Aneuploidy and cancer
- 27 July 2007
- journal article
- review article
- Published by Wiley in Journal of Cellular Biochemistry
- Vol. 102 (3) , 531-538
- https://doi.org/10.1002/jcb.21484
Abstract
The cell's euploid status is influenced by, amongst other mechanisms, an intact spindle assembly checkpoint (SAC), an accurate centrosome cycle, and proper cytokinesis. Studies in mammalian cells suggest that dysregulated SAC function, centrosome cycle, and cytokinesis can all contribute significantly to aneuploidy. Of interest, human cancers are frequently aneuploid and show altered expression in SAC genes. The SAC is a multi‐protein complex that monitors against mis‐segregation of sister chromatids. Several recent experimental mouse models have suggested a link between weakened SAC and in vivo tumorigenesis. Here, we review in brief some mechanisms which contribute to cellular aneuploidy and offer a perspective on the relationship between aneuploidy and human cancers. J. Cell. Biochem. 102: 531–538, 2007.Keywords
This publication has 55 references indexed in Scilit:
- Centrosome and retroviruses: The dangerous liaisonsRetrovirology, 2007
- New aspects of diagnosis and therapy of hepatocellular carcinomaOncogene, 2006
- The retroviral oncoprotein Tax targets the coiled-coil centrosomal protein TAX1BP2 to induce centrosome overduplicationNature Cell Biology, 2006
- Monoallelic BUB1B mutations and defective mitotic‐spindle checkpoint in seven families with premature chromatid separation (PCS) syndromeAmerican Journal of Medical Genetics Part A, 2006
- Gain of a region on 7p22.3, containing MAD1L1, is the most frequent event in small‐cell lung cancer cell linesGenes, Chromosomes and Cancer, 2005
- Checking Out the CentrosomeCell Cycle, 2004
- Abnormal Cytokinesis in Cells Deficient in the Breast Cancer Susceptibility Protein BRCA2Science, 2004
- Mechanisms of genomic instability in human cancer: Insights from studies with human papillomavirus oncoproteinsInternational Journal of Cancer, 2003
- Centromeres and KinetochoresCell, 2003
- The human papillomavirus type 16 E6 and E7 oncoproteins cooperate to induce mitotic defects and genomic instability by uncoupling centrosome duplication from the cell division cycleProceedings of the National Academy of Sciences, 2000