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Studying a complex tumor: potential and pitfalls.研究复杂肿瘤:潜力与陷阱。
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本文引用的文献

1
Mutual exclusivity analysis identifies oncogenic network modules.相互排斥分析确定致癌网络模块。
Genome Res. 2012 Feb;22(2):398-406. doi: 10.1101/gr.125567.111. Epub 2011 Sep 9.
2
Mosaic analysis with double markers reveals tumor cell of origin in glioma.双标记马赛克分析揭示了神经胶质瘤的肿瘤细胞起源。
Cell. 2011 Jul 22;146(2):209-21. doi: 10.1016/j.cell.2011.06.014. Epub 2011 Jul 7.
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Heterogeneity maintenance in glioblastoma: a social network.胶质母细胞瘤中的异质性维持:一种社交网络。
Cancer Res. 2011 Jun 15;71(12):4055-60. doi: 10.1158/0008-5472.CAN-11-0153. Epub 2011 May 31.
4
The antisense oligonucleotide trabedersen (AP 12009) for the targeted inhibition of TGF-β2.靶向抑制 TGF-β2 的反义寡核苷酸 trabedersen(AP 12009)。
Curr Pharm Biotechnol. 2011 Dec;12(12):2203-13. doi: 10.2174/138920111798808266.
5
Network modeling of the transcriptional effects of copy number aberrations in glioblastoma.脑胶质瘤中拷贝数异常的转录效应的网络建模。
Mol Syst Biol. 2011 Apr 26;7:486. doi: 10.1038/msb.2011.17.
6
SOX2 expression and amplification in gliomas and glioma cell lines.SOX2 在神经胶质瘤和神经胶质瘤细胞系中的表达和扩增。
Cancer Genomics Proteomics. 2011 May-Jun;8(3):139-47.
7
Tumour evolution inferred by single-cell sequencing.单细胞测序推断肿瘤进化。
Nature. 2011 Apr 7;472(7341):90-4. doi: 10.1038/nature09807. Epub 2011 Mar 13.
8
NFKBIA deletion in glioblastomas.胶质母细胞瘤中的 NFKBIA 缺失。
N Engl J Med. 2011 Feb 17;364(7):627-37. doi: 10.1056/NEJMoa1006312. Epub 2010 Dec 22.
9
Integrated genomic analyses identify ERRFI1 and TACC3 as glioblastoma-targeted genes.综合基因组分析确定ERRFI1和TACC3为胶质母细胞瘤靶向基因。
Oncotarget. 2010 Aug;1(4):265-77. doi: 10.18632/oncotarget.137.
10
PDGFRA gene rearrangements are frequent genetic events in PDGFRA-amplified glioblastomas.PDGFRA 基因重排是 PDGFRA 扩增型胶质母细胞瘤中常见的遗传事件。
Genes Dev. 2010 Oct 1;24(19):2205-18. doi: 10.1101/gad.1972310.

研究复杂肿瘤:潜力与陷阱。

Studying a complex tumor: potential and pitfalls.

机构信息

Department of Bioinformatics and Computational Biology, MD Anderson Cancer Center, Houston, TX, USA.

出版信息

Cancer J. 2012 Jan-Feb;18(1):107-14. doi: 10.1097/PPO.0b013e3182431c57.

DOI:10.1097/PPO.0b013e3182431c57
PMID:22290264
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3342695/
Abstract

Glioblastoma multiforme is a histopathologically heterogeneous disease with few treatment options. Therapy based on genomic alterations is rapidly gaining popularity because of the high response rate and high specificity. DNA copy number and exon-sequencing studies of glioblastoma multiforme samples have revealed recurrent genomic alterations in genes such as TP53, EGFR, and IDH1, but to date, this has not resulted in novel glioblastoma multiforme therapies. Identification of expression subtypes has resulted in new insights such as the association between genomic abnormalities and expression signatures. This review describes the types of genomic studies that have been performed and that are underway, the most prominent results, and the implications of genomic research for the development of clinical treatment modalities.

摘要

胶质母细胞瘤是一种组织病理学上具有异质性的疾病,治疗选择有限。基于基因组改变的治疗方法由于高反应率和高特异性而迅速流行。对胶质母细胞瘤样本的 DNA 拷贝数和外显子测序研究揭示了 TP53、EGFR 和 IDH1 等基因中反复出现的基因组改变,但迄今为止,这并未导致新的胶质母细胞瘤治疗方法。表达亚型的鉴定导致了新的见解,例如基因组异常与表达特征之间的关联。本文综述了已进行和正在进行的基因组研究类型、最显著的结果以及基因组研究对临床治疗模式发展的意义。