significantly improved with thalidomide (mean difference vs. placebo, -11.4 [95% CI,

233 34 months) than single-agent lenalidomide or thalidomide (median, 7 and 13 months, respectively; P =

234 ing autism to exposures in early pregnancy - thalidomide, misoprostol, and valproic acid; maternal ru

235 y and bortezomib plus dexamethasone, and (2) thalidomide monotherapy and thalidomide plus dexamethaso

236 The combination melphalan-prednisone-thalidomide (MPT) is considered a standard therapy for p

237 he combination of melphalan, prednisone, and thalidomide (MPT) is considered standard therapy for new

238 melphalan and prednisone alone (MP) and with thalidomide (MPT).

239 ] E1A06) compared melphalan, prednisone, and thalidomide (MPT-T) with melphalan, prednisone, and lena

240 ore and 48 h after a test dose exposure with thalidomide (n=42), lenalidomide (n=18), or pomalidomide

241 Here, we chronically administrated thalidomide on human APPswedish mutation transgenic (APP

242 SNP associations were related to exposure to thalidomide only or general drug-related peripheral neur

243 ence of a response to induction therapy with thalidomide or lenalidomide predicts a poorer outcome af

244 e potent anti-inflammatory agent than either Thalidomide or Lenalidomide.

245 ted to be clinically more potent than either Thalidomide or Lenalidomide.

246 e more effective and safer than single-agent thalidomide or lenalidomide.

247 duction therapy with a regimen that contains thalidomide or lenalidomide.

248 ngle-agent bortezomib or in combination with thalidomide or prednisone has been studied.

249 igned randomly to either a control group (no thalidomide) or to the experimental group (thalidomide d

250 those who were MRD negative and did receive thalidomide (P < .001).

251 disruption of LPM differentiation by atRA or thalidomide perturbed subsequent chondrogenic differenti

252 dom allocation (1:1) to maintenance therapy (thalidomide plus dexamethasone) or observation.

253 thasone, and (2) thalidomide monotherapy and thalidomide plus dexamethasone.

254 We conclude that maintenance therapy with thalidomide-prednisone after autologous stem cell transp

255 irst disease recurrence was 27.7 months with thalidomide-prednisone and 34.1 months in the observatio

256 p of 4.1 years, no differences in OS between thalidomide-prednisone and observation were detected (re

257 ted a randomized, controlled trial comparing thalidomide-prednisone as maintenance therapy with obser

258 Those allocated to thalidomide-prednisone reported worse HRQoL with respect

259 Nine second malignancies were observed with thalidomide-prednisone versus 6 in the observation group

260 respectively; hazard ratio = 0.77; P = .18); thalidomide-prednisone was associated with superior myel

261 ll types and that patients were treated with thalidomide rather than current therapies.

262 n ENL lesions and showed that treatment with thalidomide reduced its expression and the prominent neu

263 The thalidomide regimen was also associated with superior PF

264 erms of patient baseline characteristics and thalidomide regimens, there was no evidence that treatme

265 dent prognostic marker and as a predictor of thalidomide response.

266 In participants receiving thalidomide, scores from the total SGRQ, SGRQ symptom do

267 mmunomodulatory therapeutic strategies using thalidomide showed consistent efficacy, and should be co

268 Patients with adverse iFISH receiving thalidomide showed no significant PFS benefit and worse

269 Bortezomib and thalidomide significantly improved OS in multiple myelom

270 activation of both astrocytes and microglia, thalidomide significantly reduces Abeta load and plaque

271 ug discontinuation (PMDD) of bortezomib (V), thalidomide (T), and dexamethasone (D) on overall surviv

272 ds to document a novel interaction involving Thalidomide, TBX5, and HAND2.

273 enantiosensor dedicated for determination of thalidomide (TD) enantiomers (especially towards the tox

274 RL4) complex, is a direct protein target for thalidomide teratogenicity and antitumor activity of imm

275 quitin ligase is a plausible major driver of thalidomide teratogenicity.

276 Thalidomide (THD) is an immunomodulatory agent used to t

277 nt of future neuroprotective strategies with thalidomide therapy and the better use of this important

278 Thalidomide therapy was introduced.

279 The addition of thalidomide to chemoradiotherapy increased toxicities bu

280 CONCLUSION The addition of bevacizumab and thalidomide to docetaxel is a highly active combination

281 highly significant benefit to OS from adding thalidomide to MP (hazard ratio = 0.83; 95% confidence i

282 The thalidomide tragedy of the early 1960s resulted in a gre

283 of developing a peripheral neuropathy after thalidomide treatment can be mediated by polymorphisms i

284 Thalidomide treatment reduced PTX3 in the serum 7 days a

285 eding in one of our patients was achieved by thalidomide treatment, exemplifying a successful bed-to-

286 e ectopic expression of wild-type STN1 or by thalidomide treatment.

287 thalidomide) and TT3 (TT3a with bortezomib, thalidomide; TT3b with additional lenalidomide) offered

288 vestigate efficacy by incorporating low-dose thalidomide, using sub-cutaneous weekly bortezomib, and

289 This randomized trial compared VMP plus thalidomide (VMPT) induction followed by bortezomib-thal

290 mparison of maintenance with bortezomib plus thalidomide (VT) or prednisone (VP) in 178 elderly untre

291 The effect of maintenance thalidomide was assessed, with the shortest PFS demonstr

292 Thalidomide was recently shown to bind to, and inhibit,

293 Thalidomide was used by pregnant women for morning sickn

294 Responses to thalidomide were seen within 3-15 weeks, whereas respons

295 Patient 1 required long-term, low-dose thalidomide, whereas patient 2 stopped treatment and sho

296 the tragic toxicological effects of the drug thalidomide, which had been prescribed as a mild sedativ

297 s prospectively antagonized by etanercept or thalidomide, which resolved cytokine, chemokine, and rec

298 al metronomic regimen of daily celecoxib and thalidomide with alternating periods of etoposide and cy

299 from two large clinical trials that compared thalidomide with conventional-based treatment in myeloma

300 ment (including lenalidomide, bortezomib, or thalidomide), with an Eastern Cooperative Oncology Group