Chrissa Baldy | 2026 I.S. Symposium
狈补尘别:听Chrissa Baldy
罢颈迟濒别:听Understanding Chronic Pain at Its Source: How Small Molecular Changes Drive Pain in Schwannomatosis
惭补箩辞谤:听Neuroscience
础诲惫颈蝉辞谤:听Claudia Thompson
Schwannomatosis (SWN) is a rare genetic disease characterized by the formation of multiple benign peripheral nerve sheath tumors, known as schwannomas. SWN is typically associated with germline mutations in SMARCB1, LZTR1, or not otherwise classified (NOC), and consists of schwannomas that are histologically indistinguishable from solitary schwannomas (SS), which occur sporadically and account for approximately 90% of all schwannomas. Both SWN and SS tumors can induce severe pain. However, SWN pain is often debilitating and can be localized or widespread, whereas SS pain is generally localized to the tumor. Previous research has demonstrated that when cultured, painful SWN tumors can chemically condition the nearby environment by secreting pro-inflammatory factors. Additionally, both in-vivo and in-vitro analysis have demonstrated that this tumor secretome can sensitize sensory neurons to painful stimuli, suggesting the role of inflammatory mediators in SWN pain. Accordingly, this study aimed to elucidate the transcriptomic mechanisms of SWN鈥慳ssociated pain. Building off previous findings, the present study hypothesized that systemic inflammation drives the SWN pain phenotype. Within this study, gene expression of SWN and SS tumors with painful and nonpainful phenotypes were analyzed from microarray datasets. Differential expression, protein-protein interaction networks, and functional enrichment of the pain phenotypes within and between each tumor subtype were examined. Aligning with the hypothesis, the analysis identified notable upregulation of chemokines and other inflammatory mediators in painful SWN compared to both nonpainful SWN and painful SS, with strong enrichment for immune-cell chemotaxis, supporting the role of inflammation-mediated sensitization in SWN pain.
Posted in Symposium 2026 on May 1, 2026.
