Aneuploidy and cancer.
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.
Molecular Virology Section, Laboratory of Molecular Microbiology, The National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-0460, USA.
Ya-Hui
YH
Chi
Kuan-Teh
KT
Jeang
D000782:Aneuploidy; D000818:Animals; D002471:Cell Transformation, Neoplastic; D002842:Chromatids / Q000648:ultrastructure; D048749:Cytokinesis; D006801:Humans; D008938:Mitosis; D008954:Models, Biological; D009369:Neoplasms / Q000235:genetics* / Q000473:pathology*; D012854:Sister Chromatid Exchange