Why do we get cancer?
This question has bothered patients and doctors for centuries. But, perhaps the question should rather be: why do we not get cancer?
We get potential cancer many millions of times every day. Cancer is caused by missegregation, a common mistake in cell division where one daughter cell gets a chromosome too many, and the other a chromosome too few. This happens in 0.01 to 4 percent of cell divisions. It is a dangerous situation in dividing cells because, after that, cell division cannot be done correctly, as at least one new daughter cell will have a faulty chromosome number. If a cell with a surplus chromosome is allowed to divide, a daughter cell would end up with two surplus chromosomes, and the cell’s descendants would be on the way to acquire the many extra chromosomes typical of cancer cells.
The organism has a number of repair mechanisms to prevent missegrated cells from turning into cancer cells. The first is a roll-back of the division itself. If the dividing cell senses that a chromosome is not ending up in the right place, no cell wall is formed, and instead, the cell ends up with two nuclei or a nucleus with double the normal set of chromosomes. A second repair mechanism is ordering the cell never to divide again, called cell division arrest. Another important repair is ordering the cell to commit suicide, apoptosis. Finally, cells with the wrong chromosomes get eliminated by the immune system.
If a potential cancer cell slips past all these safeguards and also acquires the ability to metastasize, it can develop into a dangerous cancer. Metastases forming ability may be caused by mutation, but it may also be the result of a fusion of potential cancer cell and a white blood cell. The resultant cell moves as a white blood cell, but it does not die as a white blood cell, and instead, it divides as a cancer cell.
Carcinogenic agents typically work by disabling repair mechanisms. X-rays or radioactive substances induce mutations that inactivate a repair mechanism. People with inborn tendency to form cancers often have faulty repair mechanism genes.
Cancer increases with age. One reason is that missegregation increases with age. Another important reason is that cells can only divide about 50 times after egg cell and sperm fused. After about 50 divisions, the shoe-lace like ends of the chromosomes have been cut off and the chromosomes unravel and stick together and break up in wrong places, creating numerous mutations. Such “old” cells do not usually divide, but if they do divide, they become mutation generators. Old people are close to the 50 division limit, where potential cancer cells become mutation factories.
Large, long-lived animals like elephants rarely get cancer, while small short-lived animals like mice often get cancer. Elephants have extra genes for repair mechanisms. Mice reach the cell division limit already after 10-15 divisions. Elephants keep potential cancers in check for a long time, whereas mice often develop cancer before they are one year old.
These findings are described in the article entitled Cancer follows chromosome missegregation when all endogenous repair mechanisms fail, recently published in the journal Medical Hypotheses. This work was conducted by Kjeld C. Engvild from the Technical University of Denmark.
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