ライフサイエンスコーパス: aberrant methylation

1 that one allele of the MGMT promoter has an aberrant methylation.

2 suggesting that the CDX1 gene is a target of aberrant methylation.

3 recursor of endometrial carcinoma) for hMLH1 aberrant methylation.

4 to the protection from or susceptibility to aberrant methylation.

5 Aberrant methylation also contributes to later stages of

6 xtensive epigenetic abnormalities, including aberrant methylation and abnormal imprinted gene express

7 urther evidence for a potential link between aberrant methylation and diseases of aging.

8 d from 5-azacytidine-treated patients lacked aberrant methylation and DNMTi treatment of primary MDS

9 ning and gene expression profiling, we found aberrant methylation and epigenetic silencing of a small

10 Offspring of F0(DSS) males exhibited aberrant methylation and expression patterns of multiple

11 enome-wide epigenetic studies to investigate aberrant methylation and histone code patterns, the two

12 To provide a baseline estimate of global aberrant methylation and identify target sequences for a

13 Aberrant methylation and silencing of TMS1 was accompani

14 differ in their intrinsic susceptibility to aberrant methylation and that this susceptibility can be

15 denocarcinomas; (b) the frequency of RASSF1A aberrant methylation and the value of the methylation in

16 however, the mechanisms responsible for this aberrant methylation are poorly understood.

17 High levels of aberrant methylation at CIMP-related markers in MSH2-met

18 r (ER) alpha-negative breast tumors displays aberrant methylation at one site within the ER gene CpG

19 nts occurring at fertilization, resulting in aberrant methylation at some promoters and repetitive el

20 ific effects play a strong role in recurrent aberrant methylation at specific CpG sites across differ

21 2), indicating that PatMAn predicts not only aberrant methylation, but also PRC2 binding.

22 CXXC domain allows TET1 to protect CGIs from aberrant methylation, but it also limits its ability to

23 nance of T-cell lymphomas and contributes to aberrant methylation by both de novo and maintenance met

24 NA methyltransferases are needed, given that aberrant methylation by these enzymes is associated with

25 The aberrant methylation can begin very early in tumor progr

26 These results indicate that aberrant methylation can cooperate with chromosome delet

27 biological investigations, such as checking aberrant methylation changes during tumorigenesis, monit

28 Aberrant methylation changes, often present in a minor a

29 Methylight) to boost detection of low-level aberrant methylation-changes.

30 Aberrant methylation, consisting of DNA hypomethylation

31 Aberrant methylation contributes to the pathogenesis of

32 Our results show that most aberrant methylation events are focal and independent of

33 Sixty percent of aberrant methylation found in tumors is also present in

34 r study shows that DNMT1 mutations cause the aberrant methylation implicated in complex pathogenesis.

35 quent in breast and renal carcinoma, showing aberrant methylation in 30 and 20% of the cases, respect

36 hese results provide evidence for widespread aberrant methylation in AML, with identification of nove

37 dditional cellular factors exist that govern aberrant methylation in breast cancer cells.

38 pe from apoptosis, supporting a new role for aberrant methylation in breast tumorigenesis.

39 amine the major uses of RLGS in the study of aberrant methylation in cancer and discuss the significa

40 This is consistent with the notion that aberrant methylation in cancer may be attributable to ta

41 slands remain unmethylated, a subset accrues aberrant methylation in cancer via unknown mechanisms.

42 To study the potential mechanisms underlying aberrant methylation in cancer, we have determined the m

43 t CDH13 expression is frequently silenced by aberrant methylation in colorectal cancers and adenomas

44 f CDH13 by luciferase assay and examined its aberrant methylation in colorectal cancers, cell lines,

45 evalence of genes known to be deregulated by aberrant methylation in HCC (e.g., Ras association [RalG

46 some 12q23.1 that was affected frequently by aberrant methylation in human astrocytomas and oligodend

47 ave been previously described as targets for aberrant methylation in human cancer.

48 a non-genetic biological mechanism underlies aberrant methylation in iPSCs and that it is likely base

49 ibility that MSH2 is a target susceptible to aberrant methylation in Lynch syndrome.

50 Aberrant methylation in MDS and secondary AML tended to

51 demonstrate a relationship between SV40 and aberrant methylation in MMs.

52 Finally, we identified aberrant methylation in multiple genes also targeted by

53 omplex 2 (PRC2) complex and silenced through aberrant methylation in non-small-cell lung cancer cell

54 suggest that SPARC is a frequent target for aberrant methylation in pancreatic cancer and that SPARC

55 To identify potential targets for aberrant methylation in pancreatic cancer, we analyzed g

56 approach, we identified 7 novel targets for aberrant methylation in pancreatic cancer.

57 many of them may represent novel targets for aberrant methylation in pancreatic carcinoma.

58 the relevance of defective MGMT function by aberrant methylation in relation to the presence of K-ra

59 the relevance of defective MGMT function by aberrant methylation in relation to the presence of p53

60 nzymes and methylation-specific PCR, we find aberrant methylation in the AR expression-negative cell

61 ach to be a powerful method to uncover novel aberrant methylation in the cancer epigenome.

62 We identified aberrant methylation in the CpG island of SOCS-1 that co

63 The active role of the aberrant methylation in transcriptional silencing of gen

64 ors, most of which have never been linked to aberrant methylation in tumors.

65 RLGS was used to study aberrant methylation in two mouse models that overexpres

66 Aberrant methylation in urine and serum DNA generally wa

67 are crucial for eukaryotic development, and aberrant methylation-induced silencing of tumour suppres

68 ate tumor suppressor gene whose silencing by aberrant methylation is a common and early event in huma

69 f certain cytosines with a methyl group, and aberrant methylation is a hallmark of human diseases inc

70 Aberrant methylation is a major mech-anism for loss of f

71 t epigenetic inactivation of RASSF1A through aberrant methylation is an early step in thyroid tumorig

72 Aberrant methylation is associated with disease progress

73 ation profiling allowed us to determine that aberrant methylation is commonly present in normal aging

74 This aberrant methylation is evident in 83% of papillary thyr

75 inogenesis hinges on the question of whether aberrant methylation is sufficient to drive gene silenci

76 erestingly, LOI status did not correspond to aberrant methylation levels of the imprinted DMRs or wit

77 This aberrant methylation may be due to increased expression

78 Aberrant methylation of 5' CpG islands is thought to pla

79 Aberrant methylation of 5'CpG islands is a key epigeneti

80 expression of TMS1 that was associated with aberrant methylation of a CpG island in the promoter of

81 active maternal allele of the H19 gene, and aberrant methylation of a differentially methylated regi

82 pecific loss of transcription may arise from aberrant methylation of a nonmutated promoter region, id

83 had hMLH1 promoter hypermethylation, whereas aberrant methylation of any of the other mismatch repair

84 remission ones: in 82 of those with initial aberrant methylation of at least one gene, 59 (72%) had

85 Using MSP, we detected aberrant methylation of at least one locus in 60% of car

86 Aberrant methylation of at least one of these genes was

87 Aberrant methylation of at least one of these genes was

88 analysis in a larger panel of specimens, and aberrant methylation of at least one of these three gene

89 Aberrant methylation of CACNA1G was also examined in var

90 Aberrant methylation of candidates was further confirmed

91 Our results demonstrate frequent aberrant methylation of CDH13 in breast and lung cancers

92 Aberrant methylation of CDH13 was present in 7 of 13 (54

93 ion of a particular DNA methyltransferase to aberrant methylation of Cosmc in these cells.

94 Aberrant methylation of COX2 was also detected in 12 of

95 Aberrant methylation of CpG island DNA blocked Pol II re

96 Aberrant methylation of CpG islands acquired in tumor ce

97 Aberrant methylation of CpG islands and genomic deletion

98 Aberrant methylation of CpG islands and silencing of the

99 Aberrant methylation of CpG islands in gene promoters of

100 Aberrant methylation of CpG islands in human tumors has

101 Aberrant methylation of CpG islands in promoter regions

102 Aberrant methylation of CpG islands in promoter regions

103 TGF-beta during carcinogenesis could involve aberrant methylation of CpG islands in the 5' region of

104 ning (RLGS) is useful for global analysis of aberrant methylation of CpG islands, but has not been am

105 Aberrant methylation of CpG-dense islands in the promote

106 werful approach for studying the dynamics of aberrant methylation of critical tumor suppressor genes

107 WTs with normal imprinting of IGF2 also show aberrant methylation of CTCF binding sites, indicating t

108 Epigenetic editing of gene expression by aberrant methylation of DNA may help tumor cells escape

109 Cancers often exhibit an aberrant methylation of gene promoter regions that is as

110 we show that one category of DNA alteration, aberrant methylation of gene promoter regions, can enorm

111 Our results suggest that aberrant methylation of GSTP1 may contribute to the carc

112 human tumors originating in other organs for aberrant methylation of GSTP1 using methylation-specific

113 type-phenotype relationship in BWS, in which aberrant methylation of H19 and LIT1 and UPD are strongl

114 We thus demonstrate aberrant methylation of human TSHR as a likely molecular

115 ha) gene expression has been associated with aberrant methylation of its CpG island in a significant

116 16 cells determined that these cells possess aberrant methylation of multiple CpG dinucleotides withi

117 Aberrant methylation of multiple CpG islands has been de

118 umor and the matched urine and serum DNA for aberrant methylation of nine gene promoters (CDH1, APC,

119 Furthermore, aberrant methylation of NORE1A and SOCS3 promoters was o

120 Aberrant methylation of normally unmethylated CpG island

121 geal, and endometrial neoplasms and gliomas, aberrant methylation of p14ARF was a relatively common e

122 Aberrant methylation of p15 (>10%) was found in 27% of p

123 Aberrant methylation of p15INK4B is associated with tran

124 thermore, methylation analyses revealed that aberrant methylation of pinin CpG islands was correlated

125 These data indicate that aberrant methylation of ppENK and its transcriptional re

126 Because aberrant methylation of ppENK or p16 was more often dete

127 cing of Hsp47 in NB cells is associated with aberrant methylation of promoter CpG islands and that Hs

128 Aberrant methylation of promoter CpG islands in cancer i

129 or genes in human cancers is associated with aberrant methylation of promoter region CpG islands and

130 Gene silencing associated with aberrant methylation of promoter region CpG islands is a

131 Aberrant methylation of promoter region CpG islands is a

132 Gene silencing associated with aberrant methylation of promoter region CpG islands is o

133 Epigenetic silencing associated with aberrant methylation of promoter region CpG islands is o

134 Epigenetic silencing involving the aberrant methylation of promoter region CpG islands is w

135 Aberrant methylation of promoter sequences is observed a

136 SV40-infected HM showed progressive aberrant methylation of seven genes (RASSF1A, HPP1, DcR1

137 Lastly, aberrant methylation of several genomic loci was confirm

138 Aberrant methylation of TFPI-2 was also detected in 73%

139 Aberrant methylation of TFPI2 was detected in almost all

140 tidine (5-aza-dC) treatment, suggesting that aberrant methylation of the ABCG2 gene was associated wi

141 ndance, as measured by real-time RT-PCR, and aberrant methylation of the ATM gene promoter.

142 Aberrant methylation of the ATM promoter was independent

143 reast tumors (stage II or greater) displayed aberrant methylation of the ATM proximal promoter region

144 We investigated the possibility that aberrant methylation of the CpG island flanking the 5' t

145 These results indicate that aberrant methylation of the CpG island in the CDX1 promo

146 n of p16/CDKN2 in gliomas may be mediated by aberrant methylation of the CpG island, which is in the

147 eyed 111 ductal carcinomas of the breast for aberrant methylation of the estrogen receptor-alpha and

148 To test whether aberrant methylation of the FHIT gene may play a role in

149 whether SV40 infection of normal HM induces aberrant methylation of the genes previously studied in

150 Most of the cell lines were shown to have aberrant methylation of the GPC3 promoter region.

151 lated DNA sequences, we now demonstrate that aberrant methylation of the p16 and/or O6-methyl-guanine

152 Aberrant methylation of the p16 gene was found in 12% of

153 he first time that an epigenetic alteration, aberrant methylation of the p16 gene, can be an early ev

154 cell cycle regulation and Rb-/- cells showed aberrant methylation of the paternally expressed gene 3

155 ined bisulfite restriction analysis revealed aberrant methylation of the POU2F3 promoter in 18 of 46

156 Aberrant methylation of the ppENK gene was found in 7.7%

157 Aberrant methylation of the promoter region has emerged

158 with chromosome deletion at the FZD9 locus, aberrant methylation of the remaining allele was associa

159 ction of human mesothelial cells (HM) causes aberrant methylation of the tumor suppressor gene (TSG)

160 are pivotal in maintaining and perpetuating aberrant methylation of the VHL CpG island.

161 Here we studied the nature of aberrant methylation of the von Hippel-Lindau (VHL) dise

162 The aberrant methylation of these genes represents a new ave

163 by mutations in mismatch repair genes or by aberrant methylation of these genes stabilizing their do

164 In contrast, no such aberrant methylation of these genes was observed in norm

165 analysis of primary patient samples revealed aberrant methylation of TIMP-2 in 33/90 (36.7%) cases of

166 Aberrant methylation of TIMP-3 occurred in primary cance

167 Tumors that exhibited aberrant methylation of TMS1 generally expressed reduced

168 11 of 27) of primary breast tumors exhibited aberrant methylation of TMS1.

169 Aberrant methylation of tumor suppressor genes can lead

170 ility, epigenetic instability results in the aberrant methylation of tumor suppressor genes.

171 hylation also represents the first report of aberrant methylation on an X-linked gene associated with

172 rostate cancer cells due at least in part to aberrant methylation or gene amplification.

173 thylated CpG island in normal cells and that aberrant methylation overcomes these boundaries to direc

174 Detection of aberrant methylation pattern could serve as an excellent

175 Here, we report an aberrant methylation pattern that may be responsible for

176 required for normal development of mice, and aberrant methylation patterns are associated with certai

177 -chromosome inactivation, and imprinting yet aberrant methylation patterns are one of the most common

178 Aberrant methylation patterns have long been known to ex

179 rks from the somatic cell type of origin and aberrant methylation patterns in hiPSCs.

180 plain this suppressive effect but identified aberrant methylation patterns in MYD88 wild-type patient

181 alternative mechanism for the genesis of the aberrant methylation patterns observed in tumor cells.

182 Aberrant methylation patterns occur in several inherited

183 cal to CpG island promoters, suggesting that aberrant methylation patterns of non-CpG island promoter

184 As aberrant methylation patterns often accompany disease st

185 mutations in several driver genes can cause aberrant methylation patterns, a hallmark of cancer.

186 ool for the investigation of both normal and aberrant methylation patterns.

187 The hypothesis that aberrant methylation plays a direct causal role in carci

188 ctors (clone and passage), and we found that aberrant methylation preferentially occurs at CpGs assoc

189 y-5-azacytidine treatment of cell lines with aberrant methylation restored gene expression.

190 To examine whether this aberrant methylation results from genetic variation or n

191 ethylation levels, but specifically prevents aberrant methylation spreading into CGIs in differentiat

192 (6/20) of breast cancer cell lines, and the aberrant methylation status was strongly associated with

193 The incidence of aberrant methylation was 65% in the 26 human primary HCC

194 Aberrant methylation was also detected in four of eight

195 ted genes CD37, HDAC1, NOTCH1, and CDK5 when aberrant methylation was associated with inverse changes

196 Inactivation of MGMT by aberrant methylation was associated with the appearance

197 In gliomas and colorectal carcinomas, aberrant methylation was detected in 40% of the tumors,

198 Aberrant methylation was found in several breast cancer

199 In addition, aberrant methylation was found in three CpG islands (MIN

200 p14ARF aberrant methylation was not related to the presence of

201 Aberrant methylation was seen in every sample, on averag

202 Finally, the significance of aberrant methylation was shown by sensitivity of MPN-der

203 promoter of the RASSF1 gene, frequencies of aberrant methylation were significantly lower in MMs tha

204 in tumor cells as well as the association of aberrant methylation with long-range silencing of neighb