@article {1532777,
	title = {Dysregulation of cancer genes by recurrent intergenic fusions},
	journal = {Genome Biol},
	volume = {21},
	number = {1},
	year = {2020},
	month = {2020 Jul 06},
	pages = {166},
	abstract = {BACKGROUND: Gene fusions have been studied extensively, as frequent drivers of tumorigenesis as well as potential therapeutic targets. In many well-known cases, breakpoints occur at two intragenic positions, leading to in-frame gene-gene fusions that generate chimeric mRNAs. However, fusions often occur with intergenic breakpoints, and the role of such fusions has not been carefully examined. RESULTS: We analyze whole-genome sequencing data from 268 patients to catalog gene-intergenic and intergenic-intergenic fusions and characterize their impact. First, we discover that, in contrast to the common assumption, chimeric oncogenic transcripts-such as those involving ETV4, ERG, RSPO3, and PIK3CA-can be generated by gene-intergenic fusions through splicing of the intervening region. Second, we find that over-expression of an upstream or downstream gene by a fusion-mediated repositioning of a regulatory sequence is much more common than previously suspected, with enhancers sometimes located megabases away. We detect a number of recurrent fusions, such as those involving ANO3, RGS9, FUT5, CHI3L1, OR1D4, and LIPG in breast; IGF2 in colon; ETV1 in prostate; and IGF2BP3 and SIX2 in thyroid cancers. CONCLUSION: Our findings elucidate the potential oncogenic function of intergenic fusions and highlight the wide-ranging consequences of structural rearrangements in cancer genomes.},
	issn = {1474-760X},
	doi = {10.1186/s13059-020-02076-2},
	author = {Yun, Jae Won and Yang, Lixing and Park, Hye-Young and Lee, Chang-Woo and Cha, Hongui and Shin, Hyun-Tae and Noh, Ka-Won and Choi, Yoon-La and Park, Woong-Yang** and <b>Park, Peter J**</b>}
}
