Patrick S. Dischinger

This paper identifies an alternatively spliced NF1 isoform, NLS SE, that promotes luminal breast cancer progression by disrupting nuclear neurofibromin function and reprogramming ER signaling toward post-transcriptional regulation.

This study identifies epigenetic differences between cutaneous and plexiform neurofibromas that drive distinct RAS/MKK/P38 signaling and clinical behavior.

This study shows that P53 status modulates the response to MET and MEK inhibition in NF1-related MPNSTs, with P53 wild-type tumors showing greater suppression of RAS/MAPK and PI3K/AKT activation.