Alternative end joining, clonal evolution, and escape from a telomere-driven crisis

Eric A. Hendrickson, Duncan M. Baird

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

Telomere dysfunction and fusion play key roles in driving genomic instability and clonal evolution in many tumor types. We have recently described a role for DNA ligase III (LIG3) in facilitating the escape of cells from crisis induced by telomere dysfunction. Our data indicate that LIG3-mediated telomere fusion is important in facilitating clonal evolution.

Original languageEnglish (US)
Article numbere975623
JournalMolecular and Cellular Oncology
Volume2
Issue number1
DOIs
StatePublished - Jan 2 2015

Bibliographical note

Funding Information:
This work was supported by funding to the Baird laboratory from Cancer Research UK, Leukemia and Lymphoma Research and the National Institute for Social Care and Health Research; and to the Hendrickson laboratory from the United States National Institutes of Health (GM088351) and the National Cancer Institute (CA15446).

Keywords

  • DNA repair
  • cancer
  • ligase III
  • non-homologous end joining
  • telomerase
  • telomere

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