| Summary: | Chromosomal rearrangement and genome instability are common features of cancer cells in human. Consequently, gene duplication and gene fusion events are frequently observed in human malignancies and many of the products of these events are pathogenic, representing significant drivers of tumourigenesis and cancer evolution. In certain subsets of cancers duplicated and fused genes appear to be essential for initiation of tumour formation, and some even have the capability of transforming normal cells, highlighting the importance of understanding the events that result in their formation. The mechanisms that drive gene duplication and fusion are unregulated in cancer and they facilitate rapid evolution by selective forces akin to Darwinian survival of the fittest on a cellular level. In this review, we examine current knowledge of the landscape and prevalence of gene duplication and gene fusion in human cancers.
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