ライフサイエンスコーパス: melphalan

1 nt following intravitreous administration of melphalan.

2 s and a higher median and cumulative dose of melphalan.

3 halan and 302 to carboplatin, etoposide, and melphalan.

4 th the DNA cross-linking agents cisplatin or melphalan.

5 atologic toxicity compared with single-agent melphalan.

6 luded a combination of lenalidomide and oral melphalan.

7 th historical controls of single-agent SSOAI melphalan.

8 0%) who received carboplatin, etoposide, and melphalan.

9 muM KZ-41, following treatment with 4 mug/mL melphalan.

10 events than did carboplatin, etoposide, and melphalan.

11 ls to the DNA interstrand cross-linker (ICL) melphalan.

12 consisting of alemtuzumab, fludarabine, and melphalan.

13 in addition to omission of procarbazine and melphalan.

14 related drugs bortezomib, dexamethasone, and melphalan.

15 ho then had a complete response to high-dose melphalan.

16 systemic AL-amyloidosis receiving high-dose melphalan.

17 f the chemotherapeutic drugs doxorubicin and melphalan.

18 an compared with carboplatin, etoposide, and melphalan.

19 least 72 h after carboplatin etoposide, and melphalan.

20 gimen included alemtuzumab, fludarabine, and melphalan.

21 nation of infused gemcitabine, busulfan, and melphalan.

22 g RIC HCT with alemtuzumab, fludarabine, and melphalan.

23 men) underwent a 90-minute hyperthermic ILP (melphalan, 10 to 13 mg/L limb volume, tumor necrosis fac

24 h autologous stem cell transplantation (with melphalan 100 mg/m(2) to 140 mg/m(2)) is feasible in pat

25 Melphalan 100 mg/m(2) was administered intravenously on

26 liposomal doxorubicin-dexamethasone, tandem melphalan (100 mg/m(2)) followed by ASCT (MEL100-ASCT),

27 Half of the patients received reduced-dose melphalan (100-160 mg/m(2)).

28 eceived fludarabine 30 mg/m day (D)-7 to -3, melphalan 140 mg/m D-2, and 2 Gy TBI D-4 and -3.

29 100 mg/m(2) twice daily (days -5 to -2), and melphalan 140 mg/m(2) (day -1; B-BEAM) or rituximab 375

30 f fludarabine 25 mg/m(2) per day for 5 days, melphalan 140 mg/m(2) for one day, and TMLI radiation at

31 nditioned with fludarabine (125 mg/m(2)) and melphalan (140 mg/m(2)) plus thymoglobulin (for mismatch

32 receptor, after myeloablative chemotherapy (melphalan, 140 mg per square meter of body-surface area)

33 hone randomisation line, to either high-dose melphalan 200 mg/m(2) plus salvage ASCT or oral cyclopho

34 Patients with MM received a standard dose of melphalan 200 mg/m(2), with dose reduction for severe ki

35 ne autologous stem cell transplantation with melphalan 200 mg/m2.

36 omisation in a 1:1 ratio to either high-dose melphalan (200 mg/m(2)) and salvage ASCT or weekly oral

37 er fluoroscopic guidance was performed using melphalan (3, 5, or 7.5 mg) in every case, with addition

38 tients with an indication for SSOAI received melphalan (3-6 mg) and topotecan (0.5-1 mg; doses calcul

39 Fifty-five IAC procedures for delivery of melphalan 5 mg and possible carboplatin 30 mg.

40 All patients received melphalan 5 mg, whereas the first 6 patients also were t

41 treated with 3 cycles of SSIOAC using either melphalan (5 mg/30 mL) or carboplatin (30 mg/30 mL).

42 4000 mumol/L per min per day for 4 days) and melphalan (60 mg/m(2) per day for 2 days).

43 usion of 338 mg/m(2) per day for 4 days, and melphalan 70 mg/m(2) per day for 3 days, with doses for

44 a-arterial melphalan treatment, intravitreal melphalan (8 mug in 0.05 mL) was injected using a 32-gau

45 VMP; n = 167; bortezomib as before plus oral melphalan 9 mg/m(2) and oral prednisone 60 mg/m(2), days

46 bstituent connected to the amine nitrogen of melphalan, a large energy penalty has to be paid for sol

47 ersensitivity to the DNA crosslinking agent, melphalan; a characteristic phenotype of FANC J cells.

48 and T-cell depletion experiments showed that melphalan administration in vivo could stimulate a CD8(+

49 is and no rescue therapy within 120 hours of melphalan administration.

50 onditioning (RIC) included fludarabine (Flu)/melphalan/alemtuzumab (n = 20), Flu/busulfan (Bu)/alemtu

51 ogical second primary malignancy risk versus melphalan alone (HR 4.86 [95% CI 2.79-8.46]; p<0.0001).

52 From 1999 to 2007, use of melphalan alone dropped from 32.0% to 4.1%, and vincrist

53 ogical second primary malignancy risk versus melphalan alone.

54 ntly reduced tumor growth up to 30-fold over melphalan alone.

55 han in a concurrent matched cohort receiving melphalan, although this will need to be confirmed in a

56 n 13 (4%) patients who received busulfan and melphalan and 29 (10%) who received carboplatin, etoposi

57 were randomly assigned: 296 to busulfan and melphalan and 302 to carboplatin, etoposide, and melphal

58 atients receiving gemcitabine, busulfan, and melphalan and 34 months (25-53) in the matched control s

59 tivity by cisplatin, BCNU, chlorambucil, and melphalan and also induced endogenous AKR1C (AKR1C refer

60 phalan in patients who received busulfan and melphalan and at least 72 h after carboplatin etoposide,

61 Treatment consisted of high-dose melphalan and autograft followed by 2-Gy total body irra

62 erapy, a proteasome inhibitor, and high-dose melphalan and autologous stem cell transplantation (HDM/

63 We recommend consolidation with high-dose melphalan and autologous stem cell transplantation in th

64 ivation following treatment for myeloma with melphalan and autologous stem cell transplantation.

65 s with AL amyloidosis treated with high-dose melphalan and autologous stem-cell transplantation (HDM/

66 nd dexamethasone (PAD) followed by high-dose melphalan and autologous stem-cell transplantation.

67 s after treatment with the antimyeloma drugs melphalan and bortezomib.

68 Both melphalan and carboplatin triggered human retinal endoth

69 izes these cells to the cross-linking agents melphalan and cisplatin and to the poly(ADP-ribose) poly

70 adiation (IR), and DNA cross-linking agents (melphalan and cisplatin) through unknown mechanisms.

71 trast to our recently published results with melphalan and dexamethasone standard therapy, bortezomib

72 In addition we found cross-resistance to melphalan and doxorubicin in 8226/S-ATOR05, suggesting A

73 DNA cross-links by nitrogen mustards, e.g., melphalan and mechlorethamine.

74 mide, and dexamethasone (CTDa; n = 426) with melphalan and prednisolone (MP; n = 423) in patients wit

75 omide, and dexamethasone (CTD; intensive) or melphalan and prednisolone versus attenuated oral CTD (C

76 ed better responses and lower SRE rates than melphalan and prednisolone.

77 stigated the combination of carfilzomib with melphalan and prednisone (CMP) in patients aged >65 year

78 od, Mateos et al report that bortezomib plus melphalan and prednisone (VMP) and lenalidomide plus low

79 Bortezomib plus melphalan and prednisone (VMP) and lenalidomide plus low

80 trials, launched in or after 2000, compared melphalan and prednisone alone (MP) and with thalidomide

81 induction cycles with bortezomib plus either melphalan and prednisone or thalidomide and prednisone.

82 Melphalan and prednisone were administered orally on day

83 Therapy in Multiple Myeloma: Assessment With Melphalan and Prednisone) was conducted to determine whe

84 ostic value in elderly patients treated with melphalan and prednisone-based chemotherapy.

85 using carmustine, etoposide, cytarabine, and melphalan and received consistent management of peritran

86 d in eyes receiving higher concentrations of melphalan and repetitive injections.

87 andomly assigned to receive either high-dose melphalan and salvage ASCT (n=89) or oral weekly cycloph

88 hain (AL) amyloidosis treated with high-dose melphalan and stem cell transplantation (HDM/SCT) more t

89 models to study isolated limb infusion with melphalan and systemic chemotherapy with temozolomide.

90 There was no effect of the sequence of melphalan and topotecan administration in plasma pharmac

91 A regimen combining melphalan and topotecan for SSOAI treatment of retinobla

92 ecutive patients received 66 cycles of SSOAI melphalan and topotecan in combination.

93 Administration of combined intravitreal melphalan and topotecan in eyes not subsequently enuclea

94 ugs currently used to treat patients such as melphalan and VELCADE efficiently kills malignant plasmo

95 followed by myeloablation (with 200 mg/m2 of melphalan) and haemopoietic stem-cell rescue.

96 oning was with alemtuzumab, fludarabine, and melphalan, and additional graft-versus-host disease (GVH

97 ents received RIC consisting of fludarabine, melphalan, and alemtuzumab.

98 ding bortezomib induction, intermediate-dose melphalan, and autologous stem cell transplantation (ASC

99 frontline therapy with combined bortezomib, melphalan, and dexamethasone independently prolonged tim

100 tion also sensitized MM cells to bortezomib, melphalan, and dexamethasone, but did not downregulate I

101 hthalmic artery chemoreduction, intravitreal melphalan, and focal consolidation are being used and in

102 erential collateral resistance to cisplatin, melphalan, and temozolomide.

103 d response of vitreous seeds to intravitreal melphalan are different for each seed classification.

104 Mechlorethamine and melphalan are used as model systems in order to better u

105 h recent evidence suggesting fludarabine and melphalan as the optimal conditioning regimen.

106 with carmustine, etoposide, cytarabine, and melphalan as well as rabbit antithymocyte globulin befor

107 cular toxicities, we examined the effects of melphalan, as well as carboplatin (another chemotherapeu

108 esistance to dexamethasone, doxorubicin, and melphalan, as well as to bortezomib, and also acted syne

109 n the perfusate, followed 5 minutes later by melphalan at 1.5 mg/kg.

110 SCT in a clinical trial and instead received melphalan at 200 mg/m(2) intravenously over 30 min on 1

111 en-label, randomized, phase 3 study compared melphalan at a dose of 200 mg per square meter of body-s

112 nts who received intravitreous injections of melphalan at Memorial Sloan Kettering Cancer Center from

113 Systemic toxicity with intravitreal melphalan at these doses in humans or rabbits was not de

114 before/after 1995 (introduction of high-dose melphalan/autologous stem cell transplantation [HDM-ASCT

115 oral mucositis in adults receiving high-dose melphalan-based chemotherapy before hematopoietic stem c

116 stem cell transplantation, with busulfan- or melphalan-based conditioning.

117 Patients received a melphalan-based reduced-intensity conditioning regimen a

118 le for S0204 with THAL-DEX induction, tandem melphalan-based tandem transplantation, and THAL-prednis

119 on, before and in consolidation after tandem melphalan-based transplantation; TT3A applied VTD (borte

120 Tandem melphalan-based transplantations have yielded superior r

121 -dose carmustine, cytarabine, etoposide, and melphalan (BEAM) and autologous stem-cell transplantatio

122 n plus melphalan plus thioTEPA (BUMELTT), or melphalan before transplant.

123 is of energy profiles of mechlorethamine and melphalan binding to guanine and adenine are presented t

124 In particular, GDF15 conferred resistance to melphalan, bortezomib, and to a lesser extent, lenalidom

125 d maintenance or received a second high-dose melphalan, but the difference did not translate into a p

126 melphalan or to carboplatin, etoposide, and melphalan by minimisation, balancing age at diagnosis, s

127 endent kinase 1 (PDK1) along with cisplatin, melphalan, camptothecin, or etoposide and assayed for co

128 Melphalan can eliminate the indolent clonal plasma cells

129 Weekly injections of 30 mug of melphalan can result in a decreased ERG response, which

130 al endpoints, the gemcitabine, busulfan, and melphalan cohort had significantly longer median progres

131 Intravitreal administration of melphalan combined with topotecan produced complete cont

132 ter high-dose chemotherapy with busulfan and melphalan compared with carboplatin, etoposide, and melp

133 e deescalation in the context of fludarabine-melphalan conditioning and human leukocyte antigen (HLA)

134 SCT bortezomib induction and of unattenuated melphalan conditioning in 2010-2014 compared with earlie

135 ded 4 Gy TBI to the widely used fludarabine, melphalan conditioning regimen, in hopes of reducing rel

136 In patients who received CY/TBI or melphalan conditioning regimens, those with Gilbert's sy

137 gram responses, and used in conjunction with melphalan-containing OAC, demonstrate excellent patient

138 The remaining infusions were melphalan-containing.

139 dexamethasone (TD) versus vincristine, BCNU, melphalan, cyclophosphamide, prednisone/vincristine, BCN

140 EM2000 [VBMCP/VBAD (vincristine, carmustine, melphalan, cyclophosphamide, prednisone/vincristine, bis

141 Moreover, the enhancement of melphalan cytotoxicity by DSB/R inhibition offers a prom

142 al model, systemic ADH-1 given with regional melphalan demonstrated synergistic antitumor activity, a

143 erapy, 79% of patients in 2005-2009 received melphalan-dexamethasone, and 64% of patients in 2000-200

144 a murine melanoma model is as efficacious as melphalan, displaying antitumor activity at doses corres

145 After 24 h, an intravenous melphalan dose (140 mg/m(2)) was given.

146 er, autologous transplantation with a higher melphalan dose (200 mg per square meter) had induced onl

147 on to therapeutic agents such as bortezomib, melphalan, doxorubicin, and dexamethasone.

148 tion for PIDs using RIC with fludarabine and melphalan (Flu/Melph) and to study the effect of donor t

149 ibling donors (n = 32) receiving fludarabine/melphalan (FluMel) as a preparative regimen and patients

150 e the efficacy and toxicity of intravitreous melphalan for treatment of retinoblastoma, as a single a

151 ergoing multiple intravitreous injections of melphalan for vitreous seeding.

152 ents treated with gemcitabine, busulfan, and melphalan, grade 3 or worse adverse events included grad

153 Nine patients in the busulfan and melphalan group and 11 in the carboplatin, etoposide, an

154 ars, 146 of 296 patients in the busulfan and melphalan group and 188 of 302 in the carboplatin, etopo

155 e patients in the gemcitabine, busulfan, and melphalan group by sex, age, disease status, refractory

156 88 of 302 in the carboplatin, etoposide, and melphalan group had an event; 3-year event-free survival

157 60 (22%) of 267 patients in the busulfan and melphalan group had Bearman grades 1-3 veno-occlusive di

158 up and 11 in the carboplatin, etoposide, and melphalan group had died without relapse by 5 years.

159 14.2-35.0) in the gemcitabine, busulfan, and melphalan group had stringent complete remission compare

160 ndition (74 [26%] of 281 in the busulfan and melphalan group vs 103 [38%] of 270 in the carboplatin,

161 %] of 270 in the carboplatin, etoposide, and melphalan group), infection (55 [19%] of 283 vs 74 [27%]

162 %) of 239 in the carboplatin, etoposide, and melphalan group.

163 ter a long period in which dexamethasone and melphalan had been the standard treatment.

164 oidosis (AL) patients treated with high-dose melphalan (HDM) chemotherapy and autologous stem cell tr

165 High-dose melphalan (HDM) plus stem cell transplantation is an eff

166 Trans-pars plana intravitreal injection of melphalan hydrochloride (40 microg in 0.04 mL of diluent

167 Intravitreous injections of melphalan hydrochloride are increasingly used in the tre

168 -96.6) was observed in patients treated with melphalan hydrochloride.

169 In contrast, caffeine had no effects on melphalan-, hyperosmotic stress-, or IL-1beta-induced ac

170 fusion as a superior treatment compared with melphalan ILP allows for locoregional treatment anywhere

171 INTERPRETATION: Busulfan and melphalan improved event-free survival in children with

172 We report here that melphalan in combination with ADH-1 significantly reduce

173 ations, should be considered instead of oral melphalan in combination with lenalidomide for myeloma.

174 cts triggered by Bortezomib, doxorubicin and melphalan in Mcl-1(wt/wt) and Mcl-1(Delta/null) murine e

175 high-dose chemotherapy, at least 24 h after melphalan in patients who received busulfan and melphala

176 plications for understanding the activity of melphalan in plasma-cell diseases and support further in

177 etinal and systemic toxicity of intravitreal melphalan in retinoblastoma patients, with preclinical v

178 including bortezomib treatment and high-dose melphalan in stem cell transplant.

179 The poor performance of single-agent melphalan in this setting prompted us to study a new hig

180 induction of apoptosis in melanoma cells by melphalan in vitro did not elicit threshold levels of en

181 Melphalan increased monocytic adhesion to human retinal

182 ppears to be the primary pathway involved in melphalan-induced REC apoptosis.

183 KZ-41 protects REC against melphalan-induced upregulation of ICAM-1 and apoptosis t

184 cate that sublethal doses of doxorubicin and melphalan initiate a DNA damage response (DDR) controlli

185 All eyes received intravitreal melphalan injection (20-30 microg) by transconjunctival

186 short-term results suggest that intravitreal melphalan injection for persistent or recurrent vitreous

187 ses, such that on average each intravitreous melphalan injection was associated with a 5.3-muV decrea

188 more than 2 years after the single low-dose melphalan injection.

189 ter a single, standard low-dose intravitreal melphalan injection.

190 ate clinical response to weekly intravitreal melphalan injections and time to regression of vitreous

191 t ocular side effects following intravitreal melphalan injections are uncommon.

192 an dose, and cumulative dose of intravitreal melphalan injections required.

193 Intravitreal melphalan injections should be cautiously used for eyes

194 ERG parameters before and after intravitreal melphalan injections with histopathologic findings.

195 INTERPRETATION: Gemcitabine, busulfan, and melphalan is a comparatively safe and active regimen for

196 Intravitreal melphalan is an alternative to external beam radiation o

197 ion (HCT) with alemtuzumab, fludarabine, and melphalan is an effective approach for patients with non

198 n high doses with stem-cell transplantation, melphalan is an effective but toxic therapy for patients

199 Intra-ophthalmic artery melphalan is an effective treatment for retinoblastoma,

200 Intravitreous melphalan is an effective treatment for vitreous seeding

201 fusion (ILP) with the chemotherapeutic agent melphalan is an effective treatment option for extremity

202 Intravitreal melphalan is emerging as an effective treatment for refr

203 High-dose melphalan is of little benefit as a regimen for patients

204 ium ion is not computed to be preferred when melphalan is used.

205 ed as predictive of response to intravitreal melphalan (IVM) in patients treated predominantly with p

206 serum and performed a Cell Death ELISA after melphalan + KZ-41 treatment to determine if the treatmen

207 Isolated limb infusion (ILI) with melphalan (LPAM) or temozolomide (TMZ) was performed on

208 Melphalan (M), in combination with prednisone (MP), has

209 Isolated limb infusion (ILI) with melphalan (M-ILI) dosing corrected for ideal body weight

210 Intravitreous injection of melphalan may result in toxic effects on the anterior se

211 A sensor for the determination of melphalan (mel) using 3-thiophene acetic acid (3-TAA) as

212 We report that treatment of male mice with melphalan (MLP), a bifunctional alkylating agent widely

213 tioned with 3 different regimens:fludarabine-melphalan (n = 46); total body irradiation-etoposide (n

214 IHP employed Melphalan (n = 69) (CRC = 32, non-CRC = 37), Oxaliplatin

215 ethylnitrosourea, etoposide, cytarabine, and melphalan or cyclophosphamide) and autologous stem cell

216 Proteasome inhibitor bortezomib, but not melphalan or dexamethasone, induced similar effects, ind

217 were randomly assigned (1:1) to busulfan and melphalan or to carboplatin, etoposide, and melphalan by

218 weekly injections of 15 mug of intravitreal melphalan or vehicle to the right eye.

219 Both nongenotoxic (nutlin-3a) and genotoxic (melphalan) p53-inducing stresses increased DR5 expressio

220 t topotecan administration did not influence melphalan pharmacokinetic parameters.

221 The large variability in melphalan pharmacokinetics was explained by body weight

222 long with fluorescein angiography, CBCs, and melphalan plasma concentration.

223 dence for the improved efficacy of high-dose melphalan plus salvage ASCT when compared with cyclophos

224 We aimed to compare high-dose melphalan plus salvage ASCT with cyclophosphamide in pat

225 al cycles of RVD (350 patients) or high-dose melphalan plus stem-cell transplantation followed by two

226 ents 65 years of age or younger to high-dose melphalan plus stem-cell transplantation or MPR consolid

227 val were significantly longer with high-dose melphalan plus stem-cell transplantation than with MPR (

228 Consolidation therapy with high-dose melphalan plus stem-cell transplantation, as compared wi

229 plus cyclophosphamide (BU/CY), busulfan plus melphalan plus thioTEPA (BUMELTT), or melphalan before t

230 Melphalan, plus bortezomib, should be maintained as stan

231 lysis of baseline factors, only reduced-dose melphalan predicted shorter OS.

232 an, prednisone, and thalidomide (MPT-T) with melphalan, prednisone, and lenalidomide (mPR-R) in patie

233 splantation and one study after conventional melphalan, prednisone, and lenalidomide induction therap

234 Melphalan, prednisone, and lenalidomide, followed by len

235 The combination of melphalan, prednisone, and thalidomide (MPT) is consider

236 rative Oncology Group [ECOG] E1A06) compared melphalan, prednisone, and thalidomide (MPT-T) with melp

237 The role of thalidomide maintenance after melphalan, prednisone, and thalidomide is not well estab

238 CAD (cyclophosphamide, lomustine, vindesine, melphalan, prednisone, epidoxorubicin, vincristine, proc

239 h melphalan-prednisone-lenalidomide (MPR) or melphalan-prednisone (MP) followed by placebo in patient

240 bortezomib-melphalan-prednisone (VMP) versus melphalan-prednisone (MP) in patients with myeloma who w

241 Bortezomib-melphalan-prednisone (VMP) has improved overall survival

242 verall survival (OS) benefit with bortezomib-melphalan-prednisone (VMP) versus melphalan-prednisone (

243 idomide 100 mg, days 1 to 21), or bortezomib-melphalan-prednisone (VMP; n = 167; bortezomib as before

244 us autologous stem-cell transplantation with melphalan-prednisone-lenalidomide (MPR) and compared len

245 ntation-ineligible to receive induction with melphalan-prednisone-lenalidomide (MPR) or cyclophospham

246 wed by lenalidomide maintenance (MPR-R) with melphalan-prednisone-lenalidomide (MPR) or melphalan-pre

247 ide and low-dose dexamethasone induction and melphalan-prednisone-lenalidomide consolidation.

248 lind, multicenter, randomized study compared melphalan-prednisone-lenalidomide induction followed by

249 The combination melphalan-prednisone-thalidomide (MPT) is considered a s

250 e, and 64% of patients in 2000-2004 received melphalan-prednisone.

251 The busulfan and melphalan regimen comprised oral busulfan (150 mg/m(2) g

252 The carboplatin, etoposide, and melphalan regimen consisted of carboplatin continuous in

253 and function as underlying events leading to melphalan resistance in repeatedly exposed multiple myel

254 M) cell lines (melphalan-sensitive RPMI8226; melphalan-resistant LR5) and bone marrow plasma cells (B

255 d and causative for drug resistance in human melphalan-resistant multiple myeloma cell lines.

256 tment to determine if the treatments altered melphalan's ability to promote cell death of Y79 cells.

257 d REC apoptosis, whereas KZ-41 did not alter melphalan's effects on Y79 cells.

258 in the therapy of MM (i.e., doxorubicin and melphalan) selectively affect the shedding of MIC molecu

259 aluated in multiple myeloma (MM) cell lines (melphalan-sensitive RPMI8226; melphalan-resistant LR5) a

260 tly reduced the rates of DSB/R and increased melphalan sensitivity of the cells, with the nonhomologo

261 in diminished DNA damage repair and enhanced melphalan sensitivity.

262 Busulfan and melphalan should thus be considered standard high-dose c

263 Exposure to lenalidomide plus oral melphalan significantly increased haematological second

264 historical cohorts of patients treated with melphalan single-agent SSOAI.

265 KZ-41 inhibited melphalan-stimulation of ICAM-1 levels and REC apoptosis

266 oblasts were significantly more sensitive to melphalan than calreticulin knock-out murine embryonic f

267 s significantly more frequent with high-dose melphalan than with MPR (94.3% vs. 51.5%), as were gastr

268 o cycles of intra-arterial chemotherapy with melphalan, the main tumour displayed significant regress

269 dverse vascular toxicities with SSIOAC using melphalan, the most commonly used chemotherapeutic.

270 vage therapy with intravitreous injection of melphalan, the results suggest that the AH can serve as

271 e myeloma (MM) treatments--such as high-dose melphalan therapy plus autologous stem cell transplantat

272 17) or did not respond (n = 9) to subsequent melphalan therapy.

273 Pelvic/systemic ratios of melphalan/TNF/technetium Tc 99m were 14.2/7/3.6.

274 retinoblastoma receiving 630 intravitreous (melphalan, topotecan) or topotecan periocular injections

275 wave amplitude declined significantly in the melphalan treated eyes compared with vehicle-treated eye

276 vated protein kinase] MAPK inhibitor) before melphalan treatment to determine the involvement of NF-k

277 nd the inadequate response to intra-arterial melphalan treatment, intravitreal melphalan (8 mug in 0.

278 patients into the gemcitabine, busulfan, and melphalan trial.

279 Our results illustrate how melphalan triggers inflammatory cell death that can be l

280 show that Bortezomib, but not doxorubicin or melphalan, triggers Mcl-1 cleavage in Mcl-1(wt/wt), but

281 and promotes tumor resistance to alkylators (melphalan), tubulin disrupting agents (paclitaxel), DNA

282 predicted chemosensitivity to bortezomib and melphalan, two clinical multiple myeloma treatments, in

283 er locoregionally applied therapies, such as melphalan, used in limb perfusion for melanoma (Mel-ILP)

284 We assessed use of common chemotherapies (melphalan, vincristine, and doxorubicin), novel agents (

285 d overall survival at 6 years from high-dose melphalan was 55%, irrespective of having a donor (P = .

286 Oral melphalan was administered in escalating doses from 0.02

287 ADH-1 enhancement of response to melphalan was associated with increased formation of DNA

288 However, in this study, each injection of melphalan was associated, on average, with a decrement i

289 Intra-ophthalmic artery melphalan was offered to patients who had failed to resp

290 nts using 5FU + Oxaliplatin, Oxaliplatin, or Melphalan were 83.3%, 66.7%, and 60.9%, respectively.

291 in 2007 to 2012 and use of higher dosages of melphalan were associated with a lowered relapse risk.

292 ensitizers, genes that also sensitized MM to melphalan were excluded.

293 Doses of busulfan and melphalan were modified according to bodyweight.

294 ns and a lower median and cumulative dose of melphalan, whereas eyes with clouds received significant

295 lized lone pair on the amine nitrogen of the melphalan, which makes the subsequent cyclization more d

296 s obtained during intravitreous injection of melphalan, which matched the tumor sample postsecondary

297 at ASCT receiving gemcitabine, busulfan, and melphalan who achieved stringent complete remission in a

298 All patients were to receive high-dose melphalan with autologous stem cell support followed by

299 Overall, combination fludarabine-melphalan with low-dose TBI after haplocord stem cell tr

300 loid leukemia patients receiving fludarabine-melphalan without TBI.