IndraLab

Statements


CYLD is methylated. 49 / 49
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"Integrated Gene Expression Analysis Identified NDRG4 as One of the Top Candidates Silenced by DNA Methylation in EAC."

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"Genes (23%) on the array, including 7% of X-linked and 69% of imprinted genes, have shown statistically significant changes in methylation in EAC versus Barrett's esophagus (Wilcoxon P < 0.05)."

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"In addition, no association was observed between CREB and CYLD methylation and the occurrence and metastasis of CRC."

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"Other members of the highest ranked pathway which were aberrantly methylated in EAC are involved in chromosomal segregation and spindle assembly, these include the BUB3 , AURKA , DYNC1I1 and DCTN2 and CHFR genes."

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"SST mRNA levels in native unmethylated EACs were significantly higher than in native methylated EACs (P < ."

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"One aim of the present study was to observe whether the status of PCDH -γ- A12, SLC19A1 , CREB and CYLD promoter methylation had a correlation with the serum level of CEA and CA19-9."

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"Different from ESCC, several cancer-associated pathway genes were aberrantly methylated in EAC, including genes in the epithelial-mesenchymal transition (EMT), cell adhesion, Wingless and Int-1 (WNT), and Transforming growth factor (TGF) pathways ( xref ; xref )."

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"Among genes with frequent DNA hypermethylation, we found several gene clusters with significantly higher DNA methylation in EACs, as compared to normal tissues."

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"In contrast, the promoter of PCDH10 was specifically methylated in EAC, and this gene was respressed in EAC only (Figure  xref C and xref D)."

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"However, no significant correlation was identified between PCDH -γ- A12, SLC19A1 , CREB and CYLD methylation and the clinical features, which may be due to the lack of power in the samples used."

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"TIMP-3 gene methylation in esophageal and gastric cancer. (A) TIMP-3 gene methylation in ESCC and EAC."

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"Aberrant DNA methylation is a known hallmark of cancer, but genome-wide patterns of DNA methylation in EAC are yet to be fully characterized."

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"Notably, we also observed significant differences in the overall mutation loads between the EAC methylation subtypes ( xref )."

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"For example, a well-known marker, the promoter of the MLH1 gene, is usually highly methylated in microsatellite instability-high (MSI-H) EAC, and was unmethylated in UPSC (Figure  xref C and Additional file xref : Figure S5C)."

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"A total of 52590 CpG sites were differentially methylated (FDR < 0.01 and average beta value difference ≥ 0.20) in EAC compared with NSE (, available at Carcinogenesis Online; xref ), and 50101 sites were differentially methylated in BE compared with NSE (, available at Carcinogenesis Online)."

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"Interestingly, 74.5% of the probes aberrantly methylated in EAC were also aberrantly methylated in BE ( xref )."

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"For example, the ADCY3 promoter was specifically hypomethylated in normal endometrium, but its associated CpG island shore was highly methylated in EAC and UPSC."

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"In order to further characterize the EAC methylation subtypes, we assessed genomic alterations in the BETRNet EAC cohort."

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"Previously, 274 genes were reported as aberrantly methylated in EAC and/or BE methylation studies ( xref , xref ), of which 245 (89.4%) were also aberrantly methylated in our cohort (, available at Carcinogenesis Online)."

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"In the current study, we first profiled global DNA methylations on EAC identified by using the Illumina Human Methylation 450K BeadChips and then compared the data with gene expression data on RNA-Seq datasets."

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"Here the top pathway affected by aberrant methylation in EAC was ‘neurophysiological process dynein–dynactin motor complex in axonal transport in neurons’."

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"The extent of methylation in EAC was significantly greater than in BE for six of the nine genes (CDKN2A, ID4, RBP1, RUNX3, SFRP1 and TMEFF2) but was not different to D-EAC for any gene."

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"Considering that epigenetic regulation adds an extra layer of complexity in cancer development, further studies to gain more insight about the landscape of DNA methylation in EAC are required to better understand this complex disease."

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"Downloaded EAC DNA methylation, transcriptome, and related clinical data from TCGA database."

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"We analyzed HM450 methylation and RNA seq datasets performed on TCGA EAC to identify genes differentially regulated by promoter methylation and miRNA expression across the EAC methylation subtypes ( xref ; xref )."

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"For only CDKN2A and RUNX3 was there a significant increase in frequency of methylation in EAC compared to BE."

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"However, no significant correlation was observed between PCDH -γ- A12, SLC19A1 , CREB and CYLD promoter methylation and the serum level of CEA and CA19-9."

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"In this study, we explore methylome, transcriptome and ENCODE data to characterize the role of DNA methylation in EAC."

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"This is the first study to explore methylome, transcriptome and ENCODE data to characterize the role of methylation in EAC."

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"For example, maternally expressed gene 3 ( MEG3 ), a tumor suppressor non-coding RNA [ xref ], was highly methylated at its promoter region in EAC."

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"Results TIMP-3 Is Frequently Methylated in Human Esophageal and Gastric Cancers Using the MethyLight assay, promoter methylation of TIMP-3 in 13 EACs was assessed and compared to the corresponding[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"The current study profiled global DNA methylations on EAC and identified a large set of genomic DNA methylations on EAC, some of which were shown in previous studies."

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"Enriched pathways included known cancer signaling pathways, some previously described as aberrantly methylated in EAC: cell adhesion, regulation of epithelial-to-mesenchymal transition and TGF and WNT signaling."

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"23% genes on the array, including 7% of X-linked and 69% of imprinted genes, demonstrated statistically significant changes in methylation in EAC vs. BE (Wilcoxon P<0.05)."

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"8) was methylated only in EAC, three (No."

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"For imprinted genes, as mentioned above almost 70% of genes showed statistically significant changes in methylation in EAC vs. BE (Wilcoxon P<0.05) ( xref )."

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"All 10 genes except p14 were frequently methylated in EACs, with RUNX3, HPP1, CRBP1, RIZ1, and OST-2 representing novel methylation targets in EAC and/or BE."

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"Pathway analysis identified enrichment of known cancer signaling pathways previously described as aberrantly methylated in EAC: cell adhesion ( xref , xref ), regulation of epithelial-to-mesenchymal transition and TGF and WNT signaling ( xref )."

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"Members of this pathway are involved in the neurotrophin–Trk signaling, which was previously reported to be aberrantly methylated in EAC ( xref )."

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"However none of the genes such as p16 , APC ( xref ) and MGMT ( xref ) and a previously identified eight gene panel( xref ) were shown in this current study to be differentially methylated in EAC vs. BE."

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"MSP assay confirmed DNA methylation in EAC samples but not in normal esophagus (NE) ( xref )."

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"Mechanisms causing BE and EAC related aberrant methylation."

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"The genes with significant upregulation after 5-Aza treatment (provided in xref ) and genes with significant downregulation in EAC as compared to normal samples (provided in xref ) were considered as most likely candidate genes methylated in EAC (the experimental flow chart is shown in xref )."

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"In contrast, similar analysis of any autosome (e.g., chromosome 10) revealed no global change of DNA methylation in either EAC or UPSC (Additional file xref : Figure S7)."

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"All nine genes showed an increase in frequency of methylation in EAC compared to squamous epithelium."

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"Efficacy of cytotoxic chemotherapy differs between EAC methylation subtypes."

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"Expression of TFs with motifs enriched in EAC ce-hyperDMRs were downregulated in EAC compared to normal endometrium (Fig.  xref ), whereas TFs whose bindings motifs were enriched in EAC cancer-enhancer hypoDMRs (EAC ce-hypoDMRs) were generally upregulated in EAC (Fig.  xref ), suggesting that changes in TF expression may help dictate changes in DNA methylation at target motifs in EAC."

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"Pathways aberrantly methylated in EAC and BE."

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"Because mutations and promoter methylation of the CYLD gene could be excluded (unpublished data), we concluded that down-regulation of CYLD likely occurs at the transcriptional level."