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Cody Nesvick, MD, joined the Department of Neurological Surgery at the University of Pittsburgh School of Medicine in April 2025 as assistant professor of neurological surgery and as a pediatric neurosurgeon at UPMC Children’s Hospital of Pittsburgh. He serves as co-director of the Pediatric Skull Base Surgery Program and is surgical co-director of the UPMC Children’s Neurovascular Center of Excellence. Dr. Nesvick’s recruitment to UPMC Children’s reflects both the hospital’s clinical prowess and its strong infrastructure for translational laboratory research.
"The research enterprise at UPMC Children’s is outstanding, and the clinical program is one of the largest in North America for the diseases in which I specialize," says Dr. Nesvick. "The ability to integrate a complex surgical practice with a robust basic and translational research program in pediatric brain tumors perfectly fits my vision for a transformational brain tumor program.”
Dr. Nesvick’s clinical practice focuses on treating children with complex cranial conditions, including brain tumors, skull base tumors, and cerebrovascular diseases such as moyamoya disease and arteriovenous malformations.
“I also specialize in minimally invasive neurosurgical approaches, including endoscopic endonasal surgery for treating complex and difficult to reach diseases of the skull base."
Education and Training
Dr. Nesvick earned his medical degree at the University of Tennessee Health Science Center in Memphis. During medical school, he completed a research fellowship at the National Institutes of Health through the Medical Research Scholars Program, a joint venture between the NIH, Howard Hughes Medical Institute and medical industry, where he established roots in basic and translational neuro-oncology.
He completed his neurosurgical residency at the Mayo Clinic, where he also undertook a three-year National Cancer Institute-funded postdoctoral research fellowship in neuro-oncology. Following residency, he pursued subspecialty fellowship training in pediatric neurosurgery at the Hospital for Sick Children at the University of Toronto, followed by additional fellowship training in open and endoscopic skull base oncology at Emory University, in Atlanta.
"The combination of training across these institutions allowed me to build an integrated approach to complex pediatric neurosurgery, incorporating both highly specialized clinical skills and translational research experience," says Dr. Nesvick.
Pediatric Brain Tumor Research
During his research training prior to joining UPMC Children’s, Dr. Nesvick focused extensively on atypical teratoid rhabdoid tumor (ATRT), a rare and highly aggressive brain tumor that primarily affects infants and young children. ATRT is driven by mutations in a gene called SMARCB1, which has an important role in regulating how genes are turned on and off during normal development. These types of tumors can occur anywhere in the body, but in young children mostly manifest in the brain, spinal cord and kidneys.
"Unlike many adult cancers that accumulate mutations over time, pediatric brain tumors like ATRT often arise from disruptions in normal developmental biology," says Dr. Nesvick. "The loss of SMARCB1 alters how the cell's DNA is packaged and accessed, leading to changes in which genes are active or inactive."
Dr. Nesvick and his colleagues used patient-derived tumor models and advanced molecular techniques to study how SMARCB1 loss alters gene regulation in ATRT cells. Their work showed that SMARCB1 normally allows key transcription factors to bind to specific regions of DNA that guide normal cell development. Without SMARCB1, many of these regulatory regions become inaccessible, forcing transcription factors to activate pathways that help the tumor survive. Dr. Nesvick’s team found that this can be leveraged as a therapeutic vulnerability: these pathways can be inhibited through either direct degradation of residual SWI/SNF activity or indirect pharmacologic inhibition of the transcription factors AP-1 and TEAD.
"We identified a set of transcription factors and survival pathways that remain active even after SMARCB1 is lost," says Dr. Nesvick. "By targeting these remaining pathways with experimental therapies in the lab, we were able to disrupt tumor growth and improve survival in a preclinical model.”
"What makes these tumors challenging and scientifically interesting is that they are often genetically simple but profoundly epigenetically abnormal," says Dr. Nesvick. "The hope is that by understanding these mechanisms in detail, we can eventually design therapies that specifically disrupt the tumor's remaining survival circuits."
Building on this foundation, Dr. Nesvick is now establishing the Laboratory of Applied Epigenomics at the John G. Rangos, Sr. Research Center at UPMC Children’s, where his team will continue to study how disruptions in gene regulation contribute to pediatric brain tumor development, and to explore new treatment strategies aimed at these mechanisms.
Selection of Published Research Authored by Dr. Nesvick
Nesvick CL, Zhang L, Yan Y, Wixom AQ, Hamdan FH, Ge J, Anderson JB, Gaspar-Maia A, Johnsen SA, Daniels DJ. SWI/SNF complexes govern ontology-specific transcription factor function in MYC-subtype atypical teratoid rhabdoid tumor. Neuro Oncol. 2025 Mar 23. Online ahead of print.
Zhang L, Nesvick CL, Day CA, Choi J, Lu VM, Peterson T, Power EA, Anderson JB, Hamdan FH, Decker PA, Simons R, Welby JP, Siada R, Ge J, Kaptzan T, Johnsen SA, Hinchcliffe EH, Daniels DJ. STAT3 is a biologically relevant therapeutic target in H3K27M-mutant diffuse midline glioma. Neuro Oncol. 2022 Oct; 24(10): 1700-1711.
Nesvick CL, Lafay-Cousin L, Raghunathan A, Bouffet E, Huang AA, Daniels DJ. Atypical teratoid rhabdoid tumor: molecular insights and translation to novel therapeutics. J Neurooncol. 2020 Oct;1 50(1): 47-56.