Bivalent domains enforce transcriptional memory of DNA methylated genes in cancer cells.
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A double take on bivalent promotersDissecting epigenetic silencing complexity in the mouse lung cancer suppressor gene Cadm1Reassembly of nucleosomes at the MLH1 promoter initiates resilencing following decitabine exposureDefining the chromatin signature of inducible genes in T cellsPrognostic impact of H3K27me3 expression on locoregional progression after chemoradiotherapy in esophageal squamous cell carcinoma.Signatures of polycomb repression and reduced H3K4 trimethylation are associated with p15INK4b DNA methylation in AML.Epigenetic regulation of cell type-specific expression patterns in the human mammary epithelium.A balance between activating and repressive histone modifications regulates cystic fibrosis transmembrane conductance regulator (CFTR) expression in vivoMarek's disease virus infection induces widespread differential chromatin marks in inbred chicken lines.Multivalent epigenetic marks confer microenvironment-responsive epigenetic plasticity to ovarian cancer cells.Dnmt3a loss predisposes murine hematopoietic stem cells to malignant transformation.Epigenetic mechanisms involved in developmental nutritional programming.Treatment of breast cancer cells with DNA demethylating agents leads to a release of Pol II stalling at genes with DNA-hypermethylated regions upstream of TSS.Overlapping DNA methylation dynamics in mouse intestinal cell differentiation and early stages of malignant progressionGenome-scale analysis of aberrant DNA methylation in colorectal cancer.Haploinsufficiency of Dnmt1 impairs leukemia stem cell function through derepression of bivalent chromatin domainsDevelopment of prognostic signatures for intermediate-risk papillary thyroid cancerEpigenetics: judge, jury and executioner of stem cell fate.Stable oncogenic silencing in vivo by programmable and targeted de novo DNA methylation in breast cancer.RNA polymerase II pausing as a context-dependent reader of the genome.Decrease of 5hmC in gastric cancers is associated with TET1 silencing due to with DNA methylation and bivalent histone marks at TET1 CpG island 3'-shore.The DNA methylation landscape of small cell lung cancer suggests a differentiation defect of neuroendocrine cellsAberrant Epigenetic Modifications of LPHN2 Function as a Potential Cisplatin-Specific Biomarker for Human Gastrointestinal Cancer.NEpiC: a network-assisted algorithm for epigenetic studies using mean and variance combined signalsA primary role of TET proteins in establishment and maintenance of De Novo bivalency at CpG islands.The presence of RNA polymerase II, active or stalled, predicts epigenetic fate of promoter CpG islandsChanges of bivalent chromatin coincide with increased expression of developmental genes in cancerModulation of gene expression in ovarian cancer by active and repressive histone marks.High-wire act: the poised genome and cellular memory.Epigenetic alterations in cancer and personalized cancer treatment.Chromatin remodeling and bivalent histone modifications in embryonic stem cells.DNA methylation variations are required for epithelial-to-mesenchymal transition induced by cancer-associated fibroblasts in prostate cancer cells.The interaction of MYC with the trithorax protein ASH2L promotes gene transcription by regulating H3K27 modification.Physical interaction between MYCN oncogene and polycomb repressive complex 2 (PRC2) in neuroblastoma: functional and therapeutic implications.Promoter CpG island hypermethylation- and H3K9me3 and H3K27me3-mediated epigenetic silencing targets the deleted in colon cancer (DCC) gene in colorectal carcinogenesis without affecting neighboring genes on chromosomal region 18q21.The epigenetic landscape of Alu repeats delineates the structural and functional genomic architecture of colon cancer cells.APC promoter is frequently methylated in pancreatic juice of patients with pancreatic carcinomas or periampullary tumors.A novel subtype classification and risk of breast cancer by histone modification profiling.Long range epigenetic silencing is a trans-species mechanism that results in cancer specific deregulation by overriding the chromatin domains of normal cells.Long-range epigenetic silencing at 2q14.2 affects most human colorectal cancers and may have application as a non-invasive biomarker of disease.
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Bivalent domains enforce transcriptional memory of DNA methylated genes in cancer cells.
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
@pt
bilimsel makale
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scientific article published on 05 December 2008
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Bivalent domains enforce transcriptional memory of DNA methylated genes in cancer cells.
@en
Bivalent domains enforce transcriptional memory of DNA methylated genes in cancer cells.
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type
label
Bivalent domains enforce transcriptional memory of DNA methylated genes in cancer cells.
@en
Bivalent domains enforce transcriptional memory of DNA methylated genes in cancer cells.
@nl
prefLabel
Bivalent domains enforce transcriptional memory of DNA methylated genes in cancer cells.
@en
Bivalent domains enforce transcriptional memory of DNA methylated genes in cancer cells.
@nl
P2093
P2860
P356
P1476
Bivalent domains enforce transcriptional memory of DNA methylated genes in cancer cells
@en
P2093
Costas G Frangou
Laura Vives
Mark Groudine
P2860
P304
19809-19814
P356
10.1073/PNAS.0810133105
P407
P577
2008-12-05T00:00:00Z