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：

10400940

负责人：

MURAT GUNEL

金额：

$50.86万

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/10400940

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 Genitalia 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 Neurofibromin 2 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 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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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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