Resultados totales (Incluyendo duplicados): 2
Encontrada(s) 1 página(s)
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/235126
Dataset. 2017

DISTINCT CHROMATIN SIGNATURES OF DNA HYPOMETHYLATION IN AGING AND CANCER (DATASETS AND ADDITIONAL FILES)

  • Pérez, Raúl F.
  • Tejedor, Juan Ramón
  • Bayón, Gustavo F.
  • Fernández, Agustín F.
  • Fraga, Mario F.
Provided datasets correspond to the supplementary material generated for Perez RF et al (2018)., Distinct chromatin signatures of DNA hypomethylation in aging and cancer. Raúl F, Pérez et al. (DOI: 10.1111/acel.12744), Cancer is an aging-associated disease but the underlying molecular links between these processes are still largely unknown. Gene promoters that become hypermethylated in aging and cancer share a common chromatin signature in ES cells. In addition, there is also global DNA hypomethylation in both processes. However, any similarities of the regions where this loss of DNA methylation occurs is currently not well characterized, nor is it known whether such regions also share a common chromatin signature in aging and cancer. To address this issue we analysed TCGA DNA methylation data from a total of 2,311 samples, including control and cancer cases from patients with breast, kidney, thyroid, skin, brain and lung tumors and healthy blood, and integrated the results with histone, chromatin state and transcription factor binding site data from the NIH Roadmap Epigenomics and ENCODE projects. We identified 98,857 CpG sites differentially methylated in aging, and 286,746 in cancer. Hyper- and hypomethylated changes in both processes each had a similar genomic distribution across tissues and displayed tissue-independent alterations. The identified hypermethylated regions in aging and cancer shared a similar bivalent chromatin signature. In contrast, hypomethylated DNA sequences occurred in very different chromatin contexts. DNA hypomethylated sequences were enriched at genomic regions marked with the activating histone posttranslational modification H3K4me1 in aging, whilst in cancer, loss of DNA methylation was primarily associated with the repressive H3K9me3 mark., Peer reviewed

Proyecto: //
DOI: http://hdl.handle.net/10261/235126
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/235126
HANDLE: http://hdl.handle.net/10261/235126
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/235126
PMID: http://hdl.handle.net/10261/235126
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/235126
Ver en: http://hdl.handle.net/10261/235126
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/235126

Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/235141
Dataset. 2017

EPIGENOME-WIDE ANALYSIS REVEALS SPECIFIC DNA HYPERMETHYLATION OF T CELLS DURING HUMAN HEMATOPOIETIC DIFFERENTIATION

  • Tejedor, Juan Ramón
  • Bueno, Clara
  • Cobo, Isabel
  • Bayón, Gustavo F.
  • Prieto, Cristina
  • Mangas, Cristina
  • Pérez, Raúl F.
  • Santamarina-Ojeda, Pablo
  • Urdinguio, Rocío G.
  • Menéndez, Pablo
  • Fraga, Mario F.
  • Fernández, Agustín F.
Supplementary figures and supplementary data tables from MethylationEPIC arrays (Tejedor et al), plus a compiled dataset including raw methylation intensities, processed β-values and Phenotypic data from HumanMethylation450 arrays collected from datasets GSE63409, GSE49618, GSE88824 and GSE49031, and HumanMethylationEPIC arrays deposited in E-MTAB-6315 entry from ArrayExpress., Epigenetic regulation plays an important role in cellular development and differentiation. A detailed map of the DNA methylation dynamics that occur during cell differentiation would contribute to decipher the molecular networks governing cell fate commitment. In this study we used the most recent Illumina MethylationEPIC Beadchip platform to describe the genome-wide DNA methylation changes observed throughout hematopoietic maturation by analyzing multiple hematopoietic cell types at different developmental stages., Grants: European Commission: INFANTLEUKEMIA - GENOMIC, CELLULAR AND DEVELOPMENTAL RECONSTRUCTION OFINFANT MLL-AF4+ ACUTE LYMPHOBLASTIC LEUKEMIA (646903)., Peer reviewed

Proyecto: EC/H2020/646903
DOI: http://hdl.handle.net/10261/235141
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/235141
HANDLE: http://hdl.handle.net/10261/235141
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/235141
PMID: http://hdl.handle.net/10261/235141
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/235141
Ver en: http://hdl.handle.net/10261/235141
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/235141

Buscador avanzado