DNA methylation in cancer and aging

Michael Klutstein, Deborah Nejman, Razi Greenfield, Howard Cedar*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

558 Scopus citations

Abstract

DNA methylation is known to be abnormal in all forms of cancer, but it is not really understood how this occurs and what is its role in tumorigenesis. In this review, we take a wide view of this problem by analyzing the strategies involved in setting up normal DNA methylation patterns and understanding how this stable epigenetic mark works to prevent gene activation during development. Aberrant DNA methylation in cancer can be generated either prior to or following cell transformation through mutations. Increasing evidence suggests, however, that most methylation changes are generated in a programmed manner and occur in a subpopulation of tissue cells during normal aging, probably predisposing them for tumorigenesis. It is likely that this methylation contributes to the tumor state by inhibiting the plasticity of cell differentiation processes.

Original languageAmerican English
Pages (from-to)3446-3450
Number of pages5
JournalCancer Research
Volume76
Issue number12
DOIs
StatePublished - 15 Jun 2016

Bibliographical note

Funding Information:
This work was supported by the Rosetrees Foundation, Israel Cancer Research Fund (ICRF #210910), European Research Council (ERC #268614), Israel Science Foundation (ISF #419/10) as well as Lew Sanders and Norton Herrick.

Publisher Copyright:
©2016 AACR.

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