Abstract
The cell cycle is a complex sequence of events through which a cell duplicates its contents and divides, and involves many regulatory proteins for proper cellular reproduction, including cyclin proteins and cyclin-dependent kinases, oncogenes and tumor-suppressor genes, and mitotic checkpoint proteins. Mutations of any of these regulatory mechanisms can lead to reproduction of cells carrying genetic mutations or abnormal numbers of chromosomes, resulting in genomic instability. Chromosomal instability, contributing to genomic instability, refers to abnormalities in the number of chromosomes, and leads to aneuploidy. The role of aneuploidy in cancer cell development is often disputed, as conflicting hypotheses and research make it unclear as to whether aneuploidy is a cause or consequence of cancer. Here, we present an overview of the importance of cell-cycle checkpoint regulation and chromosomal instability in the development of cancer, and discuss evidence for conflicting arguments for the role of aneuploidy in cancer, leading us to conclude that further investigation of this role would benefit our understanding of cancer development.