Checkpoints and cancer
Checkpoint pathways can pause the cycle to permit repair, and severe damage can trigger programmed cell death. Cyclin abundance changes over the cycle; cyclins regulate CDKs, which modify target proteins. Growth-promoting genes can become overactive, while loss of growth restraints or repair mechanisms also raises cancer risk. Cancer commonly involves multiple changes rather than one universal mutation. Apoptosis removes damaged or unnecessary cells in a controlled process.
A damaged cell with a functioning checkpoint may stop before DNA replication. Loss of that checkpoint can allow mutations to be copied and inherited by daughter cells.
An inhibitor of a growth-promoting protein and a loss of a growth-suppressing protein have opposite effects. Name the protein role before predicting the outcome.