Chromatin Mechanisms Driving Cancer
- 29 June 2021
- journal article
- research article
- Published by Cold Spring Harbor Laboratory in Cold Spring Harbor Perspectives in Biology
- Vol. 14 (3), a040956
- https://doi.org/10.1101/cshperspect.a040956
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.This publication has 137 references indexed in Scilit:
- Proteomic and bioinformatic analysis of mammalian SWI/SNF complexes identifies extensive roles in human malignancyNature Genetics, 2013
- Reversible Disruption of mSWI/SNF (BAF) Complexes by the SS18-SSX Oncogenic Fusion in Synovial SarcomaCell, 2013
- Biosemiotic Entropy of the Genome: Mutations and Epigenetic Imbalances Resulting in CancerEntropy, 2013
- Architecture of the human regulatory network derived from ENCODE dataNature, 2012
- MYC on the Path to CancerCell, 2012
- BET Bromodomain Inhibition as a Therapeutic Strategy to Target c-MycCell, 2011
- RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemiaNature, 2011
- Selective inhibition of BET bromodomainsNature, 2010
- AFF4, a Component of the ELL/P-TEFb Elongation Complex and a Shared Subunit of MLL Chimeras, Can Link Transcription Elongation to LeukemiaMolecular Cell, 2010
- The language of covalent histone modificationsNature, 2000