ライフサイエンスコーパス: BCNU

1 BCNU (40 mg/m2/d) and cisplatin (40 mg/m2/d) were admini

2 BCNU and XRT together were effective against all four tu

3 BCNU blood levels were obtained before and after polymer

4 BCNU polymer alone significantly prolonged survival in m

5 BCNU sensitivity remained unchanged as well.

6 py (probability of survival: 6-BG/BCNU, 1.0; BCNU alone, >0.70; no treatment, <0.1).

7 polymers with 6.5%, 10%, 14.5%, 20%, and 28% BCNU by weight.

8 ed from infected cells were resistant to 6BG/BCNU or 6BG/TMZ.

9 G (50 mg/kg) 2 h prior to BCNU polymer (3.8% BCNU by weight) implantation had significantly improved

10 arcoma) and then randomly assigned to arm A (BCNU plus SRT), arm B (BCNU plus ART), arm C (cisplatin

11 In vivo, AdMnSOD, BCNU, and Adriamycin or ionizing radiation inhibited tum

12 After BCNU or BG + BCNU, xenografts growing from inoculums con

13 tment with MGMT transgenic C57BL/6 BMT after BCNU treatment, demonstrating full reconstitution and do

14 ce and benefit from enhanced chimerism after BCNU with less cell infiltrate and no chronic rejection

15 he MGMT gene and response and survival after BCNU.

16 nd sensitivity to the chemotherapeutic agent BCNU.

17 GMT-transduced cells survived in vivo BG and BCNU administration, only 3 of 13 mice transplanted with

18 mice were given a nonablative dose of BG and BCNU before infusion.

19 ress toward G2/M after treatment with BG and BCNU between cells expressing wild-type MGMT and mutated

20 row cells selectively survive in vivo BG and BCNU exposure, resulting in prolonged enrichment for the

21 therapy and that the combination of 6-BG and BCNU leads to uniform selection of transduced stem cells

22 acZ-transduced cells and treated with BG and BCNU or from mice transplanted with deltaMGMT-transduced

23 Thus, BG and BCNU stem cell toxicity allows triangle upMGMT-transduce

24 on were more resistant to combination BG and BCNU than CFU-C from mice transplanted with lacZ-transdu

25 more resistant to the combination of BG and BCNU than the parental cells or cells transduced with wi

26 duced cells were subjected to in vivo BG and BCNU treatment to examine the ability to enrich for tran

27 ansduced hematopoietic progenitors to BG and BCNU was much greater than we observed previously with w

28 After one cycle of BG and BCNU, deltaAGT expression was observed in 60% of bone ma

29 After 2 to 3 cycles of BG and BCNU, many mice were stably reconstituted with 75% to 10

30 After BG and BCNU, triangle upMGMT(+) CFU were frequently detected, a

31 CFU-C obtained from BG and BCNU-treated deltaMGMT animals up to 23 weeks after tran

32 dministration of O(6)-benzylguanine (BG) and BCNU every 3 to 4 weeks.

33 r treatment with O(6)-benzylguanine (BG) and BCNU.

34 r GSH level by treatment with BSO, CDNB, and BCNU resulted in a minimum change in TTase expression.

35 However, the synergy of MET depletion and BCNU observed with D-54 tumors, which do not express mea

36 n sequential administration of radiation and BCNU was abrogated.

37 Both buthionine sulfoximine and BCNU inhibited the induction of iNOS mRNA, as detected b

38 TAGT cells are resistant to temozolomide and BCNU, and treatment with BG resulted in a significantly

39 The combination of thalidomide and BCNU was well tolerated; mild myelosuppression and mild

40 xhibited the expected sensitivity to TMZ and BCNU and marked potentiation of cytotoxicity by O6-bG.

41 were also made with a co-loading of TMZ and BCNU.

42 y and SWB77 to DNA alkylating agents such as BCNU and TMZ could be attributed to the down-regulation

43 ents forming O6-alkylguanine adducts such as BCNU might be enhanced.

44 re BCNU than standard commercially available BCNU polymers and results in minimal systemic BCNU expos

45 ly assigned to arm A (BCNU plus SRT), arm B (BCNU plus ART), arm C (cisplatin plus BCNU plus SRT), or

46 rabine-based regimens and 10% with the BEAM (BCNU, etoposide, cytosine arabinoside, melphalan) protoc

47 When given i.p. 1 h before BCNU (25 mg/m2) to animals bearing s.c. tumors, dBG (134

48 After BCNU or BG + BCNU, xenografts growing from inoculums containing as lo

49 SW480 cells, treated with three cycles of BG+BCNU, maintained wt AGT and the sensitivity to BG-potent

50 CT15 (hMSH6 mutant)] with three cycles of BG+BCNU.

51 are no examples of acquired resistance to BG+BCNU in the clinical setting.

52 5) was mutated because of the exposure to BG+BCNU in these two MMR-deficient cell lines.

53 oteins were responsible for resistance to BG+BCNU, we transfected K165E and K165N MGMT cDNAs into Chi

54 chemotherapy (probability of survival: 6-BG/BCNU, 1.0; BCNU alone, >0.70; no treatment, <0.1).

55 cells; BCNU only, 51% transduced cells; 6-BG/BCNU, 93% transduced cells).

56 ed cells, animals receiving marrow from 6-BG/BCNU-treated animals reconstituted with 94% transduced c

57 entivirus-transduced human SRCs following BG/BCNU treatment.

58 a lentiviral vector and infused them into BG/BCNU-conditioned NOD/SCID mice before rounds of BG/BCNU

59 ine/1,3-bis(2-chloroethyl)-1-nitrosourea (BG/BCNU) treatment has been devised.

60 onditioned NOD/SCID mice before rounds of BG/BCNU treatment as a model for in vivo selection.

61 as not observed until the second round of BG/BCNU treatment, at which time human cells emerged to com

62 amide, cisplatin, bischloroethylnitrosourea [BCNU]) chemotherapy (SDC) or to high-dose CPB chemothera

63 oma cells resistant to cell death induced by BCNU and cisplatin.

64 ated that the DNA damage response induced by BCNU was independent of the MMR apparatus.

65 st in response to the DNA damages induced by BCNU.

66 zylfolate as an adjuvant for cell killing by BCNU appears to be a function of a cell's alpha-folate r

67 m led to much more efficient cell killing by BCNU as a result of the liberation of the more potent in

68 f AGT activity and enhancement of killing by BCNU in response to the more potent AGT inhibitor, 2,4-d

69 hematopoietic cells against cell killing by BCNU, TMZ, and MMS, which is consistent with the possibi

70 dose of 100 mg/m(2) followed 1 hour later by BCNU.

71 Following mutation of C908S, BCNU-induced eNOS uncoupling and BH4 oxidation are aboli

72 LD(50) for DNA-alkylating agent carmustine (BCNU), which is commonly used to treat glioma in clinic.

73 e combination of thalidomide and carmustine (BCNU) in patients with recurrent high-grade gliomas.

74 (CDDP), dacarbazine (DTIC), and carmustine (BCNU) significantly increased the progression-free survi

75 cyclophosphamide, cisplatin, and carmustine (BCNU) with AHPCS.

76 cyclophosphamide, cisplatin, and carmustine (BCNU) with PBPC support.

77 ts), or thiotepa, etoposide, and carmustine (BCNU; one patient).

78 lkylguanine DNA adducts, such as carmustine (BCNU), temozolomide, streptozotocin, and dacarbazine.

79 I) (67 patients) or an augmented carmustine (BCNU), cyclophosphamide, and etoposide (BCV) preparative

80 heath fiber loaded with the drug carmustine (BCNU) was evaluated in an in vivo brain tumor model.

81 cyclophosphamide (6,000 mg/m2), carmustine (BCNU; 450 mg/m2), and thiotepa (720 mg/m2) (CBT regimen)

82 We conducted a phase I trial of carmustine (BCNU) plus O(6)-BG to define the toxicity and maximum-to

83 We conducted a phase II trial of carmustine (BCNU) plus the O(6)-alkylguanine-DNA alkyltransferase in

84 maximum-tolerated dose (MTD) of carmustine (BCNU) that can be implanted in biodegradable polymers fo

85 Local delivery of carmustine (BCNU) via biodegradable polymers prolongs survival again

86 ls exposed to sublethal doses of carmustine (BCNU), a classic alkylating chemotherapeutic agent used

87 The combination of carmustine (BCNU), dacarbazine (DTIC), cisplatin (DDP), and tamoxife

88 determine whether cisplatin plus carmustine (BCNU) administered before and concurrently with radiatio

89 as correlated with resistance to carmustine (BCNU) chemotherapy.

90 ents following chemotherapy with carmustine (BCNU), etoposide, cytarabine, and melphalan (BEAM protoc

91 ients treated with chemotherapy [carmustine [BCNU], vincristine, flourouracil, and streptozocin [BOF-

92 reatment, approximately 6% transduced cells; BCNU only, 51% transduced cells; 6-BG/BCNU, 93% transduc

93 n animals given carboplatinum, chlorambucil, BCNU, and TBI, but not in animals treated with cyclophos

94 ration in animals treated with chlorambucil, BCNU, or TBI.

95 ing (streptozotocin) and 2-chloroethylating (BCNU and CCNU) chemotherapeutic genotoxic agents.

96 ARE-driven luciferase activity by cisplatin, BCNU, chlorambucil, and melphalan and also induced endog

97 s RT (arms A and B) compared with cisplatin, BCNU, and RT (arms C and D) were 10.1 v 11.5 months, res

98 ose chemotherapy (cyclophosphamide/cisplatin/BCNU) and autologous bone marrow transplant (HDC/ABMT) f

99 (1/2) NaCl on days 1 to 3 of a 3-week cycle; BCNU 150 mg/m(2) IV for 2 to 3 hours in 750 to 1,000 mL

100 1210 variants resistant to cyclophosphamide, BCNU, or melphalan.

101 exate 3 g/m(2) D1; D15, VP16 100 mg/m(2) D2, BCNU 100 mg/m(2) D3, prednisone 60 mg/kg/d D1-D5) follow

102 ity to less than 1.5% of baseline, and dBG + BCNU induced extensive perivascular apoptosis.

103 The combination of dBG + BCNU also increased the survival of animals bearing intr

104 n eNOS uncoupling induced by BH4 deficiency, BCNU exposure further exacerbates superoxide production,

105 iate the effects of interstitially delivered BCNU and, for tumors expressing significant AGT, may be

106 eeded to establish the efficacy of high-dose BCNU polymers.

107 duct formed by an important anticancer drug, BCNU, whereby an initial oxidation would occur at the ca

108 Further, the DNA cross-linking drugs BCNU and cisplatin, but not the microtubule poison vincr

109 ant melanoma were treated with CDDP + DTIC + BCNU (CDB) with or without TAM.

110 AGT activity but increased IC(50) for either BCNU or temozolomide (TMZ), compared with parental CHO c

111 according to protocols that included either BCNU or PCV adjuvant chemotherapy.

112 t significantly lower the toxicity of either BCNU or TMZ for the host.

113 arrest at 24 h after treatments with either BCNU alone or BG combined with BCNU.

114 specifically and directly protected DNA from BCNU treatment.

115 e 4, which has been previously isolated from BCNU-treated DNA, derives from alkylation on opposite st

116 rformance status (KPS), and treatment group (BCNU v PCV).

117 e other hand, radiation was found to inhibit BCNU-induced apoptosis through EGFR-mediated activation

118 posure with increasing doses of interstitial BCNU.

119 O6-benzylguanine (BG), an inhibitor of a key BCNU resistance protein, O6-alkylguanine DNA alkyltransf

120 ethyl)-1-nitrosourea (BCNU) or with 40 mg/kg BCNU alone.

121 latinum (50 mg/kg), chlorambucil (12 mg/kg), BCNU (13.2 mg/kg), or TBI (80 cGy).

122 rated significant damage 3 mo after the last BCNU dose in control animals.

123 Maximum BCNU plasma concentrations with the 20% loaded polymers

124 DNA-cross-linking agents such as melphalan, BCNU, and cisplatin.

125 nt time before being treated with melphalan, BCNU, or cisplatin for 1 h to determine clonogenic survi

126 yltransferase (MGMT), results in only modest BCNU resistance.

127 This polymer provides five times more BCNU than standard commercially available BCNU polymers

128 ure to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) alone; however, 70-80% of cells were arrested in G

129 w-dose 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and a second group receiving two cycles at the sam

130 agents 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and cis-diamminedichloroplatinum (cisplatin), in a

131 ion by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) at the O(6) position of guanine.

132 on and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) chemotherapy in three primary human glioblastoma c

133 ntiate 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) in a MGMT-positive human brain tumor xenograft, Da

134 e plus 1,3-bis(2 chloroethyl)-1-nitrosourea (BCNU) increased intracellular GSSG and decreased GSH and

135 acy of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) is being tested in clinical trials.

136 ylator 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) is cytotoxic primarily by inducing DNA monoadducts

137 either 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) or glutathione reductase-specific siRNA, results i

138 mg/kg 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) or with 40 mg/kg BCNU alone.

139 using 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) resulted in similar increases in gene marking leve

140 ng by 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) than overexpression of nucl-MGMT.

141 mine and 1,3-bis(chloroethyl)-1-nitrosourea (BCNU) to inhibit glutathione.

142 ) plus 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) would lead to an increased level of intracellular

143 cts of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a CNU commonly used for chemotherapy.

144 cts of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a commonly used CNU, on long term recovery of the

145 s from 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a stem cell toxin, and O6-benzylguanine (BG), an

146 de and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), and no further sensitization occurs in the presen

147 zymes (1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), arsenite, and phenylarsine oxide) support this co

148 agents 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), carboplatin, and camptothecin were incorporated i

149 grity (1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), cisplatin, H(2)O(2) and UV rays) enhanced the exp

150 n with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), the prodrugs were not effective adjuvants for HT2

151 agent 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), with and without AGT inhibition by 06-bG in sever

152 ); or 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU).

153 ourea, 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).

154 e CENU 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).

155 n, and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).

156 ive to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).

157 ing by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).

158 stine [1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU)] weakly induced luciferase activity in AREc32 cell

159 croM) or 1,3-bis(chloroethyl)-1-nitrosourea (BCNU, 100 microM), resulted in increased levels of ubiqu

160 agent 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU, Carmustine) into biodegradable polymer poly(lactic

161 rval in which bis(2-chloroethyl)nitrosourea (BCNU)-induced chloroethyl adducts are fully converted in

162 r agents 1,3-bis(2-chloroethyl)-nitrosourea (BCNU) and temozolomide were studied.

163 lowed by N,N-bis(2-chloroethyl)-nitrosourea (BCNU) treatment to enhance donor-cell engraftment and th

164 tion of N,N'-bis(2-chloroethyl)-nitrosourea (BCNU) were investigated using synthetic oligonucleotides

165 icity of 1,3-bis(2-chloroethyl)-nitrosourea (BCNU).

166 : vincristine, bis-chloro-ethyl nitrosourea (BCNU) melphalan, cyclophosphamide, and prednisone (VBMCP

167 2) of N,N'-bis(2-chloroethyl)-N-nitrosourea (BCNU), which was otherwise ineffective as a single thera

168 g by N,N'-bis (2-chloroethyl)-N-nitrosourea (BCNU).

169 stine [1,3-bis(2-chloroethyl)-1-nitrosourea; BCNU], lomustine [1-(2-chloroethyl)-3-cyclohexyl-1-nitro

170 skin grafts of BCNU treated mice compared no BCNU treated mice.

171 Combining the use of O6BG/BCNU with gene transfer of MGMT P140K into hematopoietic

172 /m(2) followed 1 hour later by 40 mg/m(2) of BCNU, with cycles repeated at 6-week intervals.

173 te that O6-BG can potentiate the activity of BCNU delivered intracranially via polymers in rats chall

174 agents or DTIC plus DDP, and the addition of BCNU and Tam appears to increase toxicity.

175 bsequent to an initially successful cycle of BCNU therapy, leading to minimal gains from a second cyc

176 resistant to BG-potentiated cytotoxicity of BCNU.

177 ferritin siRNA reduced the effective dose of BCNU needed for tumor suppression by more than 50%.

178 d to determine the maximal-tolerated dose of BCNU.

179 tients were treated with escalating doses of BCNU, and patients were observed for at least 6 weeks be

180 ls were exposed to low and moderate doses of BCNU, and the effects on this DNA damage signaling pathw

181 cells were treated with five weekly doses of BCNU.

182 dies, BG potentiated the cytotoxic effect of BCNU in tumors but increased toxicity to normal CD34 cel

183 When the overall effects of BCNU alone or with O6-BeG pretreatment were compared, do

184 tection from the myelosuppressive effects of BCNU and suggest a possible approach to protecting cance

185 When the clastogenic effects of BCNU and temozolomide were examined in the mouse bone ma

186 utational approach to analyze the effects of BCNU on clonal cultures of oligodendrocyte progenitor ce

187 nduction, overcame the inhibitory effects of BCNU, and increased nitrite production by intact hepatoc

188 hronic rejection in the donor skin grafts of BCNU treated mice compared no BCNU treated mice.

189 ntinuous BSO exposure increased the level of BCNU-induced DNA interstrand cross-links, and cytotoxici

190 Four dose levels of BCNU (13.5, 27, 40, and 55 mg/m(2)) were evaluated, with

191 The MTD of BCNU delivered in polymer to the surgical cavity is 20%.

192 These results indicate that the MTD of BCNU when given in combination with O(6)-BG at a dose of

193 toxicity and maximum-tolerated dose (MTD) of BCNU in conjunction with the preadministration of O(6)-B

194 We conclude that WAF1/Cip1 allows repair of BCNU- and cisplatin-damaged DNA and protects glioma cell

195 trated that WAF1/Cip1 enhances the repair of BCNU-induced DNA damage.

196 tructure together suggest that one source of BCNU interstrand cross-links is linkage of deoxyguanosin

197 tegies to minimize dose-limiting toxicity of BCNU such as regional delivery or hematopoietic stem-cel

198 Given the clinical use of BCNU polymers against malignant gliomas, concurrent trea

199 7; median survival, 22 days; P = 0.0002) or BCNU polymer alone (n = 8; median survival, 25 days; P =

200 ne (1,3-bis(2-chloroethyl)-1-nitrosourea, or BCNU).

201 were completely resistant to temozolomide or BCNU in the presence and absence of BG.

202 st cancer cells pretreated with AdMnSOD plus BCNU both in vitro and in vivo.

203 ce O(2)(*-) in combination with AdMnSOD plus BCNU may represent a powerful new antitumor regimen agai

204 In vitro, AdMnSOD plus BCNU sensitized cells to the cytotoxicity of Adriamycin

205 ectively killed by the O6-benzylguanine plus BCNU combination.

206 of the combination of O6-benzylguanine plus BCNU in clinical trials.

207 These results indicate that O(6)-BG plus BCNU at the dose schedule used in this trial is unsucces

208 ndation for a phase II trial of O(6)-BG plus BCNU in nitrosourea-resistant malignant glioma.

209 lus BCNU plus SRT), or arm D (cisplatin plus BCNU plus ART).

210 arm B (BCNU plus ART), arm C (cisplatin plus BCNU plus SRT), or arm D (cisplatin plus BCNU plus ART).

211 rated the suppressive effect of diamide plus BCNU.

212 with an equimolar dose of BG (90 mg/m2) plus BCNU and -0.6 days after treatment with BCNU alone.

213 e the capacity of BG analogues to potentiate BCNU toxicity, despite less in vitro activity than the p

214 wt AGT and the sensitivity to BG-potentiated BCNU-cytotoxicity.

215 Seventy-four patients received BCNU 15 mg/kg with identical doses of VP and Cy.

216 Patients received BCNU 200 mg/m2 on day 1 of every 6-week cycle, and 800 m

217 ear survival rates for patients who received BCNU plus RT (arms A and B) compared with cisplatin, BCN

218 enic BM in a mixed-chimerism model receiving BCNU across a major histocompatibility complex mismatch.

219 duced pancytopenia and significantly reduced BCNU-induced mortality due to bone marrow hypoplasia.

220 ludes placing biodegradable wafers releasing BCNU (Gliadel(R)) into the tumor bed at the time of surg

221 The resulting BCNU-loaded PLGA microcapsules have significantly higher

222 mphocytes observed in control mice surviving BCNU treatment was completely reversed in mice transplan

223 CNU polymers and results in minimal systemic BCNU exposure.

224 and, thus, enhance the efficacy of systemic BCNU therapy in a variety of tumor models.

225 ecurrent high-grade gliomas and the systemic BCNU exposure with increasing doses of interstitial BCNU

226 udies provide the first direct evidence that BCNU has no strong sequence preference for interstrand c

227 It was found that BCNU inhibited radiation-induced apoptosis through EGFR-

228 The BCNU was administered at 4 time points after BM transpla

229 ng significant AGT, may be necessary for the BCNU to provide a meaningful therapeutic benefit.

230 well balanced by treatment group; 61% of the BCNU group had a KPS of 90 to 100 compared with 73% of t

231 The group that received the BCNU alone wafer had a median survival of 15 days, the g

232 l of 19 days, and the group treated with the BCNU-TMZ wafer had a median survival of 28 days with 25%

233 AGT (transfected with wt MGMT cDNA) cells to BCNU or TMZ-cytotoxicity by 3-4 fold.

234 topoietic progenitor colony-forming cells to BCNU, resulting in a reduction in the dose of drug (term

235 grafts containing 1 and 100% V8MGMT cells to BCNU.

236 pulmonary function, or systemic exposure to BCNU, cyclophosphamide, or cisplatin.

237 duced Chk1 phosphorylation after exposure to BCNU.

238 analysis reveals that transient exposures to BCNU increased the cell cycle length of progenitor cells

239 of BSO to sensitize tumors and cell lines to BCNU.

240 . injection of O6-BG (50 mg/kg) 2 h prior to BCNU polymer (3.8% BCNU by weight) implantation had sign

241 bone marrow conferred in vivo resistance to BCNU-induced pancytopenia and significantly reduced BCNU

242 ld-type human AGT rendered them resistant to BCNU but this resistance could be overcome by treatment

243 0% V8MGMT cells were completely resistant to BCNU with no regressions and no growth delays.

244 /mg protein, respectively, were resistant to BCNU, but their resistance declined sharply following pr

245 ine also gave rise to CHO cells resistant to BCNU, but these mutations rendered the expressed AGT les

246 ents with the best likelihood of response to BCNU chemotherapy.

247 ation of the ATR-Chk1 pathway in response to BCNU treatment and the dependence of this response on th

248 ation of cells in the S phase in response to BCNU, an effect that was attenuated by caffeine.

249 In response to BCNU, Chk1 was found to be phosphorylated at serine 345

250 taining 0-10% V8MGMT cells were sensitive to BCNU, although partial resistance was observed as the pe

251 h less effective in restoring sensitivity to BCNU.

252 All cell lines were sensitized to BCNU by O6-bG.

253 and N,N'-bis(2-chloroethyl)-N-nitroso-urea (BCNU) stably increased the percentage of transgene-expre

254 n, cyclophosphamide, prednisone/vincristine, BCNU, doxorubicin, dexamethasone/bortezomib (VBMCP/VBAD/

255 omide/dexamethasone (TD) versus vincristine, BCNU, melphalan, cyclophosphamide, prednisone/vincristin

256 lly electrospun fiber membranes and in vitro BCNU release kinetics were measured.

257 T-transduced cells showed extensive in vitro BCNU resistance.

258 atients with AA may need to consider whether BCNU or PCV is used in the control arm.

259 ition of glutathione reductase activity with BCNU inhibited nitrite synthesis.

260 se of O6-BG will be used in combination with BCNU in another phase I trial designed to determine the

261 nstrate that thalidomide in combination with BCNU is well tolerated and has antitumor activity in pat

262 s with either BCNU alone or BG combined with BCNU.

263 therapy (RT) improves survival compared with BCNU and RT and whether survival using accelerated RT (A

264 Cisplatin administered concurrently with BCNU and RT resulted in more toxicity but provided no si

265 of s.c. tumors increased from -0.1 days with BCNU alone to 39.3 days.

266 nty-nine eligible patients were treated with BCNU 150 mg/m2/d, every 6 weeks, DTIC 220 mg/m2/d on day

267 A total of 257 patients were treated with BCNU according to RTOG protocols 70-18, 83-02, and 90-06

268 Compared with mice treated with BCNU alone, significant myeloid toxicity and death occur

269 ituted with marrow from animals treated with BCNU only demonstrated 23% transduced cells, consistent

270 s from 167 primary brain tumors treated with BCNU were quantitated with an immunofluorescence assay u

271 d-type MGMT gene transfer and treatment with BCNU alone.

272 plus BCNU and -0.6 days after treatment with BCNU alone.

273 , depleted of cellular GSH by treatment with BCNU, were subjected to oxidative stress to examine the