factors such as cigarette smoke or asbestos, for example, are all carcinogens that are known to cause cancers with excessive exposure, probably by producing one or more oncogenes .
Some defects can be repaired, but the cell's ability to repair DNA damage weakens with age. It is also thought that the genetic machinery of aging cells becomes more error-prone by accumulating unrepaired defects. The unrepaired persistence of the activated oncogene will predispose a person to develop cancer in the tissue containing that gene.
While there are several theories about the cancer-causing mechanisms of these genetic changes—such as a virus inserting its own DNA into a normal cell's chromosome, a virus acting as a random mutating agent or a single carcinogenic bullet that knocks out or rearranges a critical gene—the most commonly accepted theory suggests that multiple genetic insults, or accumulated hits, are necessary to cause cancer ( see Understanding Cancer ). A single gene loss can be inherited and lead to family histories of cancer. Other genetic hits may accumulate because of a combination of aging, environmental carcinogens or lifestyle indiscretions such as smoking or overeating.
There are more than 60 known oncogenes. They are often named for the types of cancer they induce in animals, such as ras for rat sarcoma . Oncogenes may stimulate other genes by producing increased amounts of special proteins. Some may produce abnormal amounts of growth factors or cellular receptors for growth factors. There is usually more than one oncogene activated in any given tumor and these may coordinate with each other or with the loss of tumor suppressors to produce cancer. Exactly how most oncogenes and their protein products cause cancer to develop is still not understood.
