Human Neurobeachin-like 1(NBEAL1) gene was an important member of BEACH-WD40 domain family, which was confirmed to be overexpressed in I stage glioma. In this study, we extracted total RNAs from U251 cell line, acquired its cDNA sequence by RT-PCR, and cloned part of NBEAL1 cDNA fragments into the vector pGEX-KG. The recombinant expression vector achieved high expression in E.coli BL21 as a GST fusion protein. NBEAL1 recombinant protein was purified by affinity chromatography. Monoclonal antibody was prepared against the recombinant NBEAL1 protein. Its bioactivity was identified by Western Blotting analysis. Anti-NBEAL1 antibody was conjugated with CdTe quantum dots. Resultant anti-NBEAL1 antibody-conjugated nanoprobes were injected into mice via tail vessel. After 12h, it is clearly observed that prepared nanoprobes located in brain tissues of mice model with glioma by IVIS Imaging system. In conclusion, NBEAL1 protein was successfully expressed and its monoclonal antibody was successfully prepared. Anti-NBEAL1 antibody-conjugated quantum dots may be used to image glioma. These prepared nanoprobes have great potential in early detection of glioma.

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The mutation of cancer represents a high heterogeneity characteristic, setting a big obstacle in the mechanism study of it. In this study, we explored the distributions of mutated genes in pathways in glioblastoma multiforme (GBM), and constructed networks of co-mutated pathway pairs under the false discovery rate (FDR) control. By comparing the mutation frequencies, a total of 50 mutated genes were screened with the frequency > 3, and TP53, PTEN, and EGFR were the top 3 genes. By KEGG enrichment, 18 pathways of the mutation gene spectrum of GBM were enriched. These pathways were further studied to explore the coordination between pathways, co-mutated pathway pairs, such as mismatch repair/vascular smooth muscle contraction, mismatch repair/long-term depression, mismatch repair/dopaminergic synapse, and TGF-beta signaling pathway/retrograde endocannabinoid signaling pathway were enriched in the network under FDR < 0.01; and cell cycle/p53 signaling was a co-mutated pathway pairs in the network under FDR < 0.05. Meanwhile, the samples overlap levels of enriched pathways were calculated for further confirming of the co-mutated pathway model. By the co-mutated pathway analysis, the coordination mechanism of cancer can be explored, and it may provide basis for the pathogenesis and combined therapy study of cancer.

The most common types of primary brain tumors in adults are gliomas. Glioblastoma multiforme (GBM) is the most highly aggressive type of glioma. GBM contains various numbers of cells with characteristics of activated or dysmorphic macrophages/microglia. Among them, some cell types provide significant support for tumor growth, while others are able to inhibit tumor progression. These cells are generally considered part of the tumor stroma and are often described as TAMs (tumourassociated macrophages). The presence of TAMs has been linked to increased tumor grade and poor clinical outcome in GBM, suggesting that depletion or inhibition of these cells may suppress tumor growth. A better understanding of tumor microenvironment in the brain would therefore be expected to contribute to the development of improved therapies for brain tumors that are urgently required due to a poor availability of treatments for these malignancies. This review summarizes some of the known interactions between brain tumors and different stromal cells, and also discusses potential therapeutic approaches within this context.

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