Journal
NATURE REVIEWS CANCER
Volume 13, Issue 7, Pages 443-454Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrc3537
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Funding
- NCI R00 award [RCA 160574A]
- Intramural Research Program of the National Institutes of Health, National Cancer Institute
- Center for Cancer Research
- Department of Defense [BC 102335]
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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.
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