How does a normal cell become a cancerous cell

Dia

There are many human cells involved in the process of cell division. These genes ensure that division occurs in an orderly and controlled manner. They make sure that each step in the process happens correctly such as in the right order, at the right time, with the right prompts, and the right pace. They also make sure that after divisions that a cell die. Although sometimes genes can obtain an abnormality that interferes with its ability to function. This could mean that a mutation has happened, and that the DNA within the gene is misspelled. Or, a copying error such as too many or not enough copies of genes are present. Or, translocation, in which a gene or sections of genes are mixed into the wrong section of the genome. These abnormalities can happen because of many reasons. You can get them from your parents, or from too much exposure to the sun, exposure to harmful chemicals, and lastly a mistake made during the process of DNA duplication during cell division.

Telomerase is maintained by an enzyme. Telomeres also protect chromosome ends from fusion and from being recognized as sites of DNA damage. They protect the cells which causes crucial survival cancerous cells. Telomerase allows cancerous cells to keep duplicating at a rapid rate. Telomerase activity is a good activity to have in the body, but it’s not good as well. It’s good to have cells active and alive in the body because we need them to be for the process of cell division. The bad thing is cancerous cells can also start to become active and alive too. If cancerous cells are active and alive then they will be able to produce more cancerous cells and grow rapidly without stopping it from its process.

According to the textbook essay Chronic Myeloid leukemia is the result of an uncontrolled proliferation of certain types of white blood cells. CML begins in a single white blood cell when two of its chromosomes undergo an unusual form of segment swapping with each other. When a segment from chromosome A combines with a segment of chromosome B in this process. Then the result is that the information from both chromosomes combines to create a mutant gene. A gene that does not exist in any normal white blood cells. This mutant gene is called BCR-ABL and it results in a protein that is capable of carrying out some task in the white blood cell. But the BCR-ABL protein flips a molecular switch l. Which causes white blood cells to start multiplying more rapidly even as its daughter cells start undergoing further destabilizing changes. This is not good because It means that full blown leukemia has taken place.

A scenario is when chromosomes where the BCR gene is normally located at chromosome number 22 and the ABL gene is normally on chromosome number 9. So, the BCR- ABL mutation occurs when the genes break off and switch places. The mutation then starts to rapidly develop and once this gene is activated by the Telomerase enzyme then the process of mutation will not stop. It will continue to develop rapidly and will continue to be active. Which would be difficult for cancerous cells to slow down and stop developing more bad cells.

Sal

Mutation in genes can cause cancer to develop. This development is when a cell is rapidly making cell divisions or inhibiting normal controls on the system. Cells grow; they duplicate their chromosomes and then these chromosomes separate, then one cell divides into two. When cells start to develop and when they come across a mutation then it will start rapidly developing these cancerous cells. Once these cancerous cells continue to develop there is no solution of stopping the development (unless taking antibiotics but it won’t really stop the process but rather as slowing it down) and that would lead to an outcome of developing tumors.

Telomerase is maintained by an enzyme. Telomeres protect chromosomes ends from fusion and from being recognized as sites of DNA damage. Since they protect cells this causes crucial survival cancerous cells. Telomerase allows cancerous cells to keep developing (duplicating) rapidly. This is a bad outcome to having telomerase activity because even though it is good to have cells active and alive it’s causing cancerous cells to be active and alive as well. If these cancerous cells are active and alive then they will be able to produce more its cells and grow rapidly without anything stopping it from its process.

BCR-ABL is a mutation that is developed by the combination of two genes, BCR and ABL, which can be referred to as a fusion gene. This BCR-ABL occurs due to the genes breaking off and swapping places. BCR-ABL gene allows too many white blood cells to develop. BCR-ABL causes chronic myeloid leukemia cells to grow and divide rapidly. As the cells start to grow rapidly its development of more cells leads to an outcome of having leukemia. “These white blood cells don’t grow and die like normal call” (Chronic myelogenous leukemia- Mayo Clinic)

A scenario where telomerase and BCR-ABL proteins are active in the same cell. Let’s look at a chromosome where the BCR gene is normally located at chromosome number twenty-two and the ABL gene is normally on chromosome number nine. The BCR-ABL mutation occurs when the genes break off and swap places. When this happens then this mutation starts to rapidly develop (duplicating itself) Once this gene is activated by the telomerase enzyme then the process of this mutation will not stop; it will be a bigger impact where it will continue to develop rapidly and will continue to be active. Hence, it can lead to cancerous cells to be harder to slow down its process of developing more mutation cells or to “end” the process.