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Cancer Lett. 2003 Apr 10;193(1):1-9.

DNA double strand breaks (DSB) and non-homologous end joining (NHEJ) pathways in human leukemia.

Author information

1
Department of Haematological Medicine, Leukemia Sciences Laboratories, The Rayne Institute, GKT School of Medicine, Denmark Hill, London, SE5 9NU, UK. feyruz.rassool@kcl.ac.uk

Abstract

DNA double strand breaks (DSB) are considered the most lethal form of DNA damage for eukaryotic cells. DSB can either be properly repaired, restoring genomic integrity, or misrepaired resulting in drastic consequences, such as cell death, genomic instability, and cancer. It is well established that exposure to DSB-inducing agents is associated with chromosomal abnormalities and leukemogenesis. The non-homologous end joining (NHEJ) pathway is considered a major route for the repair DSB in mammalian cells. Although the mechanism(s) by which repair of DSB lead to leukemia are poorly understood, recent evidence is beginning to emerge that a poorly defined and error-prone branch of the NHEJ pathway plays a pivotal role in this process. This review discusses some of the ways in which error-prone NHEJ repair may be involved in the development of genomic instability and leukemia.

PMID:
12691817
DOI:
10.1016/s0304-3835(02)00692-4
[Indexed for MEDLINE]

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