Mechanisms of Chromosomal Instability

被引：443

作者：

Thompson, Sarah L. ^{[1
]}

Bakhoum, Samuel F.

Compton, Duane A.

机构：

[1] Dartmouth Med Sch, Dept Biochem, Hanover, NH 03755 USA

来源：

CURRENT BIOLOGY | 2010年 / 20卷 / 06期

基金：

美国国家卫生研究院;

关键词：

KINETOCHORE-MICROTUBULE ATTACHMENT; MITOTIC-SPINDLE CHECKPOINT; CENTROMERE-ASSOCIATED KINESIN; AURORA-B; TUMOR-FORMATION; CANCER-CELLS; HUMAN BREAST; CENTROSOME AMPLIFICATION; PROMOTES TUMORIGENESIS; GENETIC INSTABILITY;

D O I：

10.1016/j.cub.2010.01.034

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Most solid tumors are aneuploid, having a chromosome number that is not a multiple of the haploid number, and many frequently mis-segregate whole chromosomes in a phenomenon called chromosomal instability (CIN). CIN positively correlates with poor patient prognosis, indicating that reduced mitotic fidelity contributes to cancer progression by increasing genetic diversity among tumor cells. Here, we review the mechanisms underlying CIN, which include defects in chromosome cohesion, mitotic checkpoint function, centrosome copy number, kinetochore-microtubule attachment dynamics, and cell-cycle regulation. Understanding these mechanisms provides insight into the cellular consequences of CIN and reveals the possibility of exploiting CIN in cancer therapy.

引用

页码：R285 / R295

页数：11

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