Tumor DNA methylation profiling of patients with Adamantinomatous craniopharyngioma (ACP)
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PROVIDER: PRJNA1000583 | ENA |
REPOSITORIES: ENA
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Project description:Abnormal DNA methylation plays a role in tumor progression and is becoming recognized as a prognostic marker in various types of cancers. In this study, we aimed to investigate the association between DNA methylation and clinicopathological features, prognosis, and outcomes in patients with Adamantinomatous craniopharyngioma (ACPs). To achieve this, we analyzed the global methylation profile of 35 tumors using the Illumina Infinium HumanMethylation850 BeadChip.
2024-03-14 | GSE239695 | GEO
Project description:Pediatric adamantinomatous craniopharyngioma (ACP) cyst may be associated with injury to critical neurological structures, such as the hypothalamus, resulting in poor quality of life and shorter lifespan. This work presents evidence that immune actors, both pro-inflammatory and immunomodulatory, and their receptors, are present at unique levels in ACP cyst fluid and tumor tissue, potentially indicating a mechanism underlying cyst growth and tumor invasion of the hypothalamus. Transcriptomic analysis revealed that ACP, when compared to other pediatric brain tumors and nomral brain, harbored overexpression of a number of inflammatory and immunosuppressive genes.
2017-02-01 | GSE94349 | GEO
Project description:Introduction: Pediatric adamantinomatous craniopharyngioma (ACP) is a histologically benign but clinically aggressive brain tumor that arises from the sellar/suprasellar region. Despite a high survival rate with current surgical and radiation therapy (75-95% at 10 years), ACP is associated with debilitating visual, endocrine, neurocognitive and psychological morbidity, resulting in exceptionally poor quality of life for survivors. Identification of an effective pharmacological therapy would drastically decrease morbidity and improve long term outcomes for children with ACP. Results: Using microarray analysis of 15 ACP patient samples, we have found several pharmaceutical targets that are significantly and consistently overexpressed in our panel of ACP relative to other pediatric brain tumors, pituitary tumors, normal pituitary and normal brain tissue. Among the most highly expressed are several targets of the kinase inhibitor dasatinib -- LCK, EPHA2 and SRC; EGFR pathway targets -- AREG, EGFR and ERBB3; and other potentially actionable cancer targets -- SHH, MMP9 and MMP12. We confirm by Western blot that a subset of these targets is highly expressed in ACP primary tumor samples. Discussion: We report here the first microarray gene expression analysis for ACP and the identification of targets for rational therapy. Experimental drugs targeting each of these gene products are currently being tested clinically and pre-clinically for the treatment of other tumor types. This study provides a rationale for further pre-clinical and clinical studies of novel pharmacological treatments for ACP. Development of pre-clinical mouse and cell culture models for ACP will further enable the translation of these targets from the lab to the clinic. Gene expression profiles were generated from surgical tumor and normal brain samples (n=210) using Affymetrix HG-U133 Plus 2.0 chips. Gene expression profiles of adamantinomatous craniopharyngioma (ACP) were compared to a cohort of other tumor samples and normal brain tissues, and analyzed via gene set enrichment (GSEA analysis) and hierarchical clustering analysis to identify high expression of potential drug targets. The sample metadata and processed data for the complete dataset, which includes reanalysis of 23 Samples from GSE26966, 33 Samples from GSE35493, and 42 Samples from GSE50385, are linked below as supplementary files.
2015-04-18 | E-GEOD-68015 | biostudies-arrayexpress
Project description:Adamantinomatous craniopharyngioma (ACP) is an intractable and histologically complex epithelial neoplasm with variable pathognomonic features, while its cellular composition, particularly the epithelial component, is poorly characterized. Herein, a single-nucleus transcriptome atlas specific to ACP was constructed by performing a single-nucleus RNA sequencing (snRNA-seq) survey of 55967 nuclei in 6 ACP samples from 3 patients. We revealed 6 epithelial subtypes with diverse molecular functions in ACP by integrating snRNA-seq, spatial transcriptomic (ST) and immunostaining data. Additionally, we investigated the potential regulatory mechanism of ACP calcification by performing a trajectory analysis and transcription factor regulon analysis. Finally, we characterized the molecular characteristics of neurons and discovered potential epithelial cell–neuron crosstalk in ACP tissues. Overall, this large-scale single-nucleus atlas combined with ST provides, for the first time, unprecedented insights into epithelial cell heterogeneity within ACP and can serve as a resource for further investigation of tumor dynamics.
2024-06-26 | GSE215932 | GEO
Project description:Introduction: Pediatric adamantinomatous craniopharyngioma (ACP) is a histologically benign but clinically aggressive brain tumor that arises from the sellar/suprasellar region. Despite a high survival rate with current surgical and radiation therapy (75-95% at 10 years), ACP is associated with debilitating visual, endocrine, neurocognitive and psychological morbidity, resulting in exceptionally poor quality of life for survivors. Identification of an effective pharmacological therapy would drastically decrease morbidity and improve long term outcomes for children with ACP. Results: Using microarray analysis of 15 ACP patient samples, we have found several pharmaceutical targets that are significantly and consistently overexpressed in our panel of ACP relative to other pediatric brain tumors, pituitary tumors, normal pituitary and normal brain tissue. Among the most highly expressed are several targets of the kinase inhibitor dasatinib -- LCK, EPHA2 and SRC; EGFR pathway targets -- AREG, EGFR and ERBB3; and other potentially actionable cancer targets -- SHH, MMP9 and MMP12. We confirm by Western blot that a subset of these targets is highly expressed in ACP primary tumor samples. Discussion: We report here the first microarray gene expression analysis for ACP and the identification of targets for rational therapy. Experimental drugs targeting each of these gene products are currently being tested clinically and pre-clinically for the treatment of other tumor types. This study provides a rationale for further pre-clinical and clinical studies of novel pharmacological treatments for ACP. Development of pre-clinical mouse and cell culture models for ACP will further enable the translation of these targets from the lab to the clinic.
2015-04-18 | GSE68015 | GEO
Project description:Laser capture microdissection of cluster cells, palisading epithelium and glial tissue from 2 cases of human adamantinomatous craniopharyngioma. 1 case performed in duplicate.
2018-04-11 | E-MTAB-5266 | biostudies-arrayexpress
Project description:RNA Sequencing of Adamantinomatous Craniopharyngioma
| PRJEB18056 | ENA
Project description:Introduction: The mechanism by which adamantinomatous craniopharyngioma (ACP) damages the hypothalamus is still unclear. Cyst fuid rich in lipids and infammatory factors is a characteristic pathological manifestation of ACP and may play a very important role in hypothalamic injury caused by tumors. Objective: The objective of this study was to construct a reliable animal model of ACP cyst fuid-induced hypotha lamic injury and explore the specifc mechanism of hypothalamic injury caused by cyst fuid. Methods: An animal model was established by injecting human ACP cyst fuid into the bilateral hypothalamus of mice. ScRNA-seq was performed on the mice hypothalamus and on an ACP sample to obtain a complete gene expression profle for analysis. Data verifcation was performed through pathological means. Results: ACP cystic fuid caused growth retardation and an increased obesity index in mice, afected the expres sion of the Npy, Fgfr2, Rnpc3, Sst, and Pcsk1n genes that regulate growth and energy metabolism in hypothalamic neurons, and enhanced the cellular interaction of Agrp–Mc3r. ACP cystic fuid signifcantly caused infammatory activation of hypothalamic microglia. The cellular interaction of CD74–APP is signifcantly strengthened between infammatory activated microglia and hypothalamic neurons. Beta-amyloid, a marker of neurodegenerative diseases, was deposited in the ACP tumor tissues and in the hypothalamus of mice injected with ACP cyst fuid. Conclusion: In this study, a novel animal model of ACP cystic fuid-hypothalamic injury was established. For the frst time, it was found that ACP cystic fuid can trigger infammatory activation of microglia to damage the hypothalamus, which may be related to the upregulation of the CD74–APP interaction and deposition of β-amyloid, implying that there may be a similar mechanism between ACP cystic fuid damage to the hypothalamus and neurodegenerative diseases.
2022-06-25 | GSE206861 | GEO
Project description:Laser Capture Microdissection and RNA Sequencing Human Adamantinomatous Craniopharyngioma
| PRJEB18054 | ENA
Project description:The purpose was to determine AcP- and AcPb-dependent gene responses to IL-1 by virally-reconstituting AcP-deficient mouse embryonic cortical neurons with CD25 (control), full length AcP, AcPb or the combination of both. A control population was transduced with a CD25-expressing virus. Half the samples were stimulated with IL-1-beta for four hours, RNA was analyzed by microarray.
2009-07-01 | GSE16104 | GEO