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How does cancer start

It is now well known to medical science that the beginning point of all cancers is a change in either one cell or in a small group of cells. This means that, in the normal course of events, some years before a patient can even feel a lump and before a doctor or specialist is able to identify a cancer on a scan the cells themselves have already begun reproducing uncontrollably.

The cells are subject to something called mutation, in which the cancer cells appear to lose many important control systems as a result of the fact that a number of genes in the cell have been either lost or damaged and thus affect a cell’s overall operations. The genes are effectively the coded messages in a cell that instruct its behavior, directing the cell how to make different proteins. Proteins are the building blocks from which the cells are made up, with some acting in the role of switches aiding the control of cellular behavior.

For example, in cellular reproduction the chain starts with a hormone signal acting on a protein whether on or actually in the cell itself. The protein subsequently sends a signal along a network of switches, and the last of these signals instructs the cell to reproduce – which it does by dividing into two. In the case of mutation a gene has been either lost or damaged, and this may result in either too much protein being produced or none at all. In specific cases proteins that operate by controlling and limiting cellular division may be permanently disabled, or a signaling protein might be permanently activated.

In terms of substances that can aid in the causing of cancer these are a number of substances currently in existence that damage cells, thereby making them more likely to become cancerous. Such substances are known as carcinogens and we can find many examples in daily life, such as cigarette smoke and other forms of pollution as well as certain fats – especially saturated fats – commonly found in fast foods.

Aging also results in the decreasing of cells’ ability to reproduce healthily and move through kinetic energy, causing oxidization In terms of what types of genes make a cell cancerous there are three primary different types. The first type are oncogenes, which encourage cells to multiply or double. This would happen very occasionally in healthy adults, and cells would usually only multiply in order for damage to be repaired – after an operation or an injury, for instance. In such cases where such genes become abnormal they actually instruct the cell to multiply continuously.

The second type are called tumor suppressor genes, and these genes halt cell doubling or multiplication. It only takes one of these genes to get damaged and cease functioning for the cell to continue multiplying endlessly. As a result the cell effectively becomes immortal-and this is one of the principle properties of a cancer cell. Perhaps the most well-known tumor suppressor genes is called P53, which acts by halting the reproduction of other damaged genes as well as encouraging such genes to destroy themselves. It is known that the P53 gene is either absent or damaged in most forms of human cancer.

Finally, there are the genes that act by repairing other damaged genes, and they repair problems associated with the DNA that constitutes the cells’ genes. If these types of cells are damaged in any way it means that other cellular mutations will not be fixed and subsequently the cell can replicate its mutations to daughter cells. These repair genes have been discovered damaged in certain forms of human cancer, including bowel cancer.

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