A diagnosisof cancer means that cancer cells have originated within tissues that growabnormally and over time became resistant to the controls that maintain anormal growth, the cancerous cells do not respond to programmed cell death andthey metastasize quickly.
So, to prevent the appearance of cancerous tumors,the correct functioning of the cell cycle control mechanisms is vital becausethese processes determine whether the cell continuous the division or is holduntil all the necessary conditions are met. The purpose of this paper is toevaluate the genes that are involved in the malfunctions of the controlmechanisms of the cell cycle that could lead to the formation of cancerous tumors. Malfunctions can come from the activation orsuppression of genes that synthesize certain proteins such as RAS. For instance,the proto- oncogenes are genes that help cell to grow and divide and when theymutate by activation, creating many copies of the gene, the cell grows out ofcontrol and can lead to cancerous tumors. The gene responsible for theuncontrolled growth of the cell is called oncogene. There are 2 ways on whichoncogenes can be activated. The first one is by chromosome rearrangements whengenes that are put side by side activate each other. And the second way is bygene duplication when too many proteins are synthesized due to the abnormalreplication of genes.
Furthermore, the malfunction of the genes called tumorsuppressors can also lead to cancerous tumors. These genes are in charge ofrepairing DNA mistakes, apoptosis (programmed cell death) and slow down the processof cell division. So whenever a mutationoccurs, suppressing these genes, cells grow out of control due to theinactivation of the tumor suppressor genes (“Oncogenes and tumor suppressorgenes”).
A common tumor suppressor is named by tumor protein p53 that actsmainly in the G1 checkpoint when it blocks the division in response to damagein the DNA. (“Cancer and the cell cycle | Biology (Article).” On the otherhand, there are specific genes involved in the cell cycle checkpointsDNA-damage, DNA- replication, and spindle-assembly that delay the cell divisionuntil certain conditions are met. During the DNA-damage induced checkpoint themrt-2 and hus-1 genes are required to produce the arrest of the cell-cyclecombine with the clk-2 gene. The activation of these genes delays the processuntil the cell can continue division. Also in the DNA- replication inducedcheckpoint the cell is not able to continue into mitosis due to the mutationcaused in the DNA replication, where the genes alt-1 and chk-1 are involved.Although, this checkpoint is active in early developmental stages of humans(embryos).
In addition, the genes involved in the spindle checkpoint or themitotic arrest deficient are mdf-2 and mdf-1. The last one is required formitotic arrest when there is a mutation in the spindle (Van Den Heuvel). All in all, cancerous tumors areformed by the mutations of genes present in the different checkpoints of thecell cycle. They are divided in positive regulators such as the oncogenes thatactive the overgrowth of cells. And negative regulators such as the tumorsuppressors that result in the overgrowth of cells if they are inactivated.Furthermore, on which checkpoint certain genes are required to preventabnormalities in the cell cycle division.