ライフサイエンスコーパス: melphalan

1 an compared with carboplatin, etoposide, and melphalan.

2 least 72 h after carboplatin etoposide, and melphalan.

3 gimen included alemtuzumab, fludarabine, and melphalan.

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

5 nt following intravitreous administration of melphalan.

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

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

8 atologic toxicity compared with single-agent melphalan.

9 luded a combination of lenalidomide and oral melphalan.

10 th historical controls of single-agent SSOAI melphalan.

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

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

13 consisting of alemtuzumab, fludarabine, and melphalan.

14 in addition to omission of procarbazine and melphalan.

15 us SCT after carmustine-etoposide-cytarabine-melphalan.

16 nation of infused gemcitabine, busulfan, and melphalan.

17 a mutational signature caused by exposure to melphalan.

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

19 0%) who received carboplatin, etoposide, and melphalan.

20 events than did carboplatin, etoposide, and melphalan.

21 Using up-front triple therapy (e.g., melphalan 0.4 mg/kg, carboplatin 50 mg, and topotecan 2

22 adiation (30-40 Gy) in 6 eyes, intravitreous melphalan (10-20 mug) in 4 eyes, enucleation of 1 eye, a

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

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

25 owing conditioning regimens: (1) fludarabine+melphalan 100 mg/m2 (FM100), (2) fludarabine+melphalan 1

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

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

28 100 mg/m(2) twice daily (days -5 to -2), and melphalan 140 mg/m(2) (day -1; B-BEAM) or rituximab 375

29 melphalan 100 mg/m2 (FM100), (2) fludarabine+melphalan 140 mg/m2 (FM140), (3) fludarabine+IV busulfan

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

31 Single-cycle melphalan 200 mg/m(2) and autologous hematopoietic cell

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

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

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

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

36 care induction therapy followed by high-dose melphalan (200 mg/m(2)) conditioning and single ASCT wit

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

41 4000 mumol/L per min per day for 4 days) and melphalan (60 mg/m(2) per day for 2 days).

42 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

43 nder the curve (AUC) of 5000 mmol-minute and melphalan 70 mg/m(2) per day on days -2 and -1 (total me

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 22, and 29 of cycles two through nine), oral melphalan (9 mg/m(2) once daily on days 1 through 4 of e

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

48 It also resulted in increased chemotherapy (melphalan) activity, as measured by formation of DNA add

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

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

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

52 versus 43.5 months (19.9-not estimated) with melphalan alone (hazard ratio 0.53 [95% CI 0.30-0.91]; p

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

54 Melphalan alone (MA) was used to treat 44 patients and 5

55 an resulted in superior outcomes compared to melphalan alone (median time to event 40.0 vs 25.0 days,

56 melphalan and 95 (97%) of 98 patients given melphalan alone achieved partial response or better.

57 t that busulfan plus melphalan could replace melphalan alone as the conditioning regimen for auto-HCT

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

59 -47.1) and 20.2 months (IQR 8.8-46.6) in the melphalan alone group.

60 group versus 14 (14%) of 98 patients in the melphalan alone group.

61 plus melphalan group and 98 patients in the melphalan alone group.

62 nger progression-free survival compared with melphalan alone in patients with multiple myeloma underg

63 conditioning of busulfan plus melphalan with melphalan alone in patients with multiple myeloma.

64 ogical second primary malignancy risk versus melphalan alone.

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

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

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

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

69 02 (98%) of 104 patients given busulfan plus melphalan and 95 (97%) of 98 patients given melphalan al

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

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

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

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

74 Both melphalan and carboplatin triggered human retinal endoth

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

76 Oral melphalan and dexamethasone (MDex) were considered a sta

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

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

79 conditioned with IV busulfan + melphalan vs melphalan and posttransplant consolidation with 2 cycles

80 risk of VTE compared with those treated with melphalan and prednisolone (MP) (16.0% [n = 68 of 425] v

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

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

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

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

85 Melphalan and prednisone were administered orally on day

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

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

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

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

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

91 ority of the patients had received high-dose melphalan and stem cell transplantation and/or treatment

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

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

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

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

96 (18)F-FDG PET/MRI before and after ILP with melphalan and tumor necrosis factor-alpha.

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

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 daratumumab in combination with bortezomib, melphalan, and prednisone (D-VMP) versus bortezomib, mel

103 n, and prednisone (D-VMP) versus bortezomib, melphalan, and prednisone (VMP) alone in patients with t

104 External beam radiation, intravitreous melphalan, and systemic checkpoint inhibition can be use

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

106 aft-versus-host disease; use of fludarabine, melphalan, and thiotepa; and receiving no pre-transplant

107 ing BEAM (carmustine, etoposide, cytarabine, melphalan)+antithymocyte globulin chemotherapeutic regim

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

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

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

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

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

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

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

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

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

117 cifically, patients who received fludarabine/melphalan-based reduced-intensity regimens were more lik

118 uding myeloablative regimens and higher dose melphalan-based reduced-intensity regimens.

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

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

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

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

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

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

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

126 Intravitreal administration of melphalan combined with topotecan produced complete cont

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

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

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

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

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

132 The remaining infusions were melphalan-containing.

133 ongoing studies, suggest that busulfan plus melphalan could replace melphalan alone as the condition

134 that conditioning therapy with busulfan plus melphalan could result in longer progression-free surviv

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

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

137 is case series, the addition of topotecan to melphalan did not alter the IAC side effect profile and

138 Importantly, dynamic control plus melphalan did not result in increased adverse events.

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

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

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

142 70 mg/m(2) per day on days -2 and -1 (total melphalan dose 140 mg/m(2)), or a melphalan dose of 200

143 -1 (total melphalan dose 140 mg/m(2)), or a melphalan dose of 200 mg/m(2) on day -2.

144 ed-intensity conditioning regimen with lower melphalan doses (FM100), which was associated with bette

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

146 Melphalan flufenamide (melflufen) is a first-in-class pe

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

148 multiple myeloma and treated with high-dose melphalan followed by autoSCT.

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

150 ergoing multiple intravitreous injections of melphalan for vitreous seeding.

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

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

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

154 treatment: 104 patients in the busulfan plus melphalan group and 98 patients in the melphalan alone g

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 7 (74%) of 104 patients in the busulfan plus melphalan group versus 14 (14%) of 98 patients in the me

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

162 The median follow-up in the busulfan plus melphalan group was 22.6 months (IQR 15.2-47.1) and 20.2

163 %] of 270 in the carboplatin, etoposide, and melphalan group), infection (55 [19%] of 283 vs 74 [27%]

164 %) of 239 in the carboplatin, etoposide, and melphalan group.

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

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

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

168 conducted to evaluate the effect of busulfan-melphalan high-dose chemotherapy with autologous stem-ce

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

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

171 -96.6) was observed in patients treated with melphalan hydrochloride.

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

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

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

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

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

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

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

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

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

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

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

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

184 is-free at a 5-year follow-up since the last melphalan injection (25-month follow-up after the combin

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

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

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

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

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

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

191 with combined intracameral and intravitreal melphalan injections given according to the previously d

192 .1 mug) and intravitreal (total dose 70 mug) melphalan injections given every 7-10 days.

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

194 Intravitreal melphalan injections should be cautiously used for eyes

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

196 mall number of intracameral and intravitreal melphalan injections.

197 here the successful management by PPV under melphalan irrigation of 2 children presenting with tract

198 PPV under melphalan irrigation, with retinectomy, if necessary, an

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

200 Intravitreal melphalan is an alternative to external beam radiation o

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

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

203 Intravitreous melphalan is an effective treatment for vitreous seeding

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

205 Intravitreal melphalan is emerging as an effective treatment for refr

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

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

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

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

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

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

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

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

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

215 Eyes were treated via IAC with either melphalan monotherapy or melphalan plus topotecan.

216 llowed by dose-reduced carboplatin/etoposide/melphalan (n = 176) or single transplant with carboplati

217 single transplant with carboplatin/etoposide/melphalan (n = 179).

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

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

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

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

222 es, with percutaneous hepatic perfusion with melphalan or with tebentafusp.

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

224 t topotecan administration did not influence melphalan pharmacokinetic parameters.

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

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

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

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

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

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

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

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

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

234 The combination of melphalan plus topotecan (MPT) was used to treat 149 pat

235 via IAC with either melphalan monotherapy or melphalan plus topotecan.

236 Treatment regimen (melphalan vs. combined melphalan plus topotecan; P < 0.05), catheterization rou

237 Melphalan, plus bortezomib, should be maintained as stan

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

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

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

241 Melphalan, prednisone, and lenalidomide, followed by len

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 The combination of dynamic control and melphalan resulted in superior outcomes compared to melp

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

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

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

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

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

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

266 Exposure to lenalidomide plus oral melphalan significantly increased haematological second

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

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

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

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

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

272 loma cell following treatment with high-dose melphalan therapy and autologous stem cell transplant.

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

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

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

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

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

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

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

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

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

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

283 vs. continuous), or concomitant intravitreal melphalan use.

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

285 s 64.7 months (32.9-64.7) with busulfan plus melphalan versus 43.5 months (19.9-not estimated) with m

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

287 splant (ASCT) conditioned with IV busulfan + melphalan vs melphalan and posttransplant consolidation

288 Treatment regimen (melphalan vs. combined melphalan plus topotecan; P < 0.0

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

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

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

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

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

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

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

298 survival with conditioning of busulfan plus melphalan with melphalan alone in patients with multiple

299 Patients received either busulfan plus melphalan, with a test dose of busulfan 32 mg/m(2) follo

300 loid leukemia patients receiving fludarabine-melphalan without TBI.