HIGHLIGHTS
SUMMARY
The authors discover neo splice sites in 18 oncogenic fusion gene pairs and demonstrate that such splice sites confer therapeutic vulnerability for etiology-based genome editing. Successes in targeted inhibition of oncogenic fusions (e_g, imatinib for BCR-ABL111) have inspired the notion of "oncogene addiction"12 that posits the therapeutic potential of targeting oncogenic fusions. Percent patient tumors with oncogenic fusion detected are indicated with gray rings. b-d Spectrum of neosplicing (b), neo-translational (c) and chimeric exon (d) fusions. e-g Spectrum of canonical fusions in leukemia (e), brain tumor (f) and . . .
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