ライフサイエンスコーパス: MGMT

1 MGMT (O(6)-methylguanine DNA methyltransferase) and APNG

2 MGMT activity in leukemia cells was quite variable and w

3 MGMT also provides resistance of tumours to alkylating a

4 MGMT expression is lost by epigenetic silencing in a var

5 MGMT expression is reduced or absent in many tumor types

6 MGMT expression provides cellular resistance to alkylato

7 MGMT expression was assessed by methylation-specific pyr

8 MGMT methylation was associated with improved OS (21.2 v

9 MGMT methylation was significantly associated with CagA-

10 MGMT methylation was significantly reduced after H pylor

11 MGMT promoter hypermethylation is currently the only kno

12 MGMT promoter methylation is partially reversible after

13 MGMT promoter methylation status remained prognostic at

14 MGMT promoter methylation was assessed on patient tumor

15 MGMT promotor methylation is associated with favourable

16 MGMT promotor methylation was quantified using Sanger se

17 MGMT, TERT, and EGFRvIII status was individually determi

18 the four dependent variables: (1) IDH1, (2) MGMT, and (3) microvascular proliferation, with an avera

19 Herein, frozen tumors from 36 MGMT methylated patients grouped according to overall su

20 uanine-DNA-methyltransferase (E.C. 2.1.1.63, MGMT).

21 ducing MGMT promoter activity and abolishing MGMT induction.

22 n of O(6)-alkylguanine DNA alkyltransferase (MGMT) is surrogate of intrinsic resistance to temozolomi

23 O(6)-Alkylguanine-DNA alkyltransferase (MGMT) is the sole repair protein for O(6)-alkylguanine l

24 of methyl groups to human alkyltransferase (MGMT).

25 ed by O6-alkylguanine-DNA alkyltransferases (MGMT) by transfer of the alkyl group to a cysteine resid

26 liminate the use of radioactivity and allows MGMT activity to be rapidly measured in minimally prepar

27 a micro-LCR-driven gamma-globin gene, and an MGMT(P140K) system that allowed for increasing the thera

28 O(6)-CMG is therefore an MGMT substrate, and hence MGMT is likely to be a protect

29 MP2 (17q25.3) were frequently amplified, and MGMT (20q26.3) and ECHS1 (10q26.3) were frequently delet

30 localization between active beta-catenin and MGMT.

31 1p/19q codeletion and MGMT promoter methylation were determined by copy-number

32 , presence of oligodendroglial elements, and MGMT promoter methylation status, analysed by intention

33 ct of these findings, the level of hTERT and MGMT expression was measured in a recurrent anaplastic e

34 the existing clinically based RPA model and MGMT promoter methylation in NRG Oncology RTOG 0525.

35 ion over both the current RTOG RPA model and MGMT promoter methylation, respectively, for patients wi

36 of heterozygosity [LOH], IDH1 mutation, and MGMT methylation), and histologic parameters.

37 ing the combined status of MMR, HR, NER, and MGMT provided a more robust prediction of temozolomide r

38 pe is conferred by the G-CIMP phenotype, and MGMT DNA methylation may be a predictive biomarker for t

39 icant correlation between Wnt signalling and MGMT expression in cancers with different origin and con

40 h not powered for efficacy, the survival and MGMT independence trends are encouraging.

41 cer revealed no methylation of the p16, ARF, MGMT, and GSTP1 gene promoters, whereas methylation of R

42 anial xenografts, we quantitatively assessed MGMT knockdown by SNAs composed of MGMT-targeting siRNA

43 E by demonstrating enrichment of RARb2, ATM, MGMT and GSTP1 promoters in multiplexed MS-NaME reaction

44 We examined the association between MGMT expression and survival duration using tumor sample

45 nt gliomas, although the association between MGMT expression status and outcome in pediatric malignan

46 The association between MGMT overexpression and adverse outcome remained signifi

47 17 for studies about the association between MGMT promoter hypermethylation and breast and gynecologi

48 survival, as well as an association between MGMT promotor-methylated tumors and PTEN positivity show

49 re was a strong positive correlation between MGMT promotor methylation and survival, as well as an as

50 marker and elucidate the discordance between MGMT methylation, expression, and patient outcome, which

51 Discrepancies between MGMT promoter methylation status and treatment response

52 tients may stem from inconsistencies between MGMT methylation and expression levels in glioblastoma.

53 toxification of O(6)-alkylguanine adducts by MGMT is stoichiometric, it has been suggested that highe

54 ects of TMZ sensitivity are not explained by MGMT promoter methylation.

55 re recognized by DNA glycosylases and not by MGMT, and so resistance to temozolomide may also be due,

56 ent sets and improved survival prediction by MGMT promoter methylation.

57 to the basic understanding of DNA repair by MGMT.

58 w that a subset of recurrent gliomas carries MGMT genomic rearrangements that lead to MGMT overexpres

59 KN1B, TP53, BRCA1, TIMP3, APC, RASSF1, CDH1, MGMT, DAPK1, GSTP1, and RARB).

60 Leukemia cell MGMT activity was higher in pediatric ALL than AML (P <

61 ancer recursive partitioning analysis class, MGMT promoter methylation, and geographical region, and

62 senchymal, RTK I "PGFRA," RTK II "classic"), MGMT promoter methylation status, and hallmark copy numb

63 was significantly associated with decreased MGMT promoter methylation and vice versa (1425.1 for met

64 re, we determined that DNA repair-deficient (MGMT(-/-)) BM displayed sensitivity to genotoxic exposur

65 al by molecular markers (1p/19q co-deletion, MGMT promoter methylation status, and IDH1/IDH2 mutation

66 vivo, with persistent and SNA dose-dependent MGMT silencing confirmed by Western blotting of tumor ti

67 We demonstrate Wnt-dependent MGMT gene expression and cellular co-localization betwee

68 Both of these patients had no detectable MGMT activity; both also had methylated MGMT promoters a

69 ore reliable methods are needed to determine MGMT activity as DNA methylation, the current standard,

70 istance model of GBM cells with differential MGMT methylation profiles, MGMT-hypermethylation enhance

71 Here, we discuss MGMT as a biomarker and elucidate the discordance betwee

72 atinums have also been found to downregulate MGMT expression and this approach is currently under exp

73 tic inhibition of Wnt activity downregulates MGMT expression and restores chemosensitivity of DNA-alk

74 transduced with lentiviral vectors encoding MGMT* and a fluorescent marker, with or without homeobox

75 s (such as O(6)-benzylguanine) of endogenous MGMT.

76 e lower than S-CRCs for all the genes except MGMT.

77 omas and one of the normal tissues expressed MGMT, hTERT was expressed in all gliomas but not in the

78 stant GBM cell lines endogenously expressing MGMT and APNG attenuated repair of TMZ-induced DNA damag

79 wo smoker cohorts to identify novel loci for MGMT methylation in sputum that were independent of the

80 mmunohistochemistry staining for MGMT or for MGMT promoter methylation.

81 enhancer SNP to empower risk prediction for MGMT methylation.

82 ighly significantly associated with risk for MGMT methylation in lung cancer and sputum from smokers.

83 and either immunohistochemistry staining for MGMT or for MGMT promoter methylation.

84 10 x 10(6) BM-cells from MGMT-transgenic-mice were transplanted into host BALB/c

85 organism that does not possess a functional MGMT homologue.

86 Furthermore, MGMT protein expression (HR, 1.84; 95% CI, 1.38-2.43; P

87 O6-methylguanine-DNA-methyltransferase gene (MGMT) promoter methylation status.

88 In patients with glioblastoma, MGMT promoter methylation in tumor tissue was not more p

89 lassemic HSCs transduced with a gamma-globin/MGMT vector initially had subtherapeutic levels of red c

90 PS, obtaining a gross total resection (GTR), MGMT promoter-methylated gene status, unifocal disease,

91 25 (44.6%) patients had MGMT hyper-methylated tumors, 6 (10.7%) were IDH1 mutate

92 MG is therefore an MGMT substrate, and hence MGMT is likely to be a protective factor in CRC under co

93 t of chemotherapeutics in cancer cells, high MGMT expressing glioblastoma (T98G) and a high ABCB1 exp

94 r, low serum folate was associated with high MGMT methylation (P = 0.001).

95 Higher MGMT protein level was significantly associated with dec

96 genic effects of alkylating agents; however, MGMT is silenced by promoter hypermethylation during car

97 reversibly inhibits methyl transfer by human MGMT.

98 We also report evidence that in human MGMT-deficient cell-free extracts, CAF-1-dependent packa

99 inhibitor of Cx43 channels, sensitized human MGMT-deficient and TMZ-resistant GBM cells to TMZ treatm

100 markers in neuro-oncology presently are: (i) MGMT promoter methylation as a prognostic and predictive

101 no differences in patient demographics, IDH/MGMT mutation status, or treatment.

102 , NEUROG1, RUNX3, SOCS1, CHFR, HIC1, IGFBP3, MGMT, MINT1, MINT31, p14 [ARF], and WRN); microsatellite

103 16/ink4a), CHFR, CRABP1, HIC1, IGF2, IGFBP3, MGMT, MINT-1, MINT-31, MLH1, NEUROG1, p14 (CDKN2A/arf),

104 egulator, which in turn led to a decrease in MGMT expression and an increased sensitivity to TMZ.

105 ctive cytotoxicity toward cells deficient in MGMT activity.

106 h patient survival, including as observed in MGMT-deficient GBM patients.

107 ed conversion of pyruvate to lactate only in MGMT-deficient cells.

108 drug-resistant, progenitor cell phenotype in MGMT-independent pediatric glioblastoma.

109 O(6)-MeG) or O(6)-CMG effectively inactivate MGMT in vitro (IC50 0.93 and 1.8 nM, respectively).

110 us, our findings suggest that BG-inactivated MGMT may be linked to cell signaling events, forcing cel

111 Several of these genes (including MGMT, RAD17, and USP44) show prior evidence of a tumour

112 nificance of miR-4516 was retained including MGMT methylation status.

113 Increased MGMT activity may account for the temozolomide resistanc

114 ed from 12.6% to 5.7% (P = .025), increasing MGMT expression.

115 uced MGMT protein and RNA levels and induced MGMT CpG methylation in gastric AGS cells.

116 As a different strategy to inhibit MGMT we investigated cellular regulators of MGMT express

117 The use of drugs inhibiting MGMT has been hindered by their haematologic toxicity an

118 injection is capable of robust intratumoral MGMT protein knockdown in vivo, with persistent and SNA

119 ity reduced beta-catenin expression, a known MGMT regulator, which in turn led to a decrease in MGMT

120 igodeoxyribonucleotides containing the known MGMT substrate O(6)-methylguanine (O(6)-MeG) or O(6)-CMG

121 a showing the direct cleavage of full-length MGMT mRNA, knockdown of MGMT protein, and increased sens

122 atform detected 5-hmC at the regional level (MGMT promoter region) in just 10 ng of genomic DNA (gDNA

123 Low MGMT expression confers significant sensitivity to DNA a

124 status tested; 926 patients had a methylated MGMT promoter, and 545 were randomly assigned to the cil

125 oven supratentorial glioblastoma, methylated MGMT promoter, and age >/=18 years) were stratified for

126 able MGMT activity; both also had methylated MGMT promoters and were MSI stable.

127 oma (particularly in tumours with methylated MGMT promoter).

128 newly diagnosed glioblastoma with methylated MGMT promoter.

129 ing the repair protein DNA methyltransferase MGMT, although other mechanisms are thought to be active

130 nt O(6)-methylguanine-DNA methyltransferase (MGMT(P140K)) into hematopoietic stem cells (HSC) has bee

131 O-6-methylguanine-DNA methyltransferase (MGMT) activity is directly correlated to TMZ sensitivity

132 in O(6)-methylguanine DNA methyltransferase (MGMT) activity, small changes in mismatch repair (MMR),

133 cell O6-methylguanine-DNA methyltransferase (MGMT) activity, tumor and plasma MGMT promoter methylati

134 me O(6)-methylguanine-DNA methyltransferase (MGMT) are resistant to this drug.

135 by O-6-methylguanine-DNA methyltransferase (MGMT) confers one mechanism of TMZ resistance.

136 tein O6-methylguanine DNA methyltransferase (MGMT) dealkylates mutagenic O6-alkylguanine lesions with

137 ed O(6)-methylguanine-DNA methyltransferase (MGMT) fare worse, presumably because of temozolomide res

138 O6-methylguanine-DNA methyltransferase (MGMT) functions to counteract the cytotoxic effects of a

139 and O6-methylguanine DNA methyltransferase (MGMT) genes were assessed by methylation-specific polyme

140 me O(6)-methylguanine-DNA methyltransferase (MGMT) in tumor correlates with resistance to alkylating

141 O(6)-Methylguanine-DNA methyltransferase (MGMT) is a DNA repair enzyme that protects cells from ca

142 O(6)-methylguanine-DNA methyltransferase (MGMT) is an enzyme that removes alkyl groups at the O(6)

143 zyme O6-methylguanine-DNA methyltransferase (MGMT) is commonly overexpressed in cancers and is implic

144 The O-6-methylguanine-DNA methyltransferase (MGMT) is responsible for the direct repair of the main T

145 O(6)-methylguanine-DNA methyltransferase (MGMT) methylation status may be an important determinant

146 ith O-6-Methylguanine-DNA Methyltransferase (MGMT) methylation.

147 tein O6-methylguanine DNA methyltransferase (MGMT) might be reduced via hypermethylation of its promo

148 in O(6)-methylguanine-DNA methyltransferase (MGMT) or a defect in the mismatch repair (MMR) pathway.

149 with O6-methylguanine-DNA methyltransferase (MGMT) promoter methylated tumors.

150 hylguanine (O(6)-MeG)-DNA methyltransferase (MGMT) promoter methylation status is accepted as a progn

151 ne O(6)-methylguanine-DNA methyltransferase (MGMT) promoter methylation status.

152 the O6-methylguanine-DNA methyltransferase (MGMT) promoter.

153 f O (6)-methylguanine-DNA methyltransferase (MGMT) remains controversial for breast and gynecologic c

154 O(6)-methylguanine-DNA methyltransferase (MGMT) repairs the most cytotoxic of lesions generated by

155 O(6)-methylguanine DNA methyltransferase (MGMT) suppresses mutations and cell death that result fr

156 of O(6)-methylguanine-DNA methyltransferase (MGMT) was assessed.

157 of O(6)-methylguanine-DNA methyltransferase (MGMT), a DNA repair protein involved in chemotherapeutic

158 ly O(6)-methylguanine-DNA methyltransferase (MGMT), a key enzyme for resistance to alkylating agents

159 din, O6-methylguanine DNA methyltransferase (MGMT), SNAP-tag, and lactoferrin, with four different pr

160 in O(6)-methylguanine-DNA methyltransferase (MGMT), which protects against the genotoxic effects of o

161 of O(6)-methylguanine-DNA methyltransferase (MGMT)-deficient mammalian cells and yeast mgt1Delta rad5

162 tein O6-methylguanine-DNA methyltransferase (MGMT).

163 zyme O6-methylguanine-DNA methyltransferase (MGMT*).

164 e of O6-methylguanine-DNA-methyltransferase (MGMT) in glioblastoma sensitivity to the DNA alkylating

165 O6-methylguanine-DNA-methyltransferase (MGMT), which repairs alkylating agent damage, is one suc

166 in O(6)-methylguanine-DNA-methyltransferase (MGMT).

167 pression of methylguanine methyltransferase (MGMT(hi)).

168 om the O(6)-methylguanine methyltransferase (MGMT) cDNA, which confers resistance to TMZ.

169 pression of methylguanine methyltransferase (MGMT) in the tumor would correlate with drug resistance

170 lements and methylguanine methyltransferase (MGMT), driven by a constitutive cellular promoter.

171 SLFN11) and methylguanine methyltransferase (MGMT), served as indicators of therapeutic resistance or

172 of the DNA repair protein methyltransferase (MGMT), a TMZ-sensitivity determinant, after exposure to

173 nd O(6)-methylguanine-DNA methyltransferase, MGMT) by liquid chromatography/electrospray ionization m

174 Furthermore, overexpression of mito-MGMT provided greater resistance to cell killing by 1,3-

175 We introduce molecular (MGMT methylation, IDH mutation, 1p/19q co-deletion, ATRX

176 trosourea (BCNU) than overexpression of nucl-MGMT.

177 The most common assays of MGMT activity are time-consuming and employ radioactivit

178 uality for immunohistochemical assessment of MGMT expression status in 109 specimens.

179 temozolomide resistance than assessments of MGMT activity alone.

180 resistance was enhanced with coexpression of MGMT.

181 In this context, a combination of MGMT activity and mismatch repair (MMR) status of the tu

182 assessed MGMT knockdown by SNAs composed of MGMT-targeting siRNA duplexes (siMGMT-SNAs).

183 The refined NRG-GBM-RPA consisting of MGMT protein, c-Met protein, and age revealed greater se

184 Correlation of MGMT promoter methylation and improved OS and PFS was re

185 tance to alkylating agents, and depletion of MGMT activity can enhance chemotherapy-induced tumor cyt

186 mozolomide results in prolonged depletion of MGMT in blood mononuclear cells and possibly in tumor.

187 We characterized expression of MGMT and its epigenetic regulation via CpG methylation i

188 zes glioma cells with elevated expression of MGMT and those deficient in MMR, two genotypes normally

189 These data show that very high expression of MGMT(P140K) has a deleterious effect on cellular prolife

190 Moreover, very high expression of MGMT(P140K) was associated with a competitive repopulati

191 ation associated with elevated expression of MGMT(P140K), but not wild-type MGMT.

192 ically low due to insufficient expression of MGMT.

193 oes not accurately reflect the expression of MGMT.

194 rade II, it is unclear whether the extent of MGMT promotor methylation and its prognostic role is ind

195 Collectively, extent of MGMT promotor methylation was strongly associated with o

196 ains, is associated with hypermethylation of MGMT and reduced levels of MGMT in the gastric epitheliu

197 the association between hypermethylation of MGMT promoter and the risk of breast and gynecologic can

198 Secondary analyses evaluated the impact of MGMT status.

199 e reported that have activity independent of MGMT, MMR, and p53.

200 ls that contain mutations K165E and K165N of MGMT, respectively, displayed a normal cell cycle progre

201 avage of full-length MGMT mRNA, knockdown of MGMT protein, and increased sensitization of GBM cells t

202 We also found that lack of MGMT expression in pretreated GBM is linked to hypermuta

203 In the majority of cell lines, a lack of MGMT promoter methylation and subsequent protein overexp

204 Conversely, the highest level of MGMT(P140K) activity did not promote efficient in vivo p

205 microfluidic chip to analyse mRNA levels of MGMT and APNG in enriched tumour exosomes obtained from

206 Organoids with reduced levels of MGMT and CHFR expression were sensitive to temozolomide

207 mide has been ascribed to elevated levels of MGMT and/or reduced mismatch repair.

208 e 97 patients whose tumors had low levels of MGMT expression versus 8.3% +/- 8% in the 12 patients wh

209 permethylation of MGMT and reduced levels of MGMT in the gastric epithelium.

210 it has been suggested that higher levels of MGMT will afford better protection to gene-modified HSC.

211 owed by down-modulation of the RNA levels of MGMT.

212 ct correlated with increased localization of MGMT(P140K) to the nucleus/chromatin.

213 CpG methylation of MGMT was more frequent in the gastric mucosa of patients

214 The prediction models of MGMT methylation, IDH mutations, 1p/19q co-deletion, ATR

215 e 109 samples demonstrated overexpression of MGMT compared with normal brain.

216 Overexpression of MGMT in childhood malignant gliomas is strongly associat

217 entially other tumors with overexpression of MGMT.

218 Furthermore, based on patterns of MGMT expression across different solid tumors, we make a

219 cant effect on the predictive performance of MGMT methylation IDH mutations, 1p/19q co-deletion, and

220 d by prolonged incubation in the presence of MGMT, again suggesting that O(6)-meG in the substrate is

221 e 7, and hypermethylation of the promoter of MGMT were available for some of the cases.

222 a-retroviral vectors that express a range of MGMT(P140K) activity, we show that MGMT(P140K) expressio

223 ith a unique 5-hmC in the promoter region of MGMT tumor suppressor gene.

224 MGMT we investigated cellular regulators of MGMT expression in multiple cancers.

225 nsfer to the active-site cysteine residue of MGMT.

226 t did confirm the prognostic significance of MGMT methylation.

227 Epigenetic silencing of MGMT has been associated with prolonged survival in adul

228 Treatment of MGMT-deficient cells with temozolomide increased sensiti

229 his process forms the basis of treatments of MGMT-deficient cancers with Sn1-type methylating drugs.

230 UBR1 attenuation reduced turnover of MGMT protein and increased repair of O6-methylguanine in

231 ween tumor cells and normal tissues based on MGMT expression, as a means to enhance selective tumor c

232 xis in a manner that was highly dependent on MGMT status.

233 effects of H pylori infection eradication on MGMT expression.

234 o study the effects of H pylori infection on MGMT RNA, protein expression, and CpG methylation.

235 This protein is called Mgmt (or MGMT) in mammals and Mgt1 in the yeast Saccharomyces cer

236 n the 12 patients whose tumors overexpressed MGMT (P = .017, exact log-rank test).

237 of 11 genes (MINT1, 2, 31, hMLH1, p16, p14, MGMT, HPP1, SFRP1, ERalpha, and LINE-1) in 48 UC-Cs, 21

238 Paradoxically, MGMT-deficient GBM patients survive longer despite still

239 ransferase (MGMT) activity, tumor and plasma MGMT promoter methylation, and microsatellite instabilit

240 h repair genes MLH1, MSH2, MLH3, MSH6, PMS2, MGMT and MLH3 via methylation specific multiplex ligatio

241 unctional congener as optimized for potency, MGMT-independence, and MMR-independence.

242 with differential MGMT methylation profiles, MGMT-hypermethylation enhanced genetic and phenotypic pl

243 pondence to two representative MDR proteins, MGMT (a DNA repair protein) and ABCB1 (an efflux protein

244 f Chk1; this effect was dependent on reduced MGMT expression.

245 H pylori reduced MGMT protein and RNA levels and induced MGMT CpG methyla

246 nchial epithelial cells, while also reducing MGMT promoter activity and abolishing MGMT induction.

247 support the importance of UBR1 in regulating MGMT homeostasis and DNA repair of alkylated DNA adducts

248 d with temozolomide to overcome the reported MGMT-mediated resistance.

249 , all but six markers (CACNA1G, IGF2, RUNX3, MGMT, MINT-1, and SOCS1) were differentially clustered w

250 Monofunctional alkylating agents sensitize MGMT-deficient tumor cells to ATR inhibitors.

251 diotherapy, kills tumor cells, has not shown MGMT dependency, and elicits an antitumor vaccine effect

252 tivity by combining them with tumor-targeted MGMT inhibitors.

253 s a novel approach for selectively targeting MGMT-deficient cells with ATR inhibitors and temozolomid

254 cute leukemia not treated with temozolomide (MGMT, n = 67; MSI, n = 65).

255 on of genes known to be methylated in TGCTs (MGMT, RASSF1A, and HOXA9).

256 This meta-analysis indicated that MGMT hypermethylation was significantly associated with

257 range of MGMT(P140K) activity, we show that MGMT(P140K) expression by weaker cellular promoter/enhan

258 The pooled results showed that MGMT promoter methylation status was significantly assoc

259 These data suggest that MGMT-based drug selection holds promise as a modality to

260 The MGMT status was prognostic.

261 Three SNPs in the MGMT gene (adjusted analysis, rs3858300; unadjusted anal

262 ide polymorphism (SNP) in an enhancer in the MGMT promoter was previously identified to be highly sig

263 Inclusion of HOXB4 in the MGMT* vectors resulted in no substantial increase in gen

264 ation in sputum that were independent of the MGMT enhancer polymorphism.

265 ylation status of the promotor region of the MGMT gene were analyzed from tumor tissue.

266 p300 was required to induce silencing of the MGMT gene.

267 methylation and subsequent silencing of the MGMT promoter are sensitive to temozolomide.

268 Methylation of the MGMT promoter in GBM correlates with increased therapeut

269 ts in glioma cells and demonstrated that the MGMT genomic rearrangements contribute to TMZ resistance

270 RGD prevented the recruitment of p300 to the MGMT promoter.

271 sequencing of the CpG sites 74-98 within the MGMT promotor region.

272 R/Cas9 technology we generated some of these MGMT rearrangements in glioma cells and demonstrated tha

273 process of aberrant DNA methylation of this MGMT promoter CpG island in lung tumours.

274 in CoMs development and that of MLH1, TIMP2, MGMT, and ECHS1 in metastatic CoMs is warranted.

275 ies MGMT genomic rearrangements that lead to MGMT overexpression, independently from changes in its p

276 We found that the predisposition to MGMT methylation arising from the 15q15.2 locus involved

277 n as a major mechanism for predisposition to MGMT methylation in the lungs of smokers, and support th

278 evolution of glioblastoma (GBM) relative to MGMT methylation remain unclear.

279 s] showing amino acid sequence similarity to MGMT, but where the cysteine at the putative active site

280 esection, methyl-guanine-methyl-transferase (MGMT) promoter methylation, age, Karnofsky performance s

281 tility of methyl-guanine-methyl-transferase (MGMT)-transgenic-C57BL/6 BM into a major histocompatibil

282 fication included clinical factors and tumor MGMT methylation status.

283 Of these patients, 3060 had tumour MGMT status tested; 926 patients had a methylated MGMT p

284 expression of MGMT(P140K), but not wild-type MGMT.

285 h 5azadC downregulated hTERT and upregulated MGMT expression in two glioma cell lines, there was no c

286 The development of clinically useful MGMT assays should permit the identification of tumors w

287 chimerism without GVHD can be achieved using MGMT transgenic BM in a mixed-chimerism model receiving

288 ongoing clinical gene therapy studies using MGMT(P140K), whereas the novel mechanistic findings are

289 identified in human GBM specimens that were MGMT methylated but showed poor survival.

290 ity towards adaptive resistance to TMZ while MGMT hypomethylation limited plasticity.

291 reater prognostic value for OS compared with MGMT promoter methylation (HR, 1.77; 95% CI, 1.28-2.44;

292 Response did not correlate with MGMT expression or promoter methylation as a continuous

293 e and high-level donor-cell engraftment with MGMT transgenic C57BL/6 BMT after BCNU treatment, demons

294 In patients with MGMT promoter methylation, temozolomide monotherapy may

295 Three patients with MGMT unmethylated glioblastoma multiforme survived 6.5,

296 7 newly diagnosed glioblastoma patients with MGMT(hi) tumors.

297 ker to predict the survival of patients with MGMT-independent TMZ resistance and that combining a Cx4

298 In 1 animal, cells transduced with MGMT* lentiviral vectors were protected and expanded aft

299 ivity of these agents to include tumors with MGMT activity by combining them with tumor-targeted MGMT

300 f GBM driver instability was observed within MGMT promoter-methylated tumors.