Tool targets cancer-causing fusions' weak spot NatureComms
The promise of therapeutically targeting oncogenic fusions is further reinforced by the recent development of genome-editing tools enabled by CRISPR-Cas9 system, where highly specific targeted editing can be achieved using a guide RNA complementary to the target DNA. Therefore, a natural hypothesis is that oncogenic fusions can harbor therapeutic vulnerability for genome editing-based therapeutics.
Here, we show general forces shaping the formation of oncogenic fusions, including gene length, splicing, translation, and protein domains. We introduce a mathematical model that can detect differential selection pressure, which is validated in-positive acute myeloid leukemia to confer superior prognostic value on event-free survival than other well-known clinical features.
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