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Essay No. 1

Benign and cancerous tumors can occur when the cell cycle checkpoints are no
longer functional.  What types of genes
may be involved in these cell cycle control mechanisms?

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A diagnosis
of cancer means that cancer cells have originated within tissues that grow
abnormally and over time became resistant to the controls that maintain a
normal growth, the cancerous cells do not respond to programmed cell death and
they metastasize quickly. So, to prevent the appearance of cancerous tumors,
the correct functioning of the cell cycle control mechanisms is vital because
these processes determine whether the cell continuous the division or is hold
until all the necessary conditions are met. The purpose of this paper is to
evaluate the genes that are involved in the malfunctions of the control
mechanisms of the cell cycle that could lead to the formation of cancerous tumors.


 Malfunctions can come from the activation or
suppression 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 they
mutate by activation, creating many copies of the gene, the cell grows out of
control and can lead to cancerous tumors. The gene responsible for the
uncontrolled growth of the cell is called oncogene. There are 2 ways on which
oncogenes can be activated. The first one is by chromosome rearrangements when
genes that are put side by side activate each other. And the second way is by
gene duplication when too many proteins are synthesized due to the abnormal
replication of genes. Furthermore, the malfunction of the genes called tumor
suppressors can also lead to cancerous tumors. These genes are in charge of
repairing DNA mistakes, apoptosis (programmed cell death) and slow down the process
of cell division. So whenever a  mutation
occurs, suppressing these genes, cells grow out of control due to the
inactivation of the tumor suppressor genes (“Oncogenes and tumor suppressor
genes”). A common tumor suppressor is named by tumor protein p53 that acts
mainly in the G1 checkpoint when it blocks the division in response to damage
in the DNA. (“Cancer and the cell cycle | Biology (Article).”


On the other
hand, there are specific genes involved in the cell cycle checkpoints
DNA-damage, DNA- replication, and spindle-assembly that delay the cell division
until certain conditions are met. During the DNA-damage induced checkpoint the
mrt-2 and hus-1 genes are required to produce the arrest of the cell-cycle
combine with the clk-2 gene. The activation of these genes delays the process
until the cell can continue division. Also in the DNA- replication induced
checkpoint the cell is not able to continue into mitosis due to the mutation
caused 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 the
mitotic arrest deficient are mdf-2 and mdf-1. The last one is required for
mitotic arrest when there is a mutation in the spindle (Van Den Heuvel).


            All in all, cancerous tumors are
formed by the mutations of genes present in the different checkpoints of the
cell cycle. They are divided in positive regulators such as the oncogenes that
active the overgrowth of cells. And negative regulators such as the tumor
suppressors that result in the overgrowth of cells if they are inactivated.
Furthermore, on which checkpoint certain genes are required to prevent
abnormalities in the cell cycle division.




















Works Cited:


and tumor suppressor genes.” American Cancer Society,


Den Heuvel, Sander. “Cell-Cycle regulation*.” Edited by James M Kramer and
Donald G Moerman , WormBook Header Image, The C. elegans Research Community, 21
Sept. 2005,


“Cancer and
the cell cycle | Biology (Article).” Khan Academy,   

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