Carrie R. Graveel

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 YAP signaling as a driver of resistance to MEK and AKT inhibitors in NF1-related MPNSTs using preclinical models and spatial transcriptomics.

This study evaluates bifunctional ER degraders with different ubiquitin ligase ligands, finding that pan-IAP antagonists enhance ER degradation and induce TNF-dependent cell death more effectively than existing therapies.

This study investigates how NF1 deficiency affects metabolic reprogramming in ER+ breast cancer and identifies potential therapeutic synergies between metabolic and targeted inhibitors.

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.

This study identifies early MET amplification in NF1-related MPNST progression and shows MET inhibition effectively targets these tumors.