TRAF7突变侵袭性脑膜瘤的分子机制-猫眼课题宝

TRAF7突变侵袭性脑膜瘤的分子机制

批准号：

9887847

负责人：

MURAT GUNEL

金额：

$56.86万

依托单位：

YALE UNIVERSITY

依托单位国家：

美国

项目类别：

财政年份：

2020

资助国家：

美国

项目状态：

未结题

起止时间：

2020-07-01 至 2025-04-30

来源：

https://reporter.nih.gov/project-details/9887847

关键词：

Acute Adult Anaplastic Meningioma Animal Model Architecture Automobile Driving Benign Benign Meningiomas Biochemical Biological Assay Blood - brain barrier anatomy Brain Brain Neoplasms Cell Line Cell Proliferation Cells ChIP-seq Clinical Trials Code Collection DNA Methylation Drug Targeting Effectiveness Event Excess Mortality Future Genes Genital system Genomic approach Genomics Glioblastoma Glioma Hand Histologic Histology Human Incidence Intracranial Neoplasms Intraneural perineurioma Invaded Malignant - descriptor Meningeal Mesothelioma Molecular Morbidity - disease rate Mutate Mutation Neurologic Neurologic Deficit Oncogenic Operative Surgical Procedures Pathway interactions Patients Pharmaceutical Preparations Population Primary Brain Neoplasms Principal Investigator Public Health Radiation Recurrence Reporting Research Resected Role Signal Pathway Signaling Molecule Stroke Structure Subgroup Testing Therapeutic United States Untranslated RNA adenoma base driver mutation drug candidate drug efficacy efficacy testing epigenomics exome exome sequencing genomic profiles inhibitor/antagonist insight meningioma mouse model mutant neurovascular new therapeutic target next generation sequencing novel therapeutics programs protein function response skull base subcutaneous transcriptome sequencing tumor ubiquitin isopeptidase ubiquitin ligase ubiquitin-protein ligase whole genome

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中文摘要

翻译

项目摘要/摘要脑膜瘤是最常见的原发脑肿瘤。虽然通常是良性组织学，但它们可以是与严重的神经系统疾病相关，并具有恶变的潜力。在我们的在之前的研究中，我们完成了700多个脑膜瘤的基因组分析，使用了完整的外显子组和靶向下一代测序，识别12个基因的驱动突变并建立互斥分子亚群。我们现在建议研究其形成的分子机制。依赖TRAF7的脑膜瘤(占所有脑膜瘤的四分之一)进行分子基因组分析用于确定TRAF7肿瘤的体细胞编码和非编码或基因组事件升到更高的年级。我们还建议使用初级药物来测试和验证候选药物的疗效从手术切除的携带TRAF7异常的脑膜瘤培养，以及小鼠模型我们已经确诊的脑膜瘤。

英文摘要

PROJECT SUMMARY / ABSTRACT Meningiomas are the most common primary brain tumors. While typically of benign histology, they can be associated with significant neurological morbidity and have the potential for malignant transformation. In our previous studies, we completed genomic analysis of over 700 meningiomas using whole exome and targeted next-generation sequencing, identifying driver mutations in 12 genes and establishing mutually exclusive molecular subgroups. We now propose to investigate the molecular mechanisms underlying the formation of TRAF7-dependent meningiomas (which represent up to one quarter of all meningiomas), undertake molecular genomic analyses to identify somatic coding and non-coding or genomic events in TRAF7 tumors that progress to higher grades. We also propose to test and validate candidate drug efficacy using primary cultures from surgically resected meningiomas carrying TRAF7 aberrations, as well as mouse models of meningioma that we have established.

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