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Analysis of 1386 epileptogenic brain lesions reveals association with <i>DYRK1A</i> and <i>EGFR</i>

  • Christian M. Bosselmann
  • , Costin Leu
  • , Tobias Bruenger
  • , Lucas Hoffmann
  • , Sara Baldassari
  • , Mathilde Chipaux
  • , Roland Coras
  • , Katja Kobow
  • , Hajo Hamer
  • , Daniel Delev
  • , Karl Roessler
  • , Christian G. Bien
  • , Thilo Kalbhenn
  • , Tom Pieper
  • , Till Hartlieb (Co-author)
  • , Kerstin Becker
  • , Lisa Ferguson
  • , Robyn M. Busch
  • , Stephanie Baulac
  • , Peter Nuernberg
  • Imad Najm, Ingmar Bluemcke, Dennis Lal
  • Cleveland Clinic Foundation
  • University of Texas System
  • Sorbonne Université
  • Fondation Adolphe de Rothschild
  • Medical University of Vienna
  • Ctr Pediat Neurol Neurorehabil & Epileptol
  • University Hospital of Cologne
  • MD, MPH Mandy Brown Belfort, Harvard University

Research output: Contribution to journalOriginal Articlepeer-review

12 Citations (Web of Science)

Abstract

Lesional focal epilepsy (LFE) is a common and severe seizure disorder caused by epileptogenic lesions, including malformations of cortical development (MCD) and low-grade epilepsy-associated tumors (LEAT). Understanding the genetic etiology of these lesions can inform medical and surgical treatment. We conducted a somatic variant enrichment mega-analysis in brain tissue from 1386 individuals who underwent epilepsy surgery, including 599 previously unpublished individuals with ultra-deep ( > 1600x) targeted panel sequencing. Here we confirm four known associations (BRAF, SLC35A2, MTOR, PTPN11), support eight associations without prior statistical support (FGFR1, PIK3CA, AKT3, NF1, PTEN, RHEB, KRAS, NRAS), and identify novel associations for two genes, DYRK1A and EGFR. Both novel genes show specific histopathological phenotypes, interact with LFE genes and pathways, and may represent promising candidates as biomarkers and potentially druggable targets.
Original languageEnglish
Article number10429
Number of pages10
JournalNature Communications
Volume15
Issue number1
DOIs
Publication statusPublished - 30 Nov 2024

Keywords

  • Growth-factor receptor
  • Somatic mutations
  • Reference panel
  • Epilepsy
  • Pathogenicity
  • Frequencies
  • System
  • Cancer

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