ライフサイエンスコーパス: temozolomide

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

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

3 75 mg/m(2) per day, with or without adjuvant temozolomide.

4 the replication of DNA lesions generated by temozolomide.

5 with the chemotherapeutic DNA-damaging agent temozolomide.

6 b1 mutants, rendering them more resistant to temozolomide.

7 apacity of cancers in predicting response to temozolomide.

8 ver instability after chemoradiotherapy with temozolomide.

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

10 ant parameters that determine sensitivity to temozolomide.

11 t drug to standard chemotherapeutics such as temozolomide.

12 ovascularization and increased resistance to Temozolomide.

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

14 istance to the widely used brain cancer drug temozolomide.

15 inhibitor bortezomib or the alkylating agent temozolomide.

16 tic drugs including cisplatin, lomustine and temozolomide.

17 ion in glioma cells enhances the efficacy of temozolomide.

18 strated to be required for DcR1 induction by temozolomide.

19 poptosis compared with standard single-agent temozolomide.

20 andard therapies consisting of radiation and temozolomide.

21 3, is also required for induction of DcR1 by temozolomide.

22 eness and resistance to the alkylating agent temozolomide.

23 ppaB-dependent expression profile induced by temozolomide.

24 r and subsequent resistance to radiation and temozolomide.

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

26 eral resistance to cisplatin, melphalan, and temozolomide.

27 er patient survival and improved response to temozolomide.

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

29 sistant cancer cells to the alkylating agent temozolomide.

30 combined radiotherapy and chemotherapy with temozolomide.

31 r after treatment with the chemotherapy drug temozolomide.

32 % response rate, while only 50% responded to temozolomide.

33 trate that irinotecan is more effective than temozolomide.

34 mouse model before and during treatment with Temozolomide.

35 for efficient transactivation in response to temozolomide.

36 l death induced by the chemotherapeutic drug temozolomide.

37 eated with radiotherapy or radiotherapy plus temozolomide.

38 cytotoxic regimens such as capecitabine and temozolomide.

39 d chemotherapy with the DNA alkylating agent temozolomide.

40 inhibition increased GB chemosensitivity to temozolomide.

41 MGMT-deficient cells with ATR inhibitors and temozolomide.

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

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

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

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

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

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

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

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

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

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

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

53 tigating the effect of combination with both temozolomide, a clinical standard-of-care chemotherapy f

54 CYC065, used together with temozolomide, a reference therapy for relapsed neuroblas

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

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

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

58 5.6 months (95% CI, 13.3-19.1 months) in the temozolomide alone group (n = 84) (HR, 0.64 [99.4% CI, 0

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

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

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

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

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

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

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

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

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

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

69 combination with chemotherapy agents such as temozolomide and cisplatin.

70 paB-dependent factors altered in response to temozolomide and found the long noncoding RNA (lncRNA) M

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

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

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

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

75 Concurrent treatment with temozolomide and radiotherapy followed by maintenance te

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

77 ed with cell death only after treatment with temozolomide and radiotherapy.

78 om patients receiving chemoradiotherapy with temozolomide and sequenced approximately 300 cancer gene

79 f MGMT and CHFR expression were sensitive to temozolomide and taxane drugs.

80 Both temozolomide and the combination of procarbazine, lomust

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

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

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

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

85 olar concentrations, complement therapy with temozolomide, and synergize strongly with everolimus.

86 treatment with concurrent chemoradiation and temozolomide, and that the model can be used to determin

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

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

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

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

91 patients are increasingly being treated with temozolomide, but early detection of response remains a

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

93 ver metastases warranted further therapy and temozolomide-capecitabine was started with morphological

94 2;Msh2(flox/-) mice to the methylating agent temozolomide caused MSH2-deficient intestinal stem cells

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

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

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

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

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

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

101 assessment in glioma patients after adjuvant temozolomide chemotherapy (TMZ).

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

103 e standard GBM treatments like radiation and temozolomide chemotherapy create DNA damage, these findi

104 While the introduction of temozolomide chemotherapy has increased long-term surviv

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

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

107 therapies including surgery, radiation, and temozolomide chemotherapy necessitating novel therapeuti

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

109 INTERPRETATION: Adjuvant temozolomide chemotherapy was associated with a signific

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

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

112 further enhanced upon nutrient starvation or temozolomide chemotherapy.

113 confers relative resistance to radiation and temozolomide chemotherapy.

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

115 strated significantly improved survival with temozolomide compared to radiation-therapy.

116 orescence guidance surgery and postoperative temozolomide concomitant chemoradiotherapy.

117 LAT1 sensitized patient-derived GBM cells to temozolomide cytotoxicity, and in vivo delivery of nanop

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

119 hat inhibition of ID1 enhances the effect of temozolomide, delays tumor recurrence, and prolongs surv

120 The combination of irinotecan, temozolomide, dintuximab, and granulocyte-macrophage col

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

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

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

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

125 y of combination olaparib PARP inhibitor and temozolomide DNA-damaging agent as an effective therapy

126 robustness of PDX studies, the PDXNet tested temozolomide drug response for three prevalidated PDX mo

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

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

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

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

131 Upon temozolomide exposure, we found a strong repression of t

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

133 % CI, 16.7-25.0 months) in the TTFields plus temozolomide group (n = 196) and 15.6 months (95% CI, 13

134 95% CI, 5.9-8.2 months) in the TTFields plus temozolomide group and 4.0 months (95% CI, 3.3-5.2 month

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

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

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

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

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

140 Irinotecan and temozolomide have activity in patients with advanced neu

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

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

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

144 tabolic changes for detection of response to temozolomide in both genetically engineered and patient-

145 icity of treatment with the alkylating agent temozolomide in combination with the PARP inhibitor (PAR

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

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

148 anti-MALAT1 siRNA increased the efficacy of temozolomide in mice bearing intracranial GBM xenografts

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

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

151 /3 caused sensitization of melanoma cells to temozolomide in vitro and in melanoma xenografts in vivo

152 Treatment of MGMT-deficient cells with temozolomide increased sensitivity to ATR inhibitors bot

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

154 Temozolomide induced growth delay, DNA double-strand bre

155 nt hypermutated gliomas was recapitulated by temozolomide-induced damage in cells with MMR deficiency

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

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

158 Temozolomide-induced senescence required functional p53

159 Inhibitor experiments revealed that temozolomide-induced senescence was initiated by damage

160 Temozolomide-induced senescence was triggered by the spe

161 ll system and did not seem to play a role in temozolomide-induced senescence.

162 e, it seems to represent a specific trait of temozolomide-induced senescence.

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

164 eal a mechanism by which the anticancer drug temozolomide induces senescence and downregulation of DN

165 rrently being tested in clinical trials, and temozolomide is a commonly used chemotherapeutic, this a

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

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

168 Temozolomide is the first line of treatment for glioblas

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

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 ifference comparing radiation-therapy versus temozolomide monotherapies.

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

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

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

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

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

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

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

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

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

183 ffer between oligodendrogliomas treated with temozolomide or carmustine.

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

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

186 Resistance to temozolomide poses a major clinical challenge in gliobla

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

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

189 sensitivity to DNA alkylating agents such as temozolomide, providing a natural therapeutic index over

190 f radiotherapy plus concomitant and adjuvant temozolomide published in 2005.

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

192 Radiation and temozolomide (radio/TMZ) resistance are major contributo

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

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

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

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

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

198 eat glioblastoma by suppressing an important temozolomide resistance mechanism.

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

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

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

202 provided an unexpectedly strong mechanism of temozolomide resistance.

203 well as preventing the emergence of acquired temozolomide resistance.

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

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

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

207 rthermore, we developed an in vitro model of temozolomide-resistant GBM that showed increased express

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

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

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

211 es, then monitored transformation status and temozolomide response.

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

213 However, combining CD47 blockade with temozolomide results in a significant pro-phagocytosis e

214 cally used chemotherapeutic drugs, including temozolomide, reverses multidrug resistance and increase

215 Temozolomide-sensitive parental cells exhibited DNA dama

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

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

218 ogen ablation or with the DNA damaging drug, temozolomide, significantly reduces cellular proliferati

219 Finally, combining AAV-ISL2-shRNA with temozolomide suppressed oligodendroglioma progression mo

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

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

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

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

224 With temozolomide the cell viability was never below 80% wher

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

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

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

228 expression enhanced the cytotoxic effects of temozolomide therapy on glioma cells and significantly p

229 M could predict patient responses to initial temozolomide therapy.

230 ical resection followed by radiotheraphy and temozolomide therapy.

231 sustained treatments with anti-cancer drugs temozolomide (TMZ) and doxorubicin (DOX) were investigat

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

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

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

235 ug nanoparticles (Hyb-D-AuNPs) based on gold-temozolomide (TMZ) complexes combined with gemcitabine (

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

237 erates at near room temperature, can enhance Temozolomide (TMZ) cytotoxicity on a glioblastoma cell l

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

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

240 Temozolomide (TMZ) is a frequently used chemotherapy for

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

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

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

244 xplore the effects of glioma development and Temozolomide (TMZ) on fecal microbiome in mice and human

245 fect of NF-kappaB inhibitor BAY 11-7082 with Temozolomide (TMZ) on the signaling pathways in GBM path

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

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

248 er pathways must be activated to escape from temozolomide (TMZ) treatment, however acquired resistanc

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

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

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

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

253 linically, we have prepared wafers releasing Temozolomide (TMZ), an anticancer drug used systemically

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

255 rapy and treatment with the alkylating agent Temozolomide (TMZ), can extend patient survival to appro

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

257 survival of GBM cells and sensitized them to temozolomide (TMZ)-induced apoptosis in vitro Likewise,

258 Temozolomide (TMZ)-resistant glioblastoma multiforme (GB

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

260 the sensitivity towards the alkylating agent temozolomide (TMZ).

261 radiation therapy (RT) and chemotherapy with temozolomide (TMZ).

262 s GBM cells to DNA damaging agents including temozolomide (TMZ).

263 a well-known and tolerated chemotherapeutic, temozolomide (TMZ).

264 GMT) is surrogate of intrinsic resistance to temozolomide (TMZ).

265 in combination treatment with radiation (RT)/temozolomide (TMZ)/PT2385 (p = 0.44, n = 10) or mean tum

266 he repurposing of imidazotetrazines (such as temozolomide, TMZ, the standard of care for glioblastoma

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 ate the mechanisms underlying the ability of temozolomide to induce senescence in glioblastoma cells.

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

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 a-ketoglutarate were significantly higher in temozolomide-treated cells compared with controls.

274 identified several metabolic alterations in temozolomide-treated cells, including a significant incr

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

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

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

278 slatable metabolic biomarkers of response to temozolomide treatment in mutant IDH1 glioma.

279 Temozolomide treatment inhibited p50 recruitment to its

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

281 f stroke-induced hippocampal neurogenesis by temozolomide treatment or using a genetic approach (Nest

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

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

284 e marker for initial therapeutic response to temozolomide treatment.

285 and from glutamine were increased following temozolomide treatment.

286 Temozolomide, unlike other alkylators, activated the ata

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

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

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

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

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

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

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

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

297 The DNA-methylating drug temozolomide, which induces cell death through apoptosis

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

299 trengthen the possibility that co-therapy of temozolomide with a CA XII inhibitor may more effectivel

300 er for early assessment of tumor response to temozolomide, with the potential to improve treatment st