Endogenous DNA damage as a source of genomic instability in cancer

• Anthony Tubbs ^[1] ; André Nussenzweig ^[1]
  1. [1] National Institutes of Health

     National Institutes of Health

     Estados Unidos

     
• Localización: Cell, ISSN 0092-8674, Vol. 168, Nº. 4, 2017 (Ejemplar dedicado a: Cancer, the road ahead), págs. 644-656
• Idioma: inglés
• Texto completo no disponible (Saber más ...)
• Resumen

  • 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.