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Medulloblastoma is the most common malignant brain tumor in childhood. Although metastasis constitutes one of the poorest prognostic indicators in this disease, the mechanisms that drive metastasis have received less attention. The aim of our study is to provide valid biological information for the metastasis mechanism of medulloblastoma. Gene expression profile of GSE468 was downloaded from GEO database and was analyzed using limma R package. Function and enrichment analyses of DEGs were performed based on PANTHER database. PPI network construction, hub gene selection and module analysis were conducted in Cytoscape software. Nine upregulated genes and 34 downregulated genes were selected as DEGs. The upregulated genes were mainly enriched in molecular function and cell component, which mainly included protein binding and nucleus respectively. A total of 120 enriched GO terms and 40 KEGG pathways were identified. The main enriched GO terms were the biological process such as apoptosis and MAPK activity. Besides, the enriched KEGG pathways also included MAPK signaling pathway. A PPI network was obtained, and JUN was identified as a hub gene. Also, we firstly investigated the role and regulatory mechanism of JUN in the metastasis of medulloblastoma. Through the bioinformatics analysis of the gene microarray in GEO, we found some crucial genes and pathways associated with the metastasis of medulloblastoma. [ABSTRACT FROM AUTHOR]

The left eye was vitrectomized for vitreous opacities, and pathological examination of the vitrectomy stained with alkaline Congo red showed amyloid deposits, which confirmed ATTRv amyloidosis. Nerve conduction studies showed the amplitude reduction of compound muscle action potentials (CMAPs) in the right common peroneal nerve. Hereditary transthyretin (ATTRv) amyloidosis is an autosomal dominant disease mainly characterised by abnormal deposition of amyloid fibrils that lead to multisystem disorders [[1]]. [Extracted from the article]