Cancer Stem Cells: The Seeds of Metastasis?

Abstract

During cell division, cells must precisely duplicate their DNA so that the resulting daughter cells are genetically identical. The DNA replication process consists of several steps: origin of replication licensing, during which sites on the genome at which replication will commence are primed; initiation, during which the replication complex, including DNA polymerase, is assembled at origins; and elongation, during which the replication complex moves along the genome, producing an identical copy of the DNA. Because endogenous and exogenous agents can damage cellular DNA during genome replication and result in dangerous mutations, cells have evolved complex “checkpoint” mechanisms to slow or stop the DNA replication process, allowing time for repair of the damage. Recent studies elegantly probe the mechanisms by which this checkpoint signal is generated, sensed, and transduced, implicating their potential utility as new therapeutic targets for cancer.