Overview
- Published in Nature Communications, researchers from the Centre for Genomic Regulation with Columbia collaborators adapted VIPER to quantify splicing edits directly rather than inferring activity from splicing factors.
- Applying the method to roughly 10,000 paired tumor and healthy samples across 14 TCGA cancer types revealed two recurrent splicing programs that recur across cancers.
- One program resembles an accelerator associated with poorer outcomes, while a second resembles a brake whose loss in tumors aligns with relatively better survival.
- The analysis nominated about 120 molecules that appear to tilt splicing toward cancer phenotypes, with FUS standing out despite limited prior study in oncology.
- The technique runs on existing RNA-seq data, enabling rapid expansion to other datasets and potentially to diseases beyond cancer, though the targets now require experimental validation.