Perineuronal net degradation in aggressive glioblastomas with KANK1::NTRK2 fusions

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ID: 325852
2026
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Abstract
Abstract Background Approximately 10% of glioblastomas harbor targetable genomic fusions. NTRK2 participates in a variety of fusion events that drive tumorigenesis. Two previous reports have described KANK1::NTRK2 fusions in adult glioblastoma patients with poor survival. Methods We performed a retrospective analysis of glioblastoma patients treated at Dartmouth-Hitchcock Medical Center (DHMC) from 2020-2025 to identify cases harboring KANK1::NTRK2 fusions. Clinical presentation, treatment, histopathologic features, and outcomes were reviewed. In addition, we conducted GeoMx whole-transcriptome and high-plex proteomic digital spatial profiling of a KANK1::NTRK2-positive glioblastoma and a comparator tumor from a long-term survivor. Candidate biomarkers were orthogonally validated using immunohistochemistry and/or immunofluorescence. Results Two patients with KANK1::NTRK2 fusion glioblastoma were identified, both demonstrating rapid progression, therapeutic resistance, and survival of less than seven months. Proteomic profiling showed increased expression and activation of canonical NTRK2 downstream signaling pathways, particularly MEK1/2 and ERK1/2. This was accompanied by upregulation of extracellular matrix remodeling enzymes, including MMP3, MMP14, and ADAM15, along with reduced expression of extracellular matrix-associated transcripts and perineuronal net components in particular compared to a non-fusion glioblastoma. Conclusions These limited, hypothesis-generating findings suggest constitutive NTRK2 signaling may promote coordinated extracellular matrix degradation and remodeling, potentially facilitating rapid and aggressive tumor growth and invasion in a subset of glioblastomas.
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Authors Madhumala K. Sadanandappa, Nishika Karbhari, Brizha Knowles, Scott Palisoul, Edward G. Hughes, Laura J. Tafe, George Zanazzi, Chun-Chieh Lin, Jennifer Hong
Journal Neuro-Oncology Advances
Year 2026
DOI
10.1093/noajnl/vdag219
URL
https://doi.org/10.1093/noajnl/vdag219
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