期刊
CELL REPORTS
卷 23, 期 1, 页码 227-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2018.03.050
关键词
-
类别
资金
- [U54 HG003273]
- [U54 HG003067]
- [U54 HG003079]
- [U24 CA143799]
- [U24 CA143835]
- [U24 CA143840]
- [U24 CA143843]
- [U24 CA143845]
- [U24 CA143848]
- [U24 CA143858]
- [U24 CA143866]
- [U24 CA143867]
- [U24 CA143882]
- [U24 CA143883]
- [U24 CA144025]
- [P30 CA016672]
- [U24 CA211006]
Gene fusions represent an important class of somatic alterations in cancer. We systematically investigated fusions in 9,624 tumors across 33 cancer types using multiple fusion calling tools. We identified a total of 25,664 fusions, with a 63% validation rate. Integration of gene expression, copy number, and fusion annotation data revealed that fusions involving oncogenes tend to exhibit increased expression, whereas fusions involving tumor suppressors have the opposite effect. For fusions involving kinases, we found 1,275 with an intact kinase domain, the proportion of which varied significantly across cancer types. Our study suggests that fusions drive the development of 16.5% of cancer cases and function as the sole driver in more than 1% of them. Finally, we identified druggable fusions involving genes such as TMPRSS2, RET, FGFR3, ALK, and ESR1 in 6.0% of cases, and we predicted immunogenic peptides, suggesting that fusions may provide leads for targeted drug and immune therapy.
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