To better understand how cancer develops, we must briefly look at the tiny building block of life called the cell and the process of cell proliferation (see animation at left). Life is dependent on normal cell proliferation - the trillions of cells that make up the body are all derived from the multiplication of a single cell. Many tissues of the body, such as the surface of the skin, are constantly being replaced by new cells as old cells wear off. If there is any injury, the healing process accelerates proliferation and the damaged tissues are repaired as well as naturally possible. The process of proliferation is so essential that it may be considered the default setting of the cells' DNA genetic program.
As with computer programs, the default setting is not always what is needed. There are also many options (or genes) which are normally in place to modify its effects. Skin cells need to be replaced on a more or less regular basis and cell proliferation is kept at the appropriate level. Certain types of cells in women's breasts only multiply under the influence of the hormone estrogen, and so these cells fluctuate with the menstrual cycle and with pregnancy. Nerve and muscle cell proliferation is normally not required since these cells do not normally wear out and therefore do not need to be replaced.
The term cancer encompasses those diseases in which there is loss of regulation of the proliferative process. According to Knudson's Multiple Hit Theory, DNA has to be hit at multiple sites for a cancer to develop. What apparently happens is that many of the controlling genes in a few cells are damaged one by one over a period of many years or decades and are rendered ineffective (or, in essence, the options are turned off - see highly simplified representation of this concept at left). Looked at another way, this is similar to syntax errors occurring in multiple lines of programming code. Normally each error causes an error message to be generated within the cell and the errors are automatically repaired. A problem arises when the repair mechanism is itself damaged. The damaged lines of genetic code are then unable to modify the default proliferation setting. Even then, there are failsafe mechanisms in place to destroy or restrict cancerous cells: a cell self-destruct process (referred to as apoptosis), the body's immune system, scar formation around the cancer, and possibly other mechanisms. Thus it can be seen that cancer cells must overcome many natural defenses before they can spread.
It is frequently difficult to pinpoint exactly what may have caused the genetic damage leading to cancer since in most cases the controlling genes are turned off unnoticeably over a long period of time. Random genetic mutations, certain chemical substances, a few types of viruses and some forms of radiation have been linked to some types of cancers. Occasionally, this is further complicated by genetic alterations that may occur over generations.
Whatever the cause, the result is a population of cells that is more or less out of control, that does not obey any boundaries, and that destroys normal cells by uninhibited growth. Different types of cancers, however, have different degrees of destructive behavior - some cancers are more aggressive than others and therefore all cancers do not have the same outlook. Examination of cancer tissue by pathologists provides information about the type and behavior of the cancer so that the appropriate treatment can be determined. On the left is an animated depiction of aggressive cancer cells and on the right is a melanoma, one of the more aggressive cancers, growing in the skin.
Note: The material provided in this web page is educational in nature and not medical advice. It is meant neither for self-diagnosis nor as a treatment recommendation. If you are concerned about any condition you think you may have, CONSULT YOUR DOCTOR.