Epigenetic plasticity and the hallmarks of cancer.

Science
Authors
Keywords
Abstract

Chromatin and associated epigenetic mechanisms stabilize gene expression and cellular states while also facilitating appropriate responses to developmental or environmental cues. Genetic, environmental, or metabolic insults can induce overly restrictive or overly permissive epigenetic landscapes that contribute to pathogenesis of cancer and other diseases. Restrictive chromatin states may prevent appropriate induction of tumor suppressor programs or block differentiation. By contrast, permissive or "plastic" states may allow stochastic oncogene activation or nonphysiologic cell fate transitions. Whereas many stochastic events will be inconsequential "passengers," some will confer a fitness advantage to a cell and be selected as "drivers." We review the broad roles played by epigenetic aberrations in tumor initiation and evolution and their potential to give rise to all classic hallmarks of cancer.

Year of Publication
2017
Journal
Science
Volume
357
Issue
6348
Date Published
2017 Jul 21
ISSN
1095-9203
DOI
10.1126/science.aal2380
PubMed ID
28729483
PubMed Central ID
PMC5940341
Links
Grant list
DP1 CA216873 / CA / NCI NIH HHS / United States