ArticleBrain pathology (Zurich, Switzerland)2007
Differential Pi3K-pathway activation in cortical tubers and focal cortical dysplasias with balloon cells.
Article in Brain pathology (Zurich, Switzerland), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 71 citations in OpenAlex.
- Iconography of abnormal non-neuronal cells in pediatric focal cortical dysplasia type IIb and tuberous sclerosis complex.Frontiers in cellular neuroscience · 2024Review
- Multi-tensor diffusion abnormalities of gray matter in an animal model of cortical dysplasia.Frontiers in neurology · 2023Article
- Epilepsy in the mTORopathies: opportunities for precision medicine.Brain communications · 2021Review
- Post-Surgical Outcome and Its Determining Factors in Patients Operated on With Focal Cortical Dysplasia Type II-A Retrospective Monocenter Study.Frontiers in neurology · 2021Article
- Mechanistic target of rapamycin complex 1 and 2 in human temporal lobe epilepsy.Annals of neurology · 2018Article
- Impaired oligodendroglial turnover is associated with myelin pathology in focal cortical dysplasia and tuberous sclerosis complex.Brain pathology (Zurich, Switzerland) · 2017Article
- Down-Regulated Expression of Liver X Receptor beta in Cortical Lesions of Patients with Focal Cortical Dysplasia.Journal of molecular neuroscience : MN · 2016Article
- Increased Expression of Transient Receptor Potential Vanilloid 4 in Cortical Lesions of Patients with Focal Cortical Dysplasia.CNS neuroscience & therapeutics · 2016Article
- Tracking and transforming neocortical progenitors by CRISPR/Cas9 gene targeting and piggyBac transposase lineage labeling.Development (Cambridge, England) · 2015Article
- PI3K/AKT pathway mutations cause a spectrum of brain malformations from megalencephaly to focal cortical dysplasia.Brain : a journal of neurology · 2015Article
- Focal Cortical Dysplasia.Seminars in neurology · 2015Review
- The enlarging spectrum of focal cortical dysplasias.Brain : a journal of neurology · 2015Article
- mTOR signaling in epilepsy: insights from malformations of cortical development.Cold Spring Harbor perspectives in medicine · 2015Review
- Contribution of tumor heterogeneity in a new animal model of CNS tumors.Molecular cancer research : MCR · 2014Article
- Mechanism-based treatment in tuberous sclerosis complex.Pediatric neurology · 2014Review
- Epilepsy related to developmental tumors and malformations of cortical development.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2014Review
- BRAF V600E mutation is associated with mTOR signaling activation in glioneuronal tumors.Brain pathology (Zurich, Switzerland) · 2014Article
- A critical review of mTOR inhibitors and epilepsy: from basic science to clinical trials.Expert review of neurotherapeutics · 2013Review
- Mammalian target of rapamycin (mTOR) activation in focal cortical dysplasia and related focal cortical malformations.Experimental neurology · 2013Review
- Differential expression of major histocompatibility complex class I in developmental glioneuronal lesions.Journal of neuroinflammation · 2013Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Balloon cells of distinct focal cortical dysplasias type IIb (FCD(IIb)) and giant cells of cortical tubers in tuberous sclerosis (TSC) constitute neuropathological hallmarks and cytological similarities. In TSC, frequent mutations in the TSC1 or TSC2 genes result in mTOR-signaling activity. Here, we addressed whether Pi3K-pathway activation differentiates balloon cells from giant cells. We used immunohistochemistry with antibodies against p-PDK1 (S241), p-Akt (S473), p-tuberin (T1462), p-p70(S6K) (T389), p-p70(S6K) (T229) and phalloidin-staining to analyze stress fiber formation in balloon cells of FCD(IIb) (n = 23) compared with cortical tuber giant cells (n = 5) and adjacent normal CNS tissue as control. We have further established an in vitro assay to assess potential phosphorylation between Akt and S6. We observed phosphorylated (p-)PDK1, p-Akt, p-tuberin, and p-p70-kDa S6-kinase (p-p70(S6K); residue T229) in balloon cells, whereas giant cells showed only equivalent levels of p-tuberin, p-p70(S6K) and stress fibers. Furthermore, Pi3K-cascade activity in balloon cells may reflect pathway "cross-talk". An in vitro assay revealed S6, a major target of p70(S6K), to increase phosphorylation of Akt. Our data suggest recruitment of different Pi3K-cascade factors in the molecular pathogenesis of giant cells in cortical tubers vs. balloon cells in FCD(IIb) and provides new implications for the development of treatment strategies for these cortical malformations.
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