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 ultiple myeloma (MM) previously treated with thalidomide.

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

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

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

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

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

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

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

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

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

23 Intended therapy consisted of daily thalidomide (200 mg for 2 weeks, then 400 mg for 50 week

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

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

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

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

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

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

30 45 mg/m(2), or 56 mg/m(2), respectively, and thalidomide 50 mg.

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

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

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

34 Thalidomide, a drug used for the treatment of multiple m

35 Lenalidomide and thalidomide abrogated this stimulatory effect of BMSCs a

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

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

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

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

40 Thalidomide also significantly improved scores on the vi

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

42 Thalidomide, an effective treatment for ENL, inhibited t

43 The administration of thalidomide, an immunomodulatory drug with antiangiogeni

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

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

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

47 recently identified class of redox-reactive thalidomide analogs that show selective killing of leuke

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

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

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

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

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

56 agents, and anthracyclines) or novel (e.g., thalidomide and bortezomib) anti-MM agents.

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

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

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

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

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

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

63 Thalidomide and its analog, Lenalidomide, are in current

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

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

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

67 Thalidomide and its derivatives lenalidomide and pomalid

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

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

70 Thalidomide and lenalidomide are immunomodulatory drugs

71 Thalidomide and lenalidomide can alleviate anemia in mye

72 Thalidomide and lenalidomide constitute an important par

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

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

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

76 reported that immunomodulatory drugs (e.g., thalidomide and lenalidomide), which are active against

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 Thalidomide and minocycline have profound immunomodulato

82 the framework for considering the effect of thalidomide and other forms of phocomelia, suggesting th

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

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

85 ravenous docetaxel and bevacizumab plus oral thalidomide and prednisone.

86 Thalidomide and related drugs are key drugs for the trea

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

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

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

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

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

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

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

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

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

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

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

98 , 75%, and 6% had received prior bortezomib, thalidomide, and lenalidomide, respectively.

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

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

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

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

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

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

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

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

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

108 osphamide, nucleoside analog, bortezomib, or thalidomide-based regimens can be considered for the fir

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

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

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

112 Thalidomide binds readily to TBX5 through amino acids R8

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

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

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

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

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

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

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

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

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

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

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

124 Thalidomide-containing regimens had better efficacy than

125 Thalidomide could be considered as a therapeutic option

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

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

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

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

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

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

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

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

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

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

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

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

138 1, 2, 4, and 5 [cycles 5 to 8]), bortezomib-thalidomide-dexamethasone (VTD; n = 167; bortezomib and

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

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

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

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

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

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

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

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

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

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

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

150 Prior thalidomide did not affect survival in lenalidomide + de

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

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

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

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

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

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

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

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

159 Of 704 patients, 39% were thalidomide exposed.

160 , ORR was higher in thalidomide-naive versus thalidomide-exposed patients (P = .04), with longer medi

161 Thalidomide-naive and thalidomide-exposed patients had similar toxicities.

162 lacebo + dexamethasone, independent of prior thalidomide exposure.

163 versus placebo + dexamethasone despite prior thalidomide exposure.

164 ents enrolled in the first clinical trial of thalidomide for advanced or refractory myeloma are updat

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

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

167 The role of thalidomide for previously untreated elderly patients wi

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

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

170 , patients with nonsquamous histology in the thalidomide group had a poorer survival: 2-year risk dif

171 The thalidomide group included significantly more untreated

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

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

174 thrombotic event was increased by 74% in the thalidomide group: HR of 1.74 (95% CI, 1.20 to 2.52; P =

175 This demonstrated that thalidomide had a teratogenic effect between approximate

176 However, whether thalidomide has any therapeutic effects on neurodegenera

177 Lower doses of thalidomide (ie, <or= 200 mg/day) should be considered g

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 Thalidomide in combination with rituximab is active and

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

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

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

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

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

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

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

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

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 Most importantly, thalidomide-induced limb deformities and microphthalmia

194 Thalidomide-induced limb truncations result from increas

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

196 Similarly, thalidomide inhibited the TBX5/HAND2 physical interactio

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

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

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

200 Thalidomide is a tumor necrosis factor alpha (TNFalpha)

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

202 Thalidomide is effective in patients with myeloma with R

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

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

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

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

207 ith the introduction of novel agents such as thalidomide, lenalidomide, and bortezomib, leading to im

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

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

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

211 Thalidomide-like drugs such as lenalidomide are clinical

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

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

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

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

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

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

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

219 Thalidomide maintenance has the potential to modulate re

220 Thalidomide maintenance significantly improves PFS and c

221 Thalidomide maintenance therapy after autologous stem ce

222 apy compared with conventional induction and thalidomide maintenance treatment.

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

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

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

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

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

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

229 34 months) than single-agent lenalidomide or thalidomide (median, 7 and 13 months, respectively; P =

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

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

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

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

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

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

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

237 Thalidomide-naive and thalidomide-exposed patients had s

238 ethasone-treated patients, ORR was higher in thalidomide-naive versus thalidomide-exposed patients (P

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

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

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

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

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

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

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

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

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

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

249 ears after initiation of therapy in favor of thalidomide (P = .09), reaching statistical significance

250 lidomide plus dexamethasone (len/dex) versus thalidomide plus dexamethasone (thal/dex) as initial the

251 The long-term impact of thalidomide plus dexamethasone (thal/dex) as primary the

252 The goal of this study was to compare thalidomide plus dexamethasone versus placebo plus dexam

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

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

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

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

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

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

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

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

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

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

263 of lenalidomide-refractory patients, 37% of thalidomide-refractory patients, and 60% of bortezomib-r

264 The thalidomide regimen was also associated with superior PF

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

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

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

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

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

270 Bortezomib and thalidomide significantly improved OS in multiple myelom

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

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

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

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

275 in 76 eligible patients with SMM, combining thalidomide (THAL, 200 mg/d) with monthly pamidronate.

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 QoL scores were similar but thalidomide was associated with less insomnia, and more

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

294 Thalidomide was used by pregnant women for morning sickn

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

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

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

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