Chromatin Mechanisms Driving Cancer
- 1Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, Ohio 44106, USA
- 2Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, USA
- Correspondence: Berkley.gryder{at}case.edu; riedt{at}mail.nih.gov; khanjav{at}mail.nih.gov
Abstract
The change in cell state from normal to malignant is driven fundamentally by oncogenic mutations in cooperation with epigenetic alterations of chromatin. These alterations in chromatin can be a consequence of environmental stressors or germline and/or somatic mutations that directly alter the structure of chromatin machinery proteins, their levels, or their regulatory function. These changes can result in an inability of the cell to differentiate along a predefined lineage path, or drive a hyperactive, highly proliferative state with addiction to high levels of transcriptional output. We discuss how these genetic alterations hijack the chromatin machinery for the oncogenic process to reveal unique vulnerabilities and novel targets for cancer therapy.