Reprogramming cancer cells to pluripotency: an experimental tool for exploring cancer epigenetics

Stefan Stricker, Steven Pollard

Research output: Contribution to journalLiterature reviewpeer-review

Abstract

The epigenetic marks displayed by a cancer cell originate from two separate processes: The most prominent epigenetic signatures are associated with the cell of origin, i.e., the lineage and cell type identity imposed during development. The second set comprises those aberrant cancer-specific epigenetic marks that appear during tumor initiation or subsequent malignant progression. These are generally thought to associate with tumor-promoting pathways. As biochemical pathways regulating epigenetic mechanisms are potentially "druggable" and reversible, there is considerable interest in defining their roles in tumor genesis and growth, as they may represent therapeutic targets for treatment of human neoplasias. (1) However, despite the potential importance of epigenetic modifications in human cancer, it has been difficult to determine when, where and how epigenetic disruptions occur, and if they have important functional roles in sustaining the malignant state.

Original languageEnglish
Pages (from-to)798-802
Number of pages5
JournalEpigenetics
Volume9
Issue number6
DOIs
Publication statusPublished - Jun 2014

Keywords

  • Animals
  • Brain Neoplasms
  • Carcinogenesis
  • Cell Line, Tumor
  • Cell Lineage
  • Cellular Reprogramming
  • DNA Methylation
  • Epigenesis, Genetic
  • Glioblastoma
  • Humans
  • Induced Pluripotent Stem Cells
  • Metabolic Networks and Pathways
  • Neoplastic Stem Cells
  • Neural Stem Cells

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