Gene Expression Analysis in an Animal Model of Cortical Dysplasia-IRRADIATED GROUP
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE13697 | GEO | 2008/12/10
SECONDARY ACCESSION(S): PRJNA109421
REPOSITORIES: GEO
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Project description:Cortical Dysplasia (CD) is the histopathological substrate in almost half of all drug-resistant epilepsy. Little is known about the gene expression profile of CD. As such information may help target therapeutics more effectively, our aim was to perform a gene expression analysis of an animal model of cortical dysplasia induced by in utero irradiation. THIS SERIES (GSE13697) INCLUDES ALL (AND ONLY) EXPERIMENTAL SAMPLES--I.E. IRRADIATED/CORTICAL DYSPLASIA (9). Nine offspring from irradiated animals, and nine age-matched controls were sacrificed at post-natal day 60. Cortex and hippocampal regions were separated, and total ribonucleic acid (RNA) was extracted using a commercially available kit (Qiagen®). RNA was then subjected to a gene expression analysis using an oligonucleotide microarray platform (Illumina®). After statistical analysis, genes were considered differentially expressed when a p value less than .001 was observed. Real-time, quantitative polymerase chain reaction (RT-qPCR) was used to confirm microarray results for three genes via the Livak method.
2008-12-09 | E-GEOD-13697 | biostudies-arrayexpress
Project description:Cortical Dysplasia (CD) is the histopathological substrate in almost half of all drug-resistant epilepsy. Little is known about the gene expression profile of CD. As such information may help target therapeutics more effectively, our aim was to perform a gene expression analysis of an animal model of cortical dysplasia induced by in utero irradiation. THIS SERIES (GSE13676) INCLUDES ALL (AND ONLY) CONTROL SAMPLES (9).
2008-12-10 | GSE13676 | GEO
Project description:Cortical Dysplasia (CD) is the histopathological substrate in almost half of all drug-resistant epilepsy. Little is known about the gene expression profile of CD. As such information may help target therapeutics more effectively, our aim was to perform a gene expression analysis of an animal model of cortical dysplasia induced by in utero irradiation. THIS SERIES (GSE13676) INCLUDES ALL (AND ONLY) CONTROL SAMPLES (9). Nine offspring from irradiated animals, and nine age-matched controls were sacrificed at post-natal day 60. Cortex and hippocampal regions were separated, and total ribonucleic acid (RNA) was extracted using a commercially available kit (Qiagen®). RNA was then subjected to a gene expression analysis using an oligonucleotide microarray platform (Illumina®). After statistical analysis, genes were considered differentially expressed when a p value less than .001 was observed. Real-time, quantitative polymerase chain reaction (RT-qPCR) was used to confirm microarray results for three genes via the Livak method.
2008-12-09 | E-GEOD-13676 | biostudies-arrayexpress
Project description:Focal cortical dysplasia (FCD), a focal brain malformation, is the most common cause of intractable epilepsy. One of the related disorders is tuberous sclerosis (TS). The dysplasia appears to result from a defect in cortical development, however, this disorder is heterogeneous, and FCD seizure therapy is non-specific and failure-prone. As a final recourse, patients may undergo multiple surgical resections to control seizures. Thus, there is a clinical need to characterize this disorder with respect to structural, molecular, and electrophysiological profiles, which will lead to development of animal models and pilot therapies that we will then apply to humans.
2015-06-01 | GSE62019 | GEO
Project description:Focal Cortical Dysplasia (FCD) is a frequent cause of drug-resistant focal epilepsy in children and young adults. The international FCD classifications of 2011 and 2022 have identified several clinico-pathological subtypes, either occurring isolated, i.e., FCD ILAE Type 1 or 2, or in association with a principal cortical lesion, i.e., FCD Type 3. Here, we addressed the DNA methylation signature of a previously described new subtype of FCD 3D occurring in the occipital lobe of very young children and microscopically defined by neuronal cell loss in cortical layer 4. We studied the DNA methylation profile using 850K BeadChip arrays in a retrospective cohort of 104 patients with FCD 1A, 2A, 2B, 3D, TLE without FCD, and 16 postmortem specimens without neurological disorders as controls, operated in China or in Germany. DNA was extracted from formalin-fixed paraffin-embedded tissue blocks with microscopically confirmed lesions, and DNA methylation profiles were bioinformatically analyzed with a recently developed deep learning algorithm. Our results revealed a distinct position of FCD 3D in the DNA methylation map of common FCD subtypes, also different from non-FCD epilepsy surgery controls or non-epileptic postmortem controls. Within the FCD 3D cohort, the DNA methylation signature separated three histopathology subtypes, i.e., fibrotic scarring around porencephalic cysts, loss of layer 4, and Rasmussen encephalitis. Differential methylation in FCD 3D with loss of layer 4 specifically mapped to biological pathways related to neurodegeneration, biogenesis of ECM components, axon guidance, and regulation of the actin cytoskeleton. Our data suggest that DNA methylation signatures in cortical malformations are not only of diagnostic value but also phenotypically relevant, providing the molecular underpinnings of structural and histopathological features associated with epilepsy. Further studies will be necessary to confirm these results and clarify their functional relevance and epileptogenic potential in these difficult-to-treat children.
2023-08-21 | GSE227239 | GEO
Project description:CpG methylation analysis of MeDIP DNA using Agilent Human DNA methylation Microarray slides (G4495A, AMADID 023795) Using methylated DNA immunoprecipitation microarray (MeDIP-chip) and Agilent Human DNA methylation Microarray slides (G4495A, AMADID 023795) we report genomic methylation signatures of tissues resected from Mesial temporal epilepsy (MTLE) and Focal cortical dysplasia (FCD) type II patients undergoing surgery. Control samples were obtained from the non-epileptic post mortem cases without any brain pathology
2018-03-10 | GSE96067 | GEO
Project description:Modeling Focal Cortical Dysplasia (FCD) using cortical organoids
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Project description:Patients with Crohn’s disease (CD) have an increased risk of small bowel adenocarcinoma (SBA). Long duration of CD is the main risk factor. SB dysplasia has been associated with SBA in 20% of cases, always described in diseased sites. The progression to neoplasia and natural history remains unknown but progression of inflammation to dysplasia and then to adenocarcinoma is suspected.
As for surveillance recommendations for colorectal carcinoma in long standing inflammatory colonic disease, endoscopic screening of SB could be proposed in CD patients with risk factors of SBA. No study can be found in literature.
The investigators propose a multicenter exploratory open study on prospective cohort of CD patients with high risk of dysplasia or cancer. The goal is evaluate the rate of dysplasia and adenocarcinoma detected by enteroscopy with biopsies in a high risk CD population
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Project description:Focal cortical dysplasia (FCD) is a type of malformation of cortical development and its main clinical manifestation is medically intractable epilepsy We aimed to investigate whether abnormal gene regulation, mediated by microRNA, could be involved in FCD type II, in view of to help clarify the molecular mechanism leading to this type of cortical malformation.
2018-04-03 | GSE97365 | GEO
Project description:Ulcerative colitis (UC) patients have a greater risk of developing colorectal cancer through inflammation-dysplasia-carcinoma sequence of transformation. The histopathological diagnosis of dysplasia is therefore of critical clinical relevance, but dysplasia may be difficult to distinguish from inflammatory changes. A proteomic pilot study on 5 UC colorectal dysplastic patients highlighted proteins differentially distributed between paired dysplastic, inflammatory and normal tissues. The best candidate marker was selected and immunohistochemistry confirmation was performed on AOM/DSS mouse model lesions, 37 UC dysplasia, 14 UC cancers, 23 longstanding UC, 35 sporadic conventional adenomas, 57 sporadic serrated lesions and 82 sporadic colorectal cancers. Differential proteomics found 11 proteins significantly more abundant in dysplasia compared to inflammation, including Solute carrier family 12 member 2 (SLC12A2) which was confidently identified with 8 specific peptides and was below the limit of quantitation in both inflammatory and normal colon. SLC12A2 immunohistochemical analysis confirmed the discrimination of preneoplastic and neoplastic lesions from inflammatory lesions in mice, UC and in sporadic contexts. A specific SLC12A2 staining pattern termed “loss of gradient” reached 89% sensitivity, 95% specificity and 92% accuracy for UC-dysplasia diagnosis together with an inter-observer agreement of 95.24% (multirater κfree of 0.90; IC95%: 0.78 – 1.00). Such discrimination could not be obtained by Ki67 staining. This specific pattern was also associated with sporadic colorectal adenomas and cancers. We found a specific SLC12A2 immunohistochemical staining pattern in precancerous and cancerous colonic UC-lesions which could be helpful for diagnosing dysplasia and cancer in UC and non-UC patients.
2020-09-16 | PXD018679 | Pride