There are more than 200 different types of cancer, all of which are characterized by abnormal cellular functioning. Normally, our cells undergo mitosis only when necessary and stop when appropriate. A cut in the skin, for example, is repaired by mitosis, usually without formation of excess tissue. The new cells fill in the damaged area, and mitosis slows when the cells make contact with surrounding cells. This is called contact inhibition, which limits the new tissue to just what is needed. Malignant (cancer) cells, however, are characterized by uncontrolled cell division. Our cells are genetically programmed to have particular life spans and to divide or die. One gene is known to act as a brake on cell division; another gene enables cells to live indefinitely, beyond their normal life span, and to keep dividing. Any imbalance in the activity of these genes may lead to abnormal cell division. Such cells are not inhibited by contact with other cells, keep dividing, and tend to spread.
A malignant tumor begins in a primary site such as the colon, then may spread or metastasize. Often the malignant cells are carried by the lymph or blood to other organs such as the liver, where secondary tumors develop. Metastasis is characteristic only of malignant cells; benign tumors do not metastasize but remain localized in their primary site.
What causes normal cells to become malignant? At present, we have only partial answers. A malignant cell is created by a mutation, a genetic change that brings about abnormal cell functions or responses and often leads to a series of mutations. Environmental substances that cause mutations are called carcinogens. One example is the tar found in cigarette smoke, which is definitely a cause of lung cancer. Ultraviolet light may also cause mutations, especially in skin that is overexposed to sunlight. For a few specific kinds of cancer, the trigger is believed to be infection with certain viruses that cause cellular mutations. Carriers of hepatitis B virus, for example, are more likely to develop primary liver cancer than are people who have never been exposed to this virus. Research has discovered two genes, one on chromosome 2 and the other on chromosome 3, that contribute to a certain form of colon cancer. Both of these genes are the codes for proteins that correct the “mistakes” that may occur when the new DNA is synthesized. When these repair proteins do not function properly, the mistakes (mutations) in the DNA lead to the synthesis of yet other faulty proteins that impair the functioning of the cell and predispose it to becoming malignant.
Once cells have become malignant, their functioning cannot return to normal, and though the immune system will often destroy such cells, sometimes it does not, especially as we get older. Therefore, the treatments for cancer are directed at removing or destroying the abnormal cells. Surgery to remove tumors, radiation to destroy cells, and chemotherapy to stop cell division or interfere with other aspects of cell metabolism are all aspects of cancer treatment.
New chemotherapy drugs are becoming more specific, with very precise targets. For example, the cells of several types of solid-tumor cancers have been found to have mutations in the gene for the cell membrane receptor for a natural growth factor (epidermal growth factor receptor, or EGFR). These altered receptors, when triggered by their usual growth factor, then cause the cell to divide uncontrollably, an abnormal response. Medications that target only these altered receptors have already been developed for some forms of lung cancer and breast cancer. Not only do they show promise in treating the cancer, they do not have the side effects of other forms of chemotherapy.