ライフサイエンスコーパス: temozolomide

1 aclitaxel, carboplatin, dacarbazine, or oral temozolomide).

2 ce temozolomide (temozolomide/radiotherapy-->temozolomide).

3 inhibitor bortezomib or the alkylating agent temozolomide.

4 tic drugs including cisplatin, lomustine and temozolomide.

5 ion in glioma cells enhances the efficacy of temozolomide.

6 strated to be required for DcR1 induction by temozolomide.

7 poptosis compared with standard single-agent temozolomide.

8 andard therapies consisting of radiation and temozolomide.

9 75 mg/m(2) per day, with or without adjuvant temozolomide.

10 3, is also required for induction of DcR1 by temozolomide.

11 eness and resistance to the alkylating agent temozolomide.

12 the replication of DNA lesions generated by temozolomide.

13 ppaB-dependent expression profile induced by temozolomide.

14 r and subsequent resistance to radiation and temozolomide.

15 iomas, and in gliomas treated with radiation/temozolomide.

16 eral resistance to cisplatin, melphalan, and temozolomide.

17 with the chemotherapeutic DNA-damaging agent temozolomide.

18 er patient survival and improved response to temozolomide.

19 b1 mutants, rendering them more resistant to temozolomide.

20 blastoma with radiotherapy (60 Gy) and daily temozolomide.

21 sistant cancer cells to the alkylating agent temozolomide.

22 combined radiotherapy and chemotherapy with temozolomide.

23 stoma is based on radiotherapy combined with temozolomide.

24 , thereby increasing the cytotoxic effect of temozolomide.

25 apacity of cancers in predicting response to temozolomide.

26 cer agents, including ionizing radiation and temozolomide.

27 lkylating agents methylmethane sulfonate and temozolomide.

28 soguanidine (MNNG), a functional analogue of temozolomide.

29 e current treatment regimen of radiation and temozolomide.

30 that had recurred after initial therapy with temozolomide.

31 synergistic enhancement in combination with temozolomide.

32 treatment with DNA alkylating agents such as temozolomide.

33 with no side effects compared to free PTX or temozolomide.

34 ant parameters that determine sensitivity to temozolomide.

35 assigned to dose-dense and 43 to metronomic temozolomide.

36 t drug to standard chemotherapeutics such as temozolomide.

37 ovascularization and increased resistance to Temozolomide.

38 with and 44.1% (36.3-51.6) without adjuvant temozolomide.

39 istance to the widely used brain cancer drug temozolomide.

40 ith vincristine 1.5 mg/m(2) on days 1 and 8, temozolomide 100 mg/m(2) on days 1-5, and bevacizumab 15

41 with irinotecan 50 mg/m(2) intravenously and temozolomide 100 mg/m(2) orally on days 1 to 5.

42 Patients in both groups received oral temozolomide (100 mg/m(2) per dose) and intravenous irin

43 cell-cycle arrest beginning three days after temozolomide (100 mumol/L, 3 hours) exposure and persist

44 fractions of 1.8 Gy) alone or with adjuvant temozolomide (12 4-week cycles of 150-200 mg/m(2) temozo

45 r intolerance, concurrent with standard oral temozolomide (150-200 mg/m(2) for 5 of 28 days) for 6-12

46 Temozolomide (150-200 mg/m2/d) was given for 5 days of e

47 a continual basis (n = 50), or chemotherapy (temozolomide, 150 mg/m2 orally daily for 5 of every 28 d

48 en 1999 and 2004, before the standard use of temozolomide, 191 patients were accrued onto New Approac

49 ; or to receive radiotherapy with concurrent temozolomide 75 mg/m(2) per day, with or without adjuvan

50 further study in this patient population are temozolomide 75 mg/m2/d plus irinotecan 60 mg/m2/d when

51 week for up to 6.5 weeks) or dose-dense oral temozolomide (75 mg/m(2) once daily for 21 days, repeate

52 dent but caspase-dependent and enhanced with temozolomide, a chemotherapeutic agent used as a present

53 Compared with temozolomide, a clinical DNA-alkylating agent against gl

54 portantly, the combination of RGD-M/sPMI and temozolomide--a standard chemotherapy drug for GBM incre

55 ther TTFields plus temozolomide (n = 466) or temozolomide alone (n = 229) (median time from diagnosis

56 d 4.0 months (95% CI, 3.3-5.2 months) in the temozolomide alone group (hazard ratio [HR], 0.62 [98.7%

57 5.6 months (95% CI, 13.3-19.1 months) in the temozolomide alone group (n = 84) (HR, 0.64 [99.4% CI, 0

58 overall survival data associated with either temozolomide alone or radiotherapy alone in elderly pati

59 nt of elderly patients with GBM using either temozolomide alone or radiotherapy alone, with considera

60 apy and temozolomide versus radiotherapy and temozolomide alone showed improvement in progression-fre

61 ity of randomized clinical studies comparing temozolomide alone with radiotherapy alone in elderly pa

62 ll survival in elderly patients treated with temozolomide alone, and 4 level 1 studies and 2 level 2

63 elds plus temozolomide and 105 randomized to temozolomide alone, and was conducted at a median follow

64 include hypofractionated radiotherapy alone, temozolomide alone, or best supportive care.

65 ort survival data from radiotherapy alone or temozolomide alone, were not restricted to an elderly po

66 the combination of siRNA targeting RRM2 and temozolomide, an analog of the current standard of care

67 he PET system analysis method was applied to temozolomide, an important alkylating agent used in the

68 Temozolomide, an oral analog of dacarbazine, also has ac

69 ded 210 patients randomized to TTFields plus temozolomide and 105 randomized to temozolomide alone, a

70 Combinatorial treatment of glioblastoma with temozolomide and a novel artificial nucleoside that inhi

71 was the MTD when combined with vincristine, temozolomide and bevacizumab administered on a 21 day sc

72 Temozolomide and bevacizumab can be safely administered

73 Combination therapy with temozolomide and bevacizumab has recently emerged as a p

74 dministered in combination with vincristine, temozolomide and bevacizumab in children with refractory

75 The combination of temozolomide and bevacizumab was associated with anticip

76 as, including the approval of agents such as temozolomide and bevacizumab, have created an evolving t

77 combination with chemotherapy agents such as temozolomide and cisplatin.

78 standard alkylating chemotherapies, such as temozolomide and cyclophosphamide, significantly inhibit

79 us murine melanoma model in combination with temozolomide and in an MX-1 breast cancer xenograft mode

80 red in 32 (14%) of 236 patients treated with temozolomide and in one (<1%) of 228 patients treated wi

81 d in eight (3%) of 236 patients treated with temozolomide and in two (1%) of 228 patients treated wit

82 potentiated the anti-tumor activity of both temozolomide and ionizing radiation.

83 has a higher antiproliferative activity than Temozolomide and is more potent than paclitaxel for the

84 Both temozolomide and O(6)-BG were administered on day 1 of a

85 f 67 patients who enrolled were treated with temozolomide and O(6)-BG.

86 plication on malignant melanoma therapy with temozolomide and other alkylating drugs suggests a combi

87 icacy in vivo, alone and in combination with temozolomide and radiation.

88 Concurrent treatment with temozolomide and radiotherapy followed by maintenance te

89 s as an enhancer of the cytotoxic effects of temozolomide and radiotherapy.

90 Both temozolomide and the combination of procarbazine, lomust

91 patients with GBM treated with radiation and temozolomide and to influence clinical decision making.

92 patients with GBM treated with radiation and temozolomide and was biologically validated in an indepe

93 Oxidative stress, temozolomide, and irradiation induced QPRT in glioma cel

94 lastoma; NCT00943826), CENTRIC (Cilengitide, Temozolomide, and Radiation Therapy in Treating Patients

95 ter Status; NCT00689221), CORE (Cilengitide, Temozolomide, and Radiation Therapy in Treating Patients

96 mission induction therapy with methotrexate, temozolomide, and rituximab (MT-R); two, feasibility of

97 were seen in 8-12% of 549 patients assigned temozolomide, and were mainly haematological and reversi

98 Patients were randomly assigned to standard temozolomide (arm 1) or DD temozolomide (arm 2) for 6 to

99 igned to standard temozolomide (arm 1) or DD temozolomide (arm 2) for 6 to 12 cycles.

100 ombination therapy using p53 activators with temozolomide as a more effective treatment for GBM.

101 vered patterns of tumor evolution, including temozolomide-associated mutations.

102 is tolerable with a standard irinotecan and temozolomide backbone and has promising response and pro

103 BM) is often treated with the cytotoxic drug temozolomide, but the disease inevitably recurs in a dru

104 2;Msh2(flox/-) mice to the methylating agent temozolomide caused MSH2-deficient intestinal stem cells

105 venously twice weekly (cilengitide group) or temozolomide chemoradiotherapy alone (control group).

106 The addition of cilengitide to temozolomide chemoradiotherapy did not improve outcomes;

107 lioblastoma and in combination with standard temozolomide chemoradiotherapy in newly diagnosed gliobl

108 We aimed to assess cilengitide combined with temozolomide chemoradiotherapy in patients with newly di

109 interactive voice response system to receive temozolomide chemoradiotherapy with cilengitide 2000 mg

110 ts to receive either radiotherapy (n=240) or temozolomide chemotherapy (n=237).

111 en treated with either radiotherapy alone or temozolomide chemotherapy alone.

112 The role of temozolomide chemotherapy in newly diagnosed 1p/19q non-

113 gies of standard radiotherapy versus primary temozolomide chemotherapy in patients with low-grade gli

114 tion therapy, adding TTFields to maintenance temozolomide chemotherapy significantly prolonged progre

115 INTERPRETATION: Adjuvant temozolomide chemotherapy was associated with a signific

116 al treatment with surgery, radiotherapy, and temozolomide chemotherapy, the prognosis is poor, with a

117 further enhanced upon nutrient starvation or temozolomide chemotherapy.

118 stemness of GSCs and also sensitized them to temozolomide chemotherapy.

119 Among these, the irinotecan/temozolomide combination induced strong tumor regression

120 elded predicted normal brain and brain tumor temozolomide concentration profiles for different temozo

121 The potentiation of temozolomide cytotoxicity by LCA owes to the conversion

122 istance of melanomas to the alkylating drugs temozolomide, dacarbazine, and fotemustine.

123 Temozolomide did not prevent immune responses.

124 INTERPRETATION: Irinotecan-temozolomide-dinutuximab met protocol-defined criteria f

125 Irinotecan-temozolomide-dinutuximab shows notable anti-tumour activ

126 Of the 17 patients assigned to irinotecan-temozolomide-dinutuximab, nine (53%; 95% CI 29.2-76.7) h

127 mozolomide-temsirolimus and 17 to irinotecan-temozolomide-dinutuximab.

128 olomide concentration profiles for different temozolomide dosing regimens (75-200 mg/m(2)/d).

129 Mechanistically, DcR1 attenuates temozolomide efficacy by blunting activation of the Fas

130 We screened a series of cell lines for temozolomide efficacy in vitro, and investigated the dif

131 tematic review to identify articles from the temozolomide era (2005-present) that reported survival d

132 fication model for glioblastoma (GBM) in the temozolomide era.

133 s et al. demonstrate that the combination of temozolomide, etoposide, doxorubicin, dexamethasone, rit

134 The higher temozolomide exposures in brain tumor relative to normal

135 e rate associated with use of irinotecan and temozolomide for children with relapsed/refractory neuro

136 did not demonstrate improved efficacy for DD temozolomide for newly diagnosed GBM, regardless of meth

137 olomide (12 4-week cycles of 150-200 mg/m(2) temozolomide given on days 1-5); or to receive radiother

138 % CI, 16.7-25.0 months) in the TTFields plus temozolomide group (n = 196) and 15.6 months (95% CI, 13

139 95% CI, 5.9-8.2 months) in the TTFields plus temozolomide group and 4.0 months (95% CI, 3.3-5.2 month

140 survival was 39 months (95% CI 35-44) in the temozolomide group and 46 months (40-56) in the radiothe

141 due to treatment-related causes: two in the temozolomide group and two in the radiotherapy group.

142 iotherapy group (grade 2) and 16 (7%) in the temozolomide group.

143 The combination of irinotecan and temozolomide has activity in these patients, and its acc

144 Resistance to DNA-damaging drugs such as temozolomide has been related to the induction of antiap

145 Irinotecan and temozolomide have activity in patients with advanced neu

146 ession-free survival than those treated with temozolomide (HR 1.86 [95% CI 1.21-2.87], log-rank p=0.0

147 This trial tested whether DD temozolomide improves overall survival (OS) or progressi

148 efficacy in potentiating the cytotoxic agent temozolomide in a B16F10 murine melanoma model.

149 of radiotherapy with concurrent and adjuvant temozolomide in adults with non-co-deleted anaplastic gl

150 dose (MTD) of oral irinotecan combined with temozolomide in children with recurrent/resistant high-r

151 a phase II study to evaluate the efficacy of temozolomide in combination with bevacizumab in patients

152 from use of the S(N)1-type alkylating agent temozolomide in combination with ionizing radiation.

153 tor augments the growth inhibitory effect of temozolomide in glioblastoma cells.

154 th as a single agent and in combination with Temozolomide in MDA-MB-436 and Capan-1 xenograft models,

155 of temsirolimus or dinutuximab to irinotecan-temozolomide in patients with relapsed or refractory neu

156 dose (MTD) of alisertib with irinotecan and temozolomide in this population.

157 /3 caused sensitization of melanoma cells to temozolomide in vitro and in melanoma xenografts in vivo

158 t hoc analysis of the registration trial for temozolomide indicated an association between valproic a

159 directly enhance HR and facilitate repair of temozolomide-induced DNA damage and temozolomide resista

160 sylase) are key enzymes capable of repairing temozolomide-induced DNA damages and their levels in tis

161 changes in MSH2 were sufficient to suppress temozolomide-induced tumor regression.

162 n of the alpha5 integrin subunit compromises temozolomide-induced tumor suppressor p53 activity in hu

163 Temozolomide is a clinical chemotherapeutic equivalent r

164 Temozolomide is a DNA-alkylating agent used to treat bra

165 The antitumor prodrug temozolomide is compromised by its dependence for activi

166 especially of brain tumours where the use of temozolomide is frequently used in treatment.

167 Sensitivity to temozolomide is restricted to a subset of glioblastoma p

168 ed radiotherapy with concurrent and adjuvant temozolomide is the standard of care after biopsy or res

169 Radiotherapy with concomitant and adjuvant temozolomide is the standard of care for newly diagnosed

170 ide and radiotherapy followed by maintenance temozolomide is the standard of care for patients with n

171 Temozolomide is used widely to treat malignant glioma, b

172 therapy including surgery, radiotherapy and temozolomide, it is essentially incurable.

173 the use of hypofractionated radiotherapy or temozolomide monotherapy in the treatment of elderly pat

174 In patients with MGMT promoter methylation, temozolomide monotherapy may have greater benefit than r

175 t studies have suggested that treatment with temozolomide monotherapy or short-course radiotherapy ma

176 ts included amoxicillin/clavulanate (n = 3), temozolomide (n = 3), various herbal products (n = 3), a

177 ntenance treatment with either TTFields plus temozolomide (n = 466) or temozolomide alone (n = 229) (

178 e) and randomly assigned to rindopepimut and temozolomide (n=371) or control and temozolomide (n=374)

179 imut and temozolomide (n=371) or control and temozolomide (n=374).

180 ine xenograft model of glioblastoma, whereas temozolomide only delayed tumor growth, its coadministra

181 induced G1 arrest, resulted in resistance to temozolomide or bortezomib.

182 ffer between oligodendrogliomas treated with temozolomide or carmustine.

183 n's choice of standard-of-care chemotherapy (temozolomide or dacarbazine).

184 es for active disease, including dacarbazine/temozolomide or interleukin-2 (IL-2).

185 that ribavirin treatment in combination with temozolomide or irradiation increases cell death in glio

186 response function that, when convolved with temozolomide plasma concentration input functions, yield

187 omly assign patients (1:1) to irinotecan and temozolomide plus either temsirolimus or dinutuximab, st

188 Resistance to temozolomide poses a major clinical challenge in gliobla

189 While GEPCOT NICs were ablated by temozolomide, pre-GEPCOT cells survived and repopulated

190 agent chemotherapy-carboplatin, vincristine, temozolomide, procarbazine, lomustine, and thioguanine-a

191 tegrin and p53 supports glioma resistance to temozolomide, providing preclinical proof-of-concept tha

192 sing the search terms glioblastoma, elderly, temozolomide, radiation, hypofractionated, and survival,

193 nd concomitant and maintenance temozolomide (temozolomide/radiotherapy-->temozolomide).

194 Predicted peak concentrations of temozolomide ranged from 2.9 to 6.7 microg/mL in human g

195 ) after completion of radiochemotherapy with temozolomide (RCX) (MRI-/FET-2), and 6-8 wk later (MRI-/

196 Here, using recurrent temozolomide-refractory glioblastoma specimens, temozolo

197 Both dose-dense and metronomic temozolomide regimens were well tolerated with modest to

198 therapies such as dose-dense and metronomic temozolomide regimens, targeted molecular agents, and ot

199 of MSH2 attenuation as a potent mediator of temozolomide resistance and argue that MMR activity offe

200 results show how DcR1 upregulation mediates temozolomide resistance and provide a rationale for DcR1

201 nation (HR) capacity contributed to acquired temozolomide resistance in PDX models and led to reduced

202 the mechanisms underlying the development of temozolomide resistance remain poorly understood.

203 nd MGMT provided a more robust prediction of temozolomide resistance than assessments of MGMT activit

204 miR-29c via c-Myc drives the acquisition of temozolomide resistance through enhancement of REV3L-med

205 provided an unexpectedly strong mechanism of temozolomide resistance.

206 well as preventing the emergence of acquired temozolomide resistance.

207 epair of temozolomide-induced DNA damage and temozolomide resistance.

208 ase (MGMT) fare worse, presumably because of temozolomide resistance.

209 equent protein overexpression were linked to temozolomide resistance.

210 ive patient tumors included clones that were temozolomide resistant, indicating that resistance to co

211 re temozolomide sensitivity in patients with temozolomide-resistant anaplastic glioma, but there seem

212 ozolomide-refractory glioblastoma specimens, temozolomide-resistant cells, and resistant-xenograft mo

213 of temozolomide sensitivity in patients with temozolomide-resistant GBM.

214 ectively reduces the growth and viability of Temozolomide-resistant glioblastoma and doxorubicin-resi

215 Through targeting "HR-addicted" temozolomide-resistant glioblastoma cells via a chemical

216 ute, we defined the decoy receptor DcR1 as a temozolomide response gene induced by a mechanism relyin

217 itors of HR may be a viable means to enhance temozolomide response in IDH1-mutant glioma.

218 es, then monitored transformation status and temozolomide response.

219 treatment in vitro of pathway inhibition and temozolomide resulted in a highly synergistic interactio

220 Adding bevacizumab to radiotherapy and temozolomide resulted in increases of 0.13 quality-adjus

221 Dose-dense (DD) temozolomide results in prolonged depletion of MGMT in b

222 MB inhibits cell proliferation in both temozolomide-sensitive and -insensitive GBM cell lines.

223 Temozolomide-sensitive parental cells exhibited DNA dama

224 regimen of temozolomide was able to restore temozolomide sensitivity in patients with temozolomide-r

225 e seemed to be no significant restoration of temozolomide sensitivity in patients with temozolomide-r

226 y constitute a mechanism by which GBM evades temozolomide sensitivity while maintaining microsatellit

227 nents MSH2 and MSH6 have profound effects on temozolomide sensitivity.

228 integrin subunit increased p53 activity and temozolomide sensitivity.

229 radiotherapy and concomitant and maintenance temozolomide (temozolomide/radiotherapy-->temozolomide).

230 nts, 18 were randomly assigned to irinotecan-temozolomide-temsirolimus and 17 to irinotecan-temozolom

231 on meriting further study whereas irinotecan-temozolomide-temsirolimus did not.

232 Of the 18 patients assigned to irinotecan-temozolomide-temsirolimus, one patient (6%; 95% CI 0.0-1

233 observed when coupling miRNA modulation with temozolomide, the first-line drug for GBM therapy.

234 erall survival alone and in combination with temozolomide, the standard-of-care chemotherapeutic agen

235 with postoperative concurrent radiation and temozolomide therapy and who underwent FDG PET/computed

236 M could predict patient responses to initial temozolomide therapy.

237 yeloid cells after O6-benzylguanine (BG) and temozolomide (TMZ) administration.

238 response during short-term chemotherapy with temozolomide (TMZ) by amide proton transfer (APT) imagin

239 of therapeutic resistance in GBM to standard temozolomide (TMZ) chemotherapy and radiotherapy (RT).

240 M) may or may not show sustained response to temozolomide (TMZ) chemotherapy.

241 BM) to the front-line chemotherapeutic agent temozolomide (TMZ) continues to challenge GBM treatment

242 openia induced by the chemotherapeutic agent temozolomide (TMZ) enhances vaccine-driven immune respon

243 ients treated with the chemotherapeutic drug temozolomide (TMZ) followed an alternative evolutionary

244 cizumab (BV) with radiation therapy (RT) and temozolomide (TMZ) for the treatment of newly diagnosed

245 ine-DNA methyltransferase promotor, standard temozolomide (TMZ) has, at best, limited efficacy.

246 the cytotoxic effect of DNA-alkylating agent Temozolomide (TMZ) in mismatch repair (MMR)-deficient an

247 he source of new tumour cells after the drug temozolomide (TMZ) is administered to transiently arrest

248 Temozolomide (TMZ) is an alkylating agent licensed for t

249 Temozolomide (TMZ) is an oral alkylating agent used for

250 Temozolomide (TMZ) is first-line treatment for gliomas a

251 Temozolomide (TMZ) is one of the most potent chemotherap

252 intrinsically resistant to chemotherapeutic temozolomide (TMZ) or develop resistance during treatmen

253 In addition, temozolomide (TMZ) treatment induced greater DNA damage

254 BMs rarely developed hypermutation following temozolomide (TMZ) treatment, indicating low risk for TM

255 pression in response to irradiation (RT) and temozolomide (TMZ) treatment.

256 limb infusion (ILI) with melphalan (LPAM) or temozolomide (TMZ) was performed on rats bearing melanom

257 e current reference drug for this condition, temozolomide (TMZ), 2OHOA combated glioma more efficient

258 Recent findings show that exposure to temozolomide (TMZ), a DNA-damaging drug used to treat gl

259 We now show that temozolomide (TMZ), a principal chemotherapeutic agent u

260 t of primary CNS lymphoma with methotrexate, temozolomide (TMZ), and rituximab, followed by hyperfrac

261 ith a combination of surgery, radiation, and temozolomide (TMZ), but these therapies ultimately fail

262 In contrast, the DNA damaging agent temozolomide (TMZ), which is used as current frontline t

263 sed the antitumor activity of coadministered temozolomide (TMZ).

264 d chemotherapy with the DNA alkylating agent temozolomide (TMZ).

265 d chemotherapy with the DNA alkylating agent temozolomide (TMZ).

266 Combined with temozolomide (TMZ; a DNA-methylating chemotherapeutic dr

267 The addition of concurrent and adjuvant temozolomide to hypofractionated radiotherapy seems to b

268 Accordingly, 5-NIdR synergized with temozolomide to increase apoptosis of tumor cells.

269 Adding the chemotherapeutic temozolomide to the treatment increased survival to 30 d

270 P, cis-platin), carboplatin, dacarbazine, or temozolomide together with velaparib, an inhibitor of po

271 was detected and enriched upon selection of temozolomide-tolerant GBM cells.

272 ral regions (DeltapHe) in both untreated and temozolomide treated (40 mg/kg) rats bearing U251 tumors

273 lyze mRNA expression patterns in tumors from temozolomide-treated GBM patients, we found that MSH2 tr

274 e found that oleandrin increases survival of temozolomide-treated mice.

275 ligibility criteria, prognostic factors, and temozolomide treatment (hazard ratio, 5.3; P = .0013; n

276 Further analysis of the role of concurrent temozolomide treatment and molecular factors is needed.

277 ced relative survival prolongation following temozolomide treatment of orthotopic mouse models in viv

278 eatment of brain tumors, as part of standard temozolomide treatment regimens in patients.

279 Whereas temozolomide treatment was not associated with either sC

280 e marker for initial therapeutic response to temozolomide treatment.

281 nged host survival, and sensitized tumors to temozolomide treatment.

282 prolonged survival in GBM-bearing mice after temozolomide treatment.

283 solid tumors, we make a case for revisiting temozolomide use in a broader spectrum of cancers based

284 itized GBM cells and CSCs to the activity of temozolomide; (v) directed its effects preferentially to

285 eated with bevacizumab plus radiotherapy and temozolomide versus radiotherapy and temozolomide alone

286 trial 0525 tested whether dose-intensifying temozolomide versus standard chemoradiotherapy improves

287 io for overall survival with use of adjuvant temozolomide was 0.65 (99.145% CI 0.45-0.93).

288 )-BG when added to a 1-day dosing regimen of temozolomide was able to restore temozolomide sensitivit

289 Temozolomide was administered after completing valacyclo

290 Adjuvant temozolomide was continued in all patients.

291 Maintenance temozolomide was given for up to six cycles, and cilengi

292 g use at the start of chemoradiotherapy with temozolomide was performed in the pooled patient cohort

293 The combination of irinotecan and temozolomide was well tolerated.

294 after two cycles of sorafenib (combined with temozolomide) was associated with prolonged survival in

295 astoma who previously received radiation and temozolomide were randomly assigned 2:2:1 to receive (1)

296 On the other hand, pretreatment with temozolomide, which induced G2 arrest, did not result in

297 to treated rats (p < 0.002), suggesting that temozolomide, which induces apoptosis and hinders prolif

298 er, melanoma SP cells were also resistant to temozolomide, which is not a substrate for ABC transport

299 Notably, these cells are also resistant to temozolomide, which is not a substrate for ATP-Binding C

300 activity and current clinical application of temozolomide, which, until now, has been largely limited