title: End-joining, translocations and cancer.
abstract: Fusion genes that are caused by chromosome translocations have been recognized for several decades as drivers of deregulated cell growth in certain types of cancer. In recent years, oncogenic fusion genes have been found in many haematological and solid tumours, demonstrating that translocations are a common cause of malignancy. Sequencing approaches have now confirmed that numerous, non-clonal translocations are a typical feature of cancer cells. These chromosome rearrangements are often highly complex and contain DNA sequence from multiple genomic sites. The factors and pathways that promote translocations are becoming clearer, with non-homologous end-joining implicated as a key source of genomic rearrangements.
authors.affiliation: Rutgers University, Center for Advanced Biotechnology and Medicine, Piscataway, New Jersey 08854, USA. bunting@cabm.rutgers.edu
authors.forename: Samuel F
authors.initials: SF
authors.lastname: Bunting
authors.forename: Andre
authors.initials: A
authors.lastname: Nussenzweig
mesh_terms: D059766:DNA End-Joining Repair / Q000502:physiology*; D042822:Genomic Instability / Q000235:genetics*; D006801:Humans; D009369:Neoplasms / Q000235:genetics* / Q000473:pathology; D050596:Oncogene Fusion / Q000502:physiology*; D014178:Translocation, Genetic / Q000235:genetics*