ライフサイエンスコーパス: CIMP

1 CIMP (CpG island methylator phenotype) is an epigenetic

2 CIMP has been reported to be useful for predicting progn

3 CIMP high was defined as methylation at 2 or more of the

4 CIMP in CRC may result from activating mutations in eith

5 CIMP is tightly correlated with cancer-specific hypermet

6 CIMP melanomas exhibited hypermethylation of genes impor

7 CIMP melanomas occurred as early as tumor stage 1b and,

8 CIMP melanomas occurred as early as tumor stage 1b and,

9 CIMP shifted the pressure-length relationship to the lef

10 CIMP+ tumors also have a high incidence of p16 and THBS1

11 CIMP-high ACC possess abnormal DNA methylation and frequ

12 CIMP-high HPs were present primarily in patients with a

13 CIMP-high unstable tumors also were more likely to have

14 5% CI: 1.34, 2.12; Pheterogeneity <= 0.001), CIMP-high CRC (OR per 5 kg/m2: 1.57; 95% CI: 1.30, 1.89;

15 uently contained BRAF mutations (P = .0041), CIMP-high (P = .013), and MSI-high (P = .037).

16 in 16 (70%) of 23 CIMP+ tumors, 1 (8%) of 12 CIMP intermediate tumors, and 1 (5%) of 21 CIMP- tumors

17 We found 9 (15.2%) CIMP-(+) EOCRC patients related with the proximal colon

18 2 CIMP intermediate tumors, and 1 (5%) of 21 CIMP- tumors (P<0.0001).

19 lation of p16 was detected in 16 (70%) of 23 CIMP+ tumors, 1 (8%) of 12 CIMP intermediate tumors, and

20 Methylation status was evaluated using 6 CIMP-related markers (MINT1, MINT2, MINT31, p16(INK4alph

21 Methylation analysis of 7 CIMP-related markers revealed that the mean number of me

22 (52 of 108) of adenomas with 25% (19 of 76) CIMP-high (two or more methylated loci) and 32% (24 of 7

23 or more methylated loci) and 32% (24 of 76) CIMP-low (one methylated locus).

24 e proximal colon (p = 0.008), and 19 (26.8%) CIMP-(+) LOCRC patients associated with tumor differenti

25 A CIMP-high (CIMP-H) subgroup, which exhibits an exception

26 A CIMP-low (CIMP-L) subgroup is enriched for KRAS mutation

27 entage of genes, whereas a subset displays a CIMP+ phenotype.

28 Although CIMP appears as a phenomenon that occurs in various canc

29 Although CIMP is probably the cause of high-frequency microsatell

30 We analyzed CIMP status of 229 individuals with CRC using an eight-m

31 ediction accuracy of CIMP/D29 MRD (0.79) and CIMP/D15 MRD (0.75) classification was comparable, indic

32 at were hypermethylated in both non-CIMP and CIMP colon cancers when compared with normal colon.

33 ethylation profiles of normal, non-CIMP, and CIMP colon specimens.

34 clearly classified as normal, non-CIMP, and CIMP, thus signifying that these three groups have disti

35 These findings suggest that CIN and CIMP represent 2 independent and inversely related mecha

36 differentially clustered with CIMP-high and CIMP-low according to KRAS and BRAF status.

37 Pheterogeneity = 0.02, between CIMP-high and CIMP-low/CIMP-negative cancer risks).

38 was associated with type 2; CDKN2A loss and CIMP in type 2 conveyed a poor prognosis.

39 d and elevated levels of DNA methylation and CIMP+ tumors have distinctive clinicopathological and mo

40 th sham, CIMP was decreased in AVF mice, and CIMP protein transfer increased plasma and LV tissue lev

41 tula (AVF) was created in C57BL/J6 mice, and CIMP was administered to AVF and sham mice by protein tr

42 RAF mutation (V600E) and tested for MLH1 and CIMP methylation, the latter including the genes, CACNA1

43 nown that oxidative stress activates MMP and CIMP inhibits MMP, it is unclear whether CIMP administra

44 cidence of MSI, KRAS/BRAF/GNAS mutations and CIMP was 51.6%, 34.4%/3.1%/6.5% and 28.1%, respectively.

45 l factor required for INK4-ARF silencing and CIMP in CRCs containing activated KRAS.

46 votal factor required for MLH1 silencing and CIMP in CRCs containing BRAF(V600E).

47 MCRC patients presented their first tumor as CIMP-(+).

48 sts the presence of KRAS mutation-associated CIMP subtype (CIMP-low, CIMP2).

49 CpG island methylator phenotype-associated (CIMP) RCCs and metabolically divergent chRCCs, and new b

50 ociations between methylation frequencies at CIMP-related markers and MSI or MSI-/LOH- sporadic CRCs

51 High levels of aberrant methylation at CIMP-related markers in MSH2-methylated tumors raise the

52 The mean methylation scores at CIMP-related markers were significantly higher in Lynch

53 ed as follows: sham; sham+CIMP; AVF; and AVF+CIMP (n=6).

54 rend = 0.25) (Pheterogeneity = 0.02, between CIMP-high and CIMP-low/CIMP-negative cancer risks).

55 There was a significant concordance between CIMP and the methylation of known genes including p16, a

56 These interactions between CIMP, K-RAS mutations, and p53 mutations were preserved

57 In SEM, the correlation structures between CIMP, locus-specific CpG island methylation, and MSI dif

58 he poor prognosis subgroup, characterized by CIMP low/D29 or D33 MRD >= 0.1%, had a cumulative incide

59 C-CIMP was furthermore characterized by silencing of genes

60 lear cell CpG island methylator phenotype (C-CIMP) subgroup associated with promoter methylation of V

61 In sporadic colon cancer, CIMP has distinct epidemiologic and clinical features an

62 status in a panel of 14 markers (7 canonical CIMP-related loci and 7 new loci), microsatellite instab

63 correlate with mutant KRAS may help clarify CIMP in future studies.

64 ropose a robust new marker panel to classify CIMP+ tumors.

65 Both cohorts revealed that combining CIMP classification at diagnosis with measurable residua

66 In contrast, the existence of a comparable CIMP subtype in gastric cancer (GC) has not been clearly

67 nine (72.2%) SCRC patients showed concordant CIMP status in their simultaneous tumors.

68 However, the current CIMP criteria are ambiguous and often result in an under

69 s, frequently observed in gliomas, establish CIMP in primary human astrocytes by remodeling the methy

70 The aim of this study was to evaluate CIMP in carcinoid tumors and PETs.

71 We therefore evaluated CIMP in 22 sporadic serrated adenomas and 6 serrated ade

72 pes (CMS), thus providing a common basis for CIMP and CMS subtypes.

73 for the elucidation of a molecular basis for CIMP.

74 1.31; p = 0.04), while it was beneficial for CIMP-High associated tumours (DFS; HR, 0.17; 95% CI, 0.0

75 Risk factors for CIMP-high-serrated lesions included Caucasian race, curr

76 uent mutations in BRAF, were more frequently CIMP- and MSI-high, and had a worse prognosis than solit

77 lation correlated with the less aggressive G-CIMP (Glioma CpG Methylator Phenotype) subset of GBM.

78 ent with those observed in IDH1-mutant and G-CIMP+ primary gliomas and can segregate IDH wild-type an

79 ylation analysis, we show that G-CIMP+ and G-CIMP-subtypes enrich distinct classes of biological proc

80 key gene expression programs, characterize G-CIMP-positive proneural glioblastomas but not other glio

81 Glioma CIMP (G-CIMP) is a powerful determinant of tumour pathogenicity,

82 iate-grade gliomas demonstrates a distinct G-CIMP phenotype that is highly dependent on the presence

83 itrate dehydrogenase 1 (IDH1), establishes G-CIMP by remodelling the methylome.

84 While the standard method for identifying G-CIMP tumors is based on genome-wide DNA methylation data

85 shion that mirrors the changes observed in G-CIMP-positive lower-grade gliomas.

86 lioma CpG island methylator phenotype (non-G-CIMP) primary tumors.

87 pathogenicity, but the molecular basis of G-CIMP remains unresolved.

88 IDH1 CNA had decreased 2HG, maintenance of G-CIMP, and DNA methylation reprogramming outside CGI.

89 glioma CpG island methylator phenotype, or G-CIMP tumors, have distinct genomic copy number aberratio

90 anifest a CpG island methylator phenotype (G-CIMP), although the functional importance of this altere

91 G island (CGI) hypermethylation phenotype (G-CIMP).

92 me-wide methylation analysis, we show that G-CIMP+ and G-CIMP-subtypes enrich distinct classes of bio

93 ted tumors as well as those exhibiting the G-CIMP phenotype in unsupervised analysis of two primary g

94 the proneural subtype is conferred by the G-CIMP phenotype, and MGMT DNA methylation may be a predic

95 oped and evaluated a method to predict the G-CIMP status of GBM samples based solely on gene expressi

96 ained all of the glioblastoma samples with G-CIMP, a known methylation phenotype driven by the IDH1 m

97 ylation changes that overlap with primary GC CIMP patterns.

98 Glioma CIMP (G-CIMP) is a powerful determinant of tumour pathog

99 at period or without prior endoscopy to have CIMP and microsatellite instability.

100 A CIMP-high (CIMP-H) subgroup, which exhibits an exceptionally high f

101 ations were stronger compared with MSI-high, CIMP-positive, BRAF-mutated, or KRAS-mutated tumors, but

102 er data were classified as type 1 (MSI-high, CIMP-positive, with pathogenic mutations in BRAF but not

103 in BRAF but not KRAS), type 2 (not MSI-high, CIMP-positive, with pathogenic mutations in BRAF but not

104 However, CIMP-high unstable tumors were significantly more likely

105 11 of 21] vs. 14% [10 of 72], P = 0.004), in CIMP+ cases (40% [19 of 48] vs. 4% [2 of 46], P < 0.001)

106 The differences in CIMP-(+) frequency between groups may reflect the import

107 cer landscape to maintain differentiation in CIMP-high ACC; off chromatin, beta-catenin bound histone

108 ions: frequent K-RAS mutations were found in CIMP(+) CRCs (28/41, 68%) compared with CIMP(-) cases (1

109 h protein levels, is significantly higher in CIMP-high or MSI subtypes than in CIMP-low or MSS subtyp

110 Genes hypermethylated in CIMP compared with those in low-methylation melanomas in

111 26 sites were found to be hypermethylated in CIMP tumors only; and importantly, 80% of these sites we

112 2 T helper cell signature, was increased in CIMP RCC.

113 Pharmacologic EZH2 inhibition in CIMP-high ACC expelled SF1/beta-catenin from chromatin a

114 es that acquired promoter DNA methylation in CIMP-H tumors.

115 that the additional hypermethylation seen in CIMP tumors occurs almost exclusively at CpG islands and

116 recurrent target of epigenetic silencing in CIMP GC.

117 analyses defined a distinct superenhancer in CIMP+ colon cancers that regulates cMYC transcription.

118 higher in CIMP-high or MSI subtypes than in CIMP-low or MSS subtypes, and is positively correlated w

119 hat were down-regulated more than twofold in CIMP-H tumors together with promoter DNA hypermethylatio

120 d previously for microsatellite instability, CIMP, and mutations of p53 and K-RAS.

121 A CIMP-low (CIMP-L) subgroup is enriched for KRAS mutations and char

122 MSI high or MSI low, CIMP high or CIMP low, CIMP negative, and positive or negative for BRAF and/or

123 satellite stable (MSS), MSI high or MSI low, CIMP high or CIMP low, CIMP negative, and positive or ne

124 f pathway-unassigned tumors (MSS or MSI low, CIMP negative, BRAF mutation negative, and KRAS mutation

125 or cases with microsatellite stable/MSI-low, CIMP-negative, BRAF-wildtype, and KRAS-wildtype tumors (

126 e 2 (microsatellite stable [MSS] or MSI-low, CIMP-positive, positive for BRAF mutation, negative for

127 = 0.001), but not with the risk of CIMP-low/CIMP-negative cancer (Ptrend = 0.25) (Pheterogeneity = 0

128 neity = 0.02, between CIMP-high and CIMP-low/CIMP-negative cancer risks).

129 nd although present in some early melanomas, CIMP was associated with worse survival independent of k

130 and cardiac inhibitor of metalloproteinase (CIMP) are coexpressed in the heart.

131 tation positive; n = 58), serrated (any MSI, CIMP high, BRAF mutation positive, and KRAS mutation neg

132 appear to be significantly modified by MSI, CIMP, LINE-1, or the other clinical and molecular variab

133 mutation negative; n = 170), alternate (MSS, CIMP low, BRAF mutation negative, and KRAS mutation posi

134 owing integrated pathways: traditional (MSS, CIMP negative, BRAF mutation negative, and KRAS mutation

135 ns in BRAF or KRAS), or type 5 (MSI-high, no CIMP, no pathogenic mutations in BRAF or KRAS).

136 Non-CIMP tumors are separated into two distinct clusters.

137 ntexts that were hypermethylated in both non-CIMP and CIMP colon cancers when compared with normal co

138 in BRAF and KRAS); and type 5 (MSI-high, non-CIMP, negative for mutations in BRAF and KRAS).

139 also transcriptionally down-regulated in non-CIMP subgroups, but this was not attributable to promote

140 sites that were also hypermethylated in non-CIMP tumors.

141 KRAS mutation); type 3 (MSS or MSI low, non-CIMP, negative for BRAF mutation, positive for KRAS muta

142 KRAS mutation); type 4 (MSS or MSI-low, non-CIMP, negative for mutations in BRAF and KRAS); and type

143 wide DNA methylation profiles of normal, non-CIMP, and CIMP colon specimens.

144 n could be clearly classified as normal, non-CIMP, and CIMP, thus signifying that these three groups

145 One non-CIMP subgroup is distinguished by a significantly higher

146 types, but it remains unclear whether or not CIMP is a universal phenomenon across human neoplasia or

147 n, integrating MRD assessment with the novel CIMP biomarker has the potential to improve risk stratif

148 , p53 mutations were found in 24% (10/41) of CIMP(+) CRCs vs. 60% (30/46) of CIMP(-) cases (P = 0.002

149 % (10/41) of CIMP(+) CRCs vs. 60% (30/46) of CIMP(-) cases (P = 0.002).

150 were measured in the presence and absence of CIMP.

151 D15, and the relapse prediction accuracy of CIMP/D29 MRD (0.79) and CIMP/D15 MRD (0.75) classificati

152 bserved in sham mice after administration of CIMP.

153 used univariate and multivariate analyses of CIMP with clinicopathologic variables and tumor mutation

154 appeared to be driven by the associations of CIMP-high cancer with microsatellite instability-high, D

155 that IDH mutation is the molecular basis of CIMP in gliomas, provide a framework for understanding o

156 The underlying cause of CIMP is not known.

157 The causes of CIMP are unknown.

158 and 3 MINT loci (acknowledged classifiers of CIMP) in 344 bladder cancers, 346 head and neck squamous

159 occur almost exclusively as a consequence of CIMP-associated methylation of MLH1.

160 m that MSI cancers arise as a consequence of CIMP.

161 identifying the true cause and definition of CIMP in different forms of human neoplasia.

162 y distinguish disease type, the existence of CIMP and the relative preponderance of hypermethylation

163 However, the existence of CIMP has been challenged.

164 These data suggest that a form of CIMP exists in these solid tumors, although its etiology

165 fer increased plasma and LV tissue levels of CIMP in AVF mice; there was no increase in sham animals.

166 Plasma and LV tissue levels of CIMP were measured by Western analysis.

167 malignant neoplasms, a greater proportion of CIMP-High tumors (75%) and more frequent genomic alterat

168 strongly supports the biologic relevance of CIMP in colon cancer.

169 ssation were associated with a lower risk of CIMP-high colorectal cancer, with multivariate hazard ra

170 y (Ptrend = 0.001), but not with the risk of CIMP-low/CIMP-negative cancer (Ptrend = 0.25) (Pheteroge

171 provided novel insight regarding the role of CIMP-specific DNA hypermethylation in gene silencing.

172 tion alterations in CRC, the significance of CIMP status, the development of treatments based on spec

173 rized by DNA hypermethylation of a subset of CIMP-H-associated markers rather than a unique group of

174 us and often result in an underestimation of CIMP frequencies in CRCs.

175 The validity of CIMP, its molecular basis, and its prognostic value rema

176 s involved in, and the mechanistic basis of, CIMP is not understood.

177 -five (64.8%) SCRC patients had at least one CIMP-(+) tumor and 20 (44.4%) MCRC patients presented th

178 the CpG island methylator phenotype (CIMP or CIMP-High) and for the V600E mutation in the BRAF gene.

179 ble (MSS), MSI high or MSI low, CIMP high or CIMP low, CIMP negative, and positive or negative for BR

180 KRAS but not BRAF), type 4 (not MSI-high or CIMP, no pathogenic mutations in BRAF or KRAS), or type

181 BRAF but not KRAS), type 3 (not MSI-high or CIMP, with pathogenic mutations in KRAS but not BRAF), t

182 ures and KRAS/BRAF/GNAS genetic mutations or CIMP were found.

183 to as 'CpG island methylator phenotype', or 'CIMP'.

184 is bound at the promoters of MLH1 and other CIMP genes, and recruits a corepressor complex that incl

185 bound at the promoters of INK4-ARF and other CIMP genes.

186 lity (MSI), LINE-1 hypomethylation, and p53, CIMP, KRAS and BRAF mutation.

187 se tumors have the hypermethylator phenotype CIMP.

188 ), and the CpG island methylation phenotype (CIMP).

189 ence of the CpG island methylator phenotype (CIMP or CIMP-High) and for the V600E mutation in the BRA

190 ized by the CpG island methylator phenotype (CIMP) (multivariate odds ratio, 2.19; 95% CI, 1.14 to 4.

191 nstability, CpG Island Methylator Phenotype (CIMP) and chromosomal instability, as assessed by Next G

192 2) have the CpG island methylator phenotype (CIMP) and significantly longer patient survival time tha

193 RCs) have a CpG island methylator phenotype (CIMP) characterized by aberrant DNA hypermethylation and

194 0E]) have a CpG island methylator phenotype (CIMP) characterized by aberrant hypermethylation of many

195 rs with the CpG island methylator phenotype (CIMP) constitute a subset of tumours with extensive epig

196 islands as CpG island methylator phenotype (CIMP) has been described in tumors.

197 ity and the CpG island methylator phenotype (CIMP) in colon cancer.

198 CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal

199 hway termed CpG island methylator phenotype (CIMP) in CRC, which is characterized by the simultaneous

200 The CpG island methylator phenotype (CIMP) is a newly described mechanism for carcinogenesis

201 The CpG island methylator phenotype (CIMP) is a recently described mechanism for tumorigenesi

202 cancer, the CpG island methylator phenotype (CIMP) is defined as widespread and elevated levels of DN

203 The CpG island methylator phenotype (CIMP) is one of the mechanisms involved in colorectal ca

204 (CRC) with CpG island methylator phenotype (CIMP) is recognized as a subgroup of CRC that shows asso

205 rmethylated CpG island methylator phenotype (CIMP) observed in EBV-associated carcinomas.

206 s) with the CpG island methylator phenotype (CIMP) often associate with epigenetic silencing of hMLH1

207 tability or CpG island methylator phenotype (CIMP) positivity.

208 methylation CpG island methylator phenotype (CIMP) risk stratification in 2 pediatric T-ALL patient c

209 lthough the CpG island methylator phenotype (CIMP) was first identified and has been most extensively

210 A CpG island methylator phenotype (CIMP) was observed in a distinct subgroup of type 2 papi

211 to have the CpG island methylator phenotype (CIMP), a higher propensity for CpG island DNA methylatio

212 mutations, CpG island methylator phenotype (CIMP), and immunostaining including mucin phenotype and

213 lity (MSI), CpG island methylator phenotype (CIMP), and mutations in BRAF and KRAS.

214 lity (MSI), CpG island methylator phenotype (CIMP), and mutations in KRAS and BRAF in tumors.

215 lity (MSI), CpG island methylator phenotype (CIMP), and somatic mutations in BRAF and KRAS genes, and

216 lity (MSI), CpG island methylator phenotype (CIMP), B-Raf proto-oncogene serine/threonine kinase (BRA

217 tion, and a CpG island methylator phenotype (CIMP), but precursors are poorly established.

218 oncept of a CpG island methylator phenotype (CIMP), especially in microsatellite stable colon cancer,

219 o status of CpG island methylator phenotype (CIMP), microsatellite instability, v-raf murine sarcoma

220 The CpG island methylator phenotype (CIMP), thoroughly described in colorectal cancer and to

221 guanosine (CpG) island methylator phenotype (CIMP), which appears to be a defining event in approxima

222 type termed CpG island methylator phenotype (CIMP), which includes methylation of such genes as p16 a

223 AS, and the CpG island methylator phenotype (CIMP).

224 Is, underpinning a CGI methylator phenotype (CIMP).

225 display the CpG island methylator phenotype (CIMP).

226 o display a CpG island methylator phenotype (CIMP).

227 nown as the CpG island methylator phenotype (CIMP).

228 nd methylation, or the methylator phenotype (CIMP).

229 ized by the CpG island methylator phenotype (CIMP).

230 (MSI); the CpG island methylator phenotype (CIMP); 18q loss of heterozygosity; KRAS, BRAF, and PIK3C

231 rs have the CpG island methylator phenotype (CIMP+) with methylation and transcriptional silencing of

232 The CpG island methylator phenotype (CIMP-high, CIMP1) is a distinct phenotype associated wit

233 [MSI]-high, CpG island methylator phenotype [CIMP] -positive, positive for BRAF mutation, negative fo

234 -island promoter DNA methylation phenotypes (CIMPs), in CRCs and other cancers.

235 displaying CpG island methylator phenotypes (CIMPs), defined as DNA hypermethylation at specific CpG

236 We found that CIMP-positive (CIMP+) tumors convincingly represent a distinct subset,

237 s "CpG island-methylator-phenotype positive (CIMP+)." Two of four carcinomas with microsatellite inst

238 is subgroup was also identified representing CIMP high/D29 or D33 MRD < 0.1% with pCIR5yr of 0% and 3

239 Mice were grouped as follows: sham; sham+CIMP; AVF; and AVF+CIMP (n=6).

240 Compared with sham, CIMP was decreased in AVF mice, and CIMP protein transfe

241 Analysis of transcriptionally silenced CIMP genes in KRAS-positive CRCs indicates that differen

242 Concordant methylation of two or more sites (CIMP-high) was also more frequent in sporadic serrated a

243 ABP1, IGF2, MLH1, NEUROG1, RUNX3 and SOCS1); CIMP-(+) tumors were defined as having >= 5 methylated m

244 s' characterization according to MMR status, CIMP phenotype and TYMS mRNA expression may provide a mo

245 We studied CIMP in hyperplastic polyps (HPs), with emphasis on pati

246 The differentiated ACC subtype CIMP-high is prevalent, incurable, and routinely fatal.

247 ce of KRAS mutation-associated CIMP subtype (CIMP-low, CIMP2).

248 cordance between synchronous tumors suggests CIMP status is generally maintained in SCRC patients.

249 this mutation was related to poor survival, CIMP high, advanced American Joint Committee on Cancer (

250 nt perspective discusses the use of the term CIMP in cancer, its significance in clinical practice, a

251 vely studied in colorectal cancer, the term "CIMP" has been repeatedly used over the past decade to d

252 We find that CIMP defines two groups of tumors with significantly dif

253 We found that CIMP-positive (CIMP+) tumors convincingly represent a di

254 These observations indicate that CIMP tumors have specific defects in controlling both DN

255 These results suggest that CIMP may be one of the major pathways that contribute to

256 The CIMP phenotype is an early event in gastric cancer, bein

257 Among the CIMP genes are the tumor suppressors p14(ARF), p15(INK4B

258 The evaluation of the biology behind the CIMP subgroups revealed associations with transcriptome

259 the majority of these tumors evolve through CIMP.

260 Thus, CIMP is also characterized by more extensive methylation

261 est that there may be a genetic component to CIMP in CRC.

262 sought to discover molecular contributors to CIMP in GC, by performing global DNA methylation, gene e

263 on-related carcinogenesis pathway leading to CIMP-high colorectal cancer.

264 unique molecular profile that is similar to CIMP-high, BRAF-mutated colorectal cancers.

265 te analysis of microsatellite stable tumors, CIMP high was related significantly to the V600E BRAF mu

266 g gastric cancer (GC), mechanisms underlying CIMP remain poorly understood.

267 rated lesions harbored mutant BRAF, 26% were CIMP-high, and 5% had methylated MLH1.

268 permethylation of hMLH1, and both cases were CIMP+.

269 instability, and all three of the cases were CIMP+.

270 erplastic glands and adenomatous glands were CIMP-high.

271 Sporadic HPs were CIMP-negative (not methylated at any locus), but 43% of

272 le/large HPs, or hyperplastic polyposis were CIMP-high (two or more methylated loci, P = 0.00001).

273 To study whether CIMP is present in gastric cancer, the methylation statu

274 and CIMP inhibits MMP, it is unclear whether CIMP administration attenuates oxidative stress and MMP-

275 BRAF but mutant KRAS may also associate with CIMP in CRC.

276 imutations are significantly associated with CIMP in various other cancers, occurring even in premali

277 ic CRCs without CIN would be associated with CIMP.

278 nd SOCS1) were differentially clustered with CIMP-high and CIMP-low according to KRAS and BRAF status

279 d in CIMP(+) CRCs (28/41, 68%) compared with CIMP(-) cases (14/47, 30%, P = 0.0005).

280 Treatment of AVF mice with CIMP significantly abrogated the contractile dysfunction

281 Patients with CIMP melanomas had worse melanoma-specific survival (haz

282 mice and decreased in AVF mice treated with CIMP.

283 mice compared with sham, and treatment with CIMP decreased MMP activity.

284 a panel of colorectal tumors with or without CIMP.