Pathways that suppress programmed DNA breaks from progressing to chromosomal breaks and translocations

Sonia Franco, Frederick W. Alt, John P. Manis

Research output: Contribution to journalArticlepeer-review


Guarding the genome against internal and external assaults requires the coordinated interaction of multiple cellular networks to sense, respond to, and repair breaks in chromosomal DNA. Both external factors such as ionizing radiation or internal events like oxidative damage can cause DNA double stranded breaks (DSBs) [1,2]. DSBs are also part of the normal lymphocyte developmental program where they are an integral element of the mechanisms that generate a diverse immune repertoire in the context of V(D)J and immunoglobulin heavy chain (IgH) class switch recombination (CSR) [3-5]. DSBs initiate a cascade of cellular events that direct cells to pause and properly repair potentially lethal chromosomal breaks. Errors in the repair of both general and lymphocyte-specific DSBs can lead to oncogenic chromosomal translocations [6-8]. Here, we review recent advances in understanding factors and protein complexes involved in the response to DNA DSBs with a focus on the B lymphocyte specific process of CSR.

Original languageEnglish (US)
Pages (from-to)1030-1041
Number of pages12
JournalDNA Repair
Issue number9-10
StatePublished - Sep 8 2006
Externally publishedYes


  • Class switch recombination
  • DNA damage response
  • Lymphoma

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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