Several genetic pathways help control cell division.
The inhibition or activation of CDKs inhibits or activates G1-to-S and G2-to-M transitions.
The measured synthesis and degradation of different cyclins guides CDKs to the appropriate targets at the appropriate times.
Checkpoints that integrate repair of chromosomal damage with events of the cell cycle minimize the replication of DNA damage.
The genes and proteins of various signal transduction systems relay signals about whether or not to enter the cell cycle.
Cancer is a genetic disease resulting from the growth of a clone of mutant cells.
A cell requires many mutations to become cancerous. Exposure to environmental mutagens probably generates most of these mutations.
Many mutations that lead to cancer jeopardize cell-cycle regulation.
Mutations in growth factors, receptors, and other elements of signal transduction pathways can release cells from the signals normally required for proliferation.
Mutations in CDKs and the proteins that control them may also lead to inappropriate proliferation or genomic instability.
Mutations in DNA repair and checkpoint controls lead to genomic instability and, often, to loss of the surveillance system that kills aberrant cells by apoptosis.
Mutations that lead to genomic instability permit the rapid evolution of abnormal tumor cells.
