Neurofibromatosis is a very common genetic disorder affecting 1 out of 3,000 children and adults. NF1 patients can develop brain and nerve tumors that can compromise brain and nerve structure and function. We aim to pursue cancer research, and primarily study nerve tumors, with the goal of improving the quality of life of >110,000 people in the U.S., and many more worldwide.
My research interests include glial cell biology, intracellular signaling, preclinical therapeutics, and peripheral nerve tumorigenesis. My laboratory team and I share the goal of finding innovative treatments for neurofibromatosis by utilizing our knowledge of developmental biology together and levels of ribonucleic acid (RNA) and proteins in neurofibroma tumor and immune cell types as guides for drug selection and testing.
Some of the notable discoveries my team and I have made in our lab include: 1) developing and producing transcriptome data for investigating NF1 cells and nerve tumors and 2) pioneering the use of mitogen-activated protein kinase (MEK) inhibitors in a new and original preclinical model of the peripheral nerve tumor. This research led clinicians to pursue clinical trials, and in 2020, the Food and Drug Administration (FDA) granted approval for use of MEK inhibitors as a therapy for plexiform neurofibromas.
I also recruit and mentor neuro-oncology and rasopathy faculty at the Cincinnati Children’s, and mentor students and postdoctoral fellows in my laboratory.
Throughout my career, I received awards, including:
I joined the Cincinnati Children’s team in 2006. I now have more than 30 years of experience in Schwann cell biology and cancer research. My research has been consistently funded by the National Institutes of Health, the Department of Defense Program on Neurofibromatosis and other agencies. My work has been published in numerous journals, including Cancer Cell, Cell Reports, Scientific Reports, Cancer Research, PNAS and Clinical Cancer Research.
PhD: Indiana University, 1982
BA: Brown University, 1975
Fellowship: Washington University St. Louis, 1987
Preclinical testing in neurofibromatosis
Genetic mutations in tumor suppressor genes; development and tumorigenesis of the nervous system; peripheral NF1, NF2
Multi-Echo Resting-State Functional Magnetic Resonance Imaging Analysis of Attention-Deficit/Hyperactivity Disorder Severity and Motor Dysfunction in a Pediatric Sample of Neurofibromatosis Type 1. Pediatric Neurology. 2026.
MAPK-dependent release of GDNF from Schwann cells mediates tumor-independent pain in neurofibromatosis 1. Science Signaling. 2026; 19(939):eaee5174.
Decreased PP2A expression and activity represent a therapeutic target for plexiform neurofibroma. Acta Neuropathologica Communications. 2026.
Valosin-Containing Protein Contributes to Plexiform Neurofibroma Formation and Represents a Novel Therapeutic Target. Cells. 2026; 15(9).
A Randomized, Double-Blind, Pilot Study of N-Acetylcysteine for Motor and Cognitive Symptoms in Youth With Neurofibromatosis Type 1. Pediatric Neurology. 2026; 180:129-137.
Genetic activation of ERK2 recapitulates core neurodevelopmental features of Rasopathy syndromes in mice. HGG Advances. 2026; 7(3):100621.
Abstract 2269: Two-step mechanism of plexiform neurofibroma formation: Role of the NF-κB pathway in neurofibroma formation. Cancer Research. 2026; 86(7_Supplement):2269-2269.
The 9th International RASopathies Symposium. American Journal of Medical Genetics, Part A. 2026.
Pharmacogenomic Synthetic Lethal Screens Reveal Hidden Vulnerabilities and New Therapeutic Approaches for Treatment of NF1-Associated Tumors. Molecular Cancer Therapeutics. 2026; 25(2):230-243.
Daytime SHP2 inhibitor dosing, when immune cell numbers are elevated, shrinks neurofibromas. Life Science Alliance. 2025; 8(12).