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 provides cellular resistance to alkylato

6 MGMT expression was assessed by methylation-specific pyr

7 MGMT methylation was associated with G-to-A mutation in

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 methylation is partially reversible after

12 MGMT promoter methylation was assessed on patient tumor

13 MGMT(P140K) overexpression prevented the substantial mye

14 cinomas at p14 (P = 0.04), hMLH1 (P = 0.04), MGMT (P = 0.01), MINT1 (P = 0.01), MINT25 (P = 0.01), MI

15 resistance related proteins, such as BCRP-1, MGMT, MDR-1, MRP-1 and MRP-3, after TRP-2 transfection.

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

17 ducing MGMT promoter activity and abolishing MGMT induction.

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

19 of methyl groups to human alkyltransferase (MGMT).

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

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

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

23 %), MT1G (20%), NORE1A (19%), CDH1 (16%) and MGMT (9%) and not or rarely at SDHB (4%), RARB2 (0%), p1

24 incidence of methylation at CASP8 (43%) and MGMT (30%), intermediate frequencies at NORE1A (15%), p1

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

26 localization between active beta-catenin and MGMT.

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

28 epair/drug detoxification (BRCA1, GSTP1, and MGMT) was associated with improved response to chemother

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

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

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

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

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

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

35 GCT component was methylated for RASSF1A and MGMT, while the seminoma component was methylated only f

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

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

38 eta, but methylation at p14, p16, THBS1, and MGMT was tumor-specific.

39 thylation of nine gene promoters (CDH1, APC, MGMT, RASSF1A, GSTP1, p16, RAR-beta2, and ARF) from 17 p

40 ally inactivated in cancer (p16(INK4A), APC, MGMT, GSTP1, DAPK, CDH1, CDH13, RARbeta and FHIT) in 24

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

42 A combination of only four genes (p16, ARF, MGMT, and GSTP1) would theoretically allow us to detect

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

44 re frequent in carcinoid tumors than PETs at MGMT (25 versus 0%, p = 0.03), THBS1 (44 versus 9%, p =

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

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

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

48 The association between MGMT overexpression and adverse outcome remained signifi

49 17 for studies about the association between MGMT promoter hypermethylation and breast and gynecologi

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

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

52 date genes were methylated in seminomas, but MGMT (44%), APC (29%) and FHIT (29%) were frequently met

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

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

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

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

62 ter methylation at CASP8, CDH1, CDH13, DAPK, MGMT, NORE1A, p14ARF and RARB2 in primary Wilms' tumours

63 tumours and CASP8, CDH1, CDH13, CRBP1, DAPK, MGMT, MT1G, NORE1A, p16INK4a, SDHB and RARB2 in primary

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

65 e methylguanine methyltransferase deficient (MGMT(-)), were treated with the methylating agent MNNG t

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

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

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

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

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

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

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 humans - with a novel drug-resistance gene, MGMT, which is not expressed in normal HSCs (see the rel

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

90 lts were extended using a novel gamma-globin/MGMT dual gene lentiviral vector.

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

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

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

94 Higher MGMT protein level was significantly associated with dec

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

96 reversibly inhibits methyl transfer by human MGMT.

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

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

99 31) demonstrated circulating hypermethylated MGMT, RAR-beta2, and RASSF1A DNA for at least one of the

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

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

102 16/ink4a), CHFR, CRABP1, HIC1, IGF2, IGFBP3, MGMT, MINT-1, MINT-31, MLH1, NEUROG1, p14 (CDKN2A/arf),

103 ctive cytotoxicity toward cells deficient in MGMT activity.

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

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

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

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

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

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

110 Increased MGMT activity may account for the temozolomide resistanc

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

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

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

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

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

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

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

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

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

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

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

122 newly diagnosed glioblastoma with methylated MGMT promoter.

123 and O6-methylguanine DNA methylatransferase (MGMT) (34%), and death-associated protein kinase (DAPK)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 et O(6)-methylguanine DNA methyltransferase (MGMT) to the mitochondria and examine its impact on cell

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

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

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

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

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

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

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

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

154 ss O(6)-methylguanine-DNA-methyltransferase (MGMT) displayed a transient cell cycle G2/M arrest in re

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

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

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

158 140K O6-methylguanine-DNA-methyltransferase (MGMT[P140K]) gene transduction and O6-benzylguanine/1,3-

159 OX2), O(6)-methyl-guanine methyltransferase (MGMT), estrogen receptor (ER), retinoic acid receptor be

160 OX2), O(6)-methyl-guanine methyltransferase (MGMT), estrogen receptor (ER), thrombospondin 1 (THBS1),

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

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

163 transfer a methylguanine methyltransferase (MGMT) drug-resistance gene into normal bone marrow cells

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

165 beta), O(6)-methylguanine methyltransferase (MGMT), and human mutL homologue 1 (hMLH1) genes as deter

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

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

168 stance gene methylguanine methyltransferase (MGMT), which encodes a DNA-repair enzyme that confers re

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

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

171 ted O(6)-benzylguanine (6BG)-resistant MGMT (MGMT(P140K)) to the nucleus or the mitochondria, committ

172 not enhance the resistance provided by mito-MGMT alone.

173 Overexpression of either mito-MGMT or nucl-MGMT also conferred a similar level of resi

174 l-MGMT) or mitochondrial-targeted MGMT (mito-MGMT).

175 Simultaneous overexpression of mito-MGMT and nucl-MGMT did not enhance the resistance provid

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

177 fected with human wild type and K165E mutant MGMT cDNA, respectively.

178 cells expressing wild-type MGMT and mutated MGMT were confirmed in CHO cells transfected with human

179 taneous overexpression of mito-MGMT and nucl-MGMT did not enhance the resistance provided by mito-MGM

180 transfected with nuclear-targeted MGMT (nucl-MGMT) or mitochondrial-targeted MGMT (mito-MGMT).

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

182 Overexpression of either mito-MGMT or nucl-MGMT also conferred a similar level of resistance to met

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

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

185 temozolomide resistance than assessments of MGMT activity alone.

186 resistance was enhanced with coexpression of MGMT.

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

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

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

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

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

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

193 large-animal data support the evaluation of MGMT(P140K) in conjunction with O(6)BG and temozolomide

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

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

196 icient lentiviral transfer and expression of MGMT into relatively few HSCs led to repopulation of mos

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

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

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

200 oes not accurately reflect the expression of MGMT.

201 ically low due to insufficient expression of MGMT.

202 The frequency of MGMT methylation was higher in stage 1 and 2 tumours (50

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

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

205 Hypermethylation of MGMT, RASSF1A, and DAPK was significantly lower in prima

206 Secondary analyses evaluated the impact of MGMT status.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 Overexpression of MGMT in childhood malignant gliomas is strongly associat

222 entially other tumors with overexpression of MGMT.

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

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

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

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

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

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

229 irst evidence of potent in vivo selection of MGMT(P140K) lentivirus-transduced human SRCs following B

230 t did confirm the prognostic significance of MGMT methylation.

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

232 e that mitochondrial or nuclear targeting of MGMT protects hematopoietic cells against cell killing b

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

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

235 effects of H pylori infection eradication on MGMT expression.

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

237 ted between methylation of RASSF1A, CASP8 or MGMT in individual tumours.

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

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

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

241 UNX3, RIZ1, CRBP1, 3-OST-2, APC, TIMP3, p16, MGMT, p14) for promoter hypermethylation in 77 EAC, 93 B

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

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

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

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

246 Two dogs received MGMT(P140K)-transduced autologous CD34(+)-selected cells

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

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

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

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

251 targeted O(6)-benzylguanine (6BG)-resistant MGMT (MGMT(P140K)) to the nucleus or the mitochondria, c

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

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

254 d MGMT (nucl-MGMT) or mitochondrial-targeted MGMT (mito-MGMT).

255 cells were transfected with nuclear-targeted MGMT (nucl-MGMT) or mitochondrial-targeted MGMT (mito-MG

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

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

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

259 These studies demonstrate that MGMT-based in vivo selection may be useful to increase g

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

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

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

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

264 The MGMT status was prognostic.

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

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

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

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

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

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

271 confers resistance to the combination of the MGMT inhibitor O(6)-benzylguanine (O(6)BG) and nitrosour

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

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

274 rinary cancer revealed no methylation of the MGMT, GSTP1, p16, and ARF genes, whereas methylation of

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

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

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

278 al tissues; and CpG islands at DAPK1, TIMP3, MGMT, CDKN2b, p14/ARF, and CDH1 were not abnormally hype

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

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

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

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

283 fication included clinical factors and tumor MGMT methylation status.

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

285 and BCNU between cells expressing wild-type MGMT and mutated MGMT were confirmed in CHO cells transf

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

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

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

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

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

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 uman NOD/SCID repopulating cells (SRCs) with MGMT(P140K) using a lentiviral vector and infused them i

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

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