ArticleJournal of neuropathology and experimental neurology2010
Early progenitor cell marker expression distinguishes type II from type I focal cortical dysplasias.
Article in Journal of neuropathology and experimental neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Pathogenetic mechanisms of focal cortical dysplasia.Epilepsia · 2014Pooled it
- Balloon cells in type II focal cortical dysplasia: developmental origins, molecular signatures, and epileptogenic mechanisms.Frontiers in cell and developmental biology · 2026Review
- Transcriptomic and morphologic vascular aberrations underlying FCDIIb etiology.Nature communications · 2025Article
- Multiparameter quantitative analyses of diagnostic cells in brain tissues from tuberous sclerosis complex.Cytometry. Part B, Clinical cytometry · 2025Article
- Multimodal single-cell profiling reveals neuronal vulnerability and pathological cell states in focal cortical dysplasia.iScience · 2024Article
- Krüppel-like factors: potential roles in blood-brain barrier dysfunction and epileptogenesis.Acta pharmacologica Sinica · 2024Review
- Balloon cells in malformations of cortical development: friends or foes?Acta epileptologica · 2024Review
- Iconography of abnormal non-neuronal cells in pediatric focal cortical dysplasia type IIb and tuberous sclerosis complex.Frontiers in cellular neuroscience · 2024Review
- Dynamic expression of NR2F1 and SOX2 in developing and adult human cortex: comparison with cortical malformations.Brain structure & function · 2021Article
- Metabolic Profile and Neurogenic Potential of Human Amniotic Fluid Stem Cells From Normal vs. Fetus-Affected Gestations.Frontiers in cell and developmental biology · 2021Article
- Increased expression of Fragile X mental retardation protein in malformative lesions of patients with focal cortical dysplasia.Neuroreport · 2020Article
- Dissecting the genetic basis of focal cortical dysplasia: a large cohort study.Acta neuropathologica · 2019Article
- Malformations of Cerebral Cortex Development: Molecules and Mechanisms.Annual review of pathology · 2019Review
- Multinodular and vacuolating neuronal tumors in epilepsy: dysplasia or neoplasia?Brain pathology (Zurich, Switzerland) · 2018Article
- Mechanistic target of rapamycin complex 1 and 2 in human temporal lobe epilepsy.Annals of neurology · 2018Article
- Contribution of Altered Endocannabinoid System to Overactive mTORC1 Signaling in Focal Cortical Dysplasia.Frontiers in pharmacology · 2018Article
- Identification and characterization of a new source of adult human neural progenitors.Cell death & disease · 2017Article
- Expression of pannexin 1 and 2 in cortical lesions from intractable epilepsy patients with focal cortical dysplasia.Oncotarget · 2017Article
- Clinical and immunohistochemical characteristics of type II and type I focal cortical dysplasia.Oncotarget · 2016Article
- Focal Cortical Dysplasia.Seminars in neurology · 2015Review
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Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
Type I and type II focal cortical dysplasias (FCDs) exhibit distinct histopathologic features that suggest different pathogenic mechanisms. Type I FCDs are characterized by mild laminar disorganization and hypertrophic neurons, whereas type II FCDs exhibit dramatic laminar disorganization and cytomegalic cells (balloon cells). Both FCD types are associated with intractable epilepsy; therefore, identifying cellular or molecular differences between these lesion types that explains the histologic differences could provide new diagnostic and therapeutic insights. Type II FCDs express nestin, a neuroglial progenitor protein that is modulated in vitro by the stem cell proteins c-Myc, sex-determining region Y-box 2 (SOX2), and Octamer-4 (Oct-4) after activation of mammalian target of rapamycin complex 1 (mTORC1). Because mTORC1 activation has been demonstrated in type II FCDs, we hypothesized that c-Myc, SOX2, and Oct-4 expression would distinguish type II from type I FCDs. In addition, we assayed the expression of progenitor cell proteins forkhead box G1 (FOXG1), Kruppel-like factor 4 (KLF4), Nanog, and SOX3. Differential expression of 7 stem cellproteins and aberrant phosphorylation of2mTORC1 substrates, S6 andS6 kinase 1 proteins, clearly distinguished type II from type I FCDs(n = 10 each). Our results demonstrate new potential pathogenic pathways in type II FCDs and suggest biomarkers for diagnostic pathology in resected epilepsy specimens.
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