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G1 期 Cdk 调节中心体周期并介导癌基因依赖性中心体扩增。

The G1 phase Cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification.

机构信息

Emory University, Department of Radiation Oncology, Winship Cancer Institute, 1701 Uppergate Drive, Atlanta, Georgia, 30322, USA.

出版信息

Cell Div. 2011 Jan 27;6:2. doi: 10.1186/1747-1028-6-2.

Abstract

Because centrosome amplification generates aneuploidy and since centrosome amplification is ubiquitous in human tumors, a strong case is made for centrosome amplification being a major force in tumor biogenesis. Various evidence showing that oncogenes and altered tumor suppressors lead to centrosome amplification and aneuploidy suggests that oncogenes and altered tumor suppressors are a major source of genomic instability in tumors, and that they generate those abnormal processes to initiate and sustain tumorigenesis. We discuss how altered tumor suppressors and oncogenes utilize the cell cycle regulatory machinery to signal centrosome amplification and aneuploidy.

摘要

由于中心体扩增会产生非整倍体,并且中心体扩增在人类肿瘤中普遍存在,因此可以强有力地证明中心体扩增是肿瘤发生的主要力量。各种证据表明,癌基因和改变的肿瘤抑制因子导致中心体扩增和非整倍体,这表明癌基因和改变的肿瘤抑制因子是肿瘤基因组不稳定性的主要来源,并且它们产生这些异常过程来启动和维持肿瘤发生。我们讨论了改变的肿瘤抑制因子和癌基因如何利用细胞周期调节机制来发出中心体扩增和非整倍体的信号。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e179/3038874/2aaa68efe0e8/1747-1028-6-2-1.jpg

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