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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 (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

98 1210 variants resistant to cyclophosphamide, BCNU, or melphalan.

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

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

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

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

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

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

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

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

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

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

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

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

111 specifically and directly protected DNA from BCNU treatment.

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

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

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

115 posure with increasing doses of interstitial BCNU.

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

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

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

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

120 Maximum BCNU plasma concentrations with the 20% loaded polymers

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 resistant to BG-potentiated cytotoxicity of BCNU.

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

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

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

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

176 cells were treated with five weekly doses of BCNU.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

194 7; median survival, 22 days; P = 0.0002) or BCNU polymer alone (n = 8; median survival, 25 days; P =

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

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

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

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

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

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

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

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

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

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

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

206 rated the suppressive effect of diamide plus BCNU.

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

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

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

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

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

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

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

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

215 The resulting BCNU-loaded PLGA microcapsules have significantly higher

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

217 CNU polymers and results in minimal systemic BCNU exposure.

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

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

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

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

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

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

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

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

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

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

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

229 duced Chk1 phosphorylation after exposure to BCNU.

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

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

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

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

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

235 0% V8MGMT cells were completely resistant to BCNU with no regressions and no growth delays.

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

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

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

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

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

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

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

243 h less effective in restoring sensitivity to BCNU.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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