One of the most remarkable safeguards is an inbuilt system which is controlled by the genes in the cells which limits the number of times that a particular cell line can divide. When a cell divides the chromosomes which are made of the genetic material also divide and each time a small section at their ends fails to replicate. Therefore as the cell line continues to divide the chromosomes get shorter. The end parts of the chromosomes are called the telomeres and it is these which become progressively shorter each time the cell divides. After a predestined number of cell divisions the telomeres are shortened sufficiently to cause the cells to stop any further dividing. This is known as the cells becoming senescent. Cells in senescence will eventually die but a few of the millions of cells concerned will not be caught by this safeguard system and will continue further division. After a few more decisions the telomeres are even further shortened and there is a stop to the cycling of even the remaining cells. This second "last resort" stop is called crisis. Again the cells will stop dividing and will die out.

A few of these cells will even evade crisis and escape this second safety net. Such cells will continue to divide indefinitely and will thus become so-called immortal cells. In some cancer cells an enzyme is produced that rebuilds the telomeres of the chromosomes as they become shortened thus enabling the cells to evade these two safety nets and becoming immortal cells. The enzyme is produced by genes in the DNA of affected cancer cells. This is one mechanism whereby the genetic error in a cell can lead to cancer. In normally dividing cells the change to the cell division part of the life cycle as opposed to the resting phase is regulated by genes know as proto-oncogenes which stimulate cell division and tumour suppressor genes which inhibit cell division. The balance between these two types of genes leads to an orderly regulation of cell division.

During cell division there will be a small percentage of cases where the division is faulty and the genetic material (genes) become damaged. If this occurs to proto-oncogenes they can be transformed into oncogenes which become increasingly overactive and thus there is an unregulated increase in cell division, and these cells will all contain the genetic error. There are some special genes in each cell of which the gene P53 is probably the best known, that trigger self destruction of the cell if the DNA becomes damaged. This self destruction is known as apoptosis. This mechanism is extremely important to the clinician since both radiotherapy and some chemotherapeutic drugs work by damaging the DNA structure and relying upon apoptosis to complete the destruction of the cancer cells. Another error can occur when there is a faulty division which can stop the tumour suppressor genes working. This again results in an uncontrolled division of cells with damaged DNA.