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Cell. 2017 Feb 9;168(4):644-656. doi: 10.1016/j.cell.2017.01.002.

Endogenous DNA Damage as a Source of Genomic Instability in Cancer.

Author information

1
Laboratory of Genome Integrity, NIH, Bethesda, MD 20892, USA.
2
Laboratory of Genome Integrity, NIH, Bethesda, MD 20892, USA. Electronic address: andre_nussenzweig@nih.gov.

Abstract

Genome instability, defined as higher than normal rates of mutation, is a double-edged sword. As a source of genetic diversity and natural selection, mutations are beneficial for evolution. On the other hand, genomic instability can have catastrophic consequences for age-related diseases such as cancer. Mutations arise either from inactivation of DNA repair pathways or in a repair-competent background due to genotoxic stress from celluar processes such as transcription and replication that overwhelm high-fidelity DNA repair. Here, we review recent studies that shed light on endogenous sources of mutation and epigenomic features that promote genomic instability during cancer evolution.

KEYWORDS:

DNA damage; DNA repair; DNA replication; Genome instability; cancer; mutagenesis; transcription

PMID:
28187286
DOI:
10.1016/j.cell.2017.01.002
[Indexed for MEDLINE]
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