6.3 Cancer and the Cell Cycle

The cycle will not proceed until the kinetochores of each pair of sister chromatids are firmly anchored to the poles of the cell.

You can see what happens at the G1, G2, and M checkpoint by visiting the cell cycle.

By the end of this section, you will be able to: Errors occur despite the redundant levels of cell-cycle control.

The cell-cycle checkpoint surveillance mechanism monitors the proper replication of DNA during the S phase.
When the cell-cycle controls are fully functional, a small percentage of replication errors will be passed on to the daughter cells.
The process of cell reproduction is involved in all cancers.
The change in the cell may be small.
Minor mistakes may allow subsequent mistakes to occur more easily.
As each generation of cells produces more non-functional proteins from uncorrected DNA damage, small, uncorrected errors are passed from parent to daughter cells.
As the effectiveness of the control and repair mechanisms decreases, the pace of the cell cycle increases.
Uncontrolled growth of the cells that are not normal can lead to a tumor.

Consider what might happen to a cell with a recently acquired oncogene.
Alteration of the DNA sequence will result in a less functional or non-functional protein.
The result is detrimental to the cell and will likely prevent the cell from completing the cycle; however, the organism is not harmed because the mutation will not be carried forward.
The damage is minimal if a cell cannot reproduce.
A change in a genes activity can increase the activity of a positive regulator.
The cell cycle could be pushed past a checkpoint before all of the required conditions are met if the Cdk mutation allowed it to be activated before it should be.
If the daughter cells are too damaged to undertake further cell divisions, there would be no harm to the organisms.
If the atypical daughter cells are able to divide further, the subsequent generation of cells will likely accumulate more genes that regulate the cell cycle.

Anyprotein that influences the cycle can be altered in such a way as to override the cell-cycle checkpoint.
An oncogene is an altered Proto-oncogene that has an increase in the rate of the cell cycle.

Many of the negative cell-cycle regulatory proteins were found in cells that had become cancer.

A roadblock to cellcycle progress is put up by the collective function of the bestunderstood tumor suppressor genes.
If there is a problem, a cell that carries a negative regulator might not be able to stop the cell cycle.

The multiple roles that the p53 protein plays at the G1 checkpoint is not surprising.
The p53 protein causes other genes to stop the cell cycle, causes genes that participate in DNA repair to stop, and causes genes that initiate cell death when DNA damage cannot be repaired.
A damaged p53 gene can cause the cell to behave as if there are no changes.
The damaged version of p53 can't cause cell death.