Research is proceeding into the various genes responsible for cell growth and replication and the mechanisms that activate or inhibit the activities of these genes. Discoveries to date include genes that repair DNA, genes that program cell death (apoptosis), genes that cause cancer (oncogenes), and tumor-suppressor genes. Changes in cell DNA are at the root of malignant transformation.
Carcinogenesis is the process by which normal cells are transformed into cancer cells. Malignant tumors develop from a sequence of changes over a relatively long period of time. A combination of factors or repeated exposure to a single risk factor leads to changes in the gene or chromosome and leads to the transformation of the normal cell into a malignant cell. Some specific cancers have well-established risk factors (e.g., bronchogenic carcinoma or lung cancer and cigarette smoking). The multiplicity of developmental steps in carcinogenesis is supported by the fact that not all cigarette smokers develop cancer. It is difficult to establish precise predisposing or causative (etiologic) factors for each cancer because it takes many years to gather sufficient documentation, and frequently there are multiple factors involved. The role of oncogenic viruses has been confirmed with evidence of some strains of human papillomavirus triggering cervical cancer. Exposure to radiation continues to lead to leukemia and ultraviolet radiation (sun) leads to skin cancer. Also, the incidence of some cancers has changed without adequate explanation. Diagnostic techniques have improved also, which may affect statistics somewhat.
The stages in carcinogenesis have been organized into:
- 1. "Initiating" factors or procarcinogens cause the first irreversible changes in the cell DNA. Genetic changes or exposure to an environmental risk may cause this first mutation. This initial change does not create an active neoplasm.
- 2. Exposure to "promoters" later causes further changes in DNA, resulting in less differentiation and an increased rate of mitosis. Dysplasia or anaplasia may be evident at this time. This process leads to the development of the tumor. Promoters include hormones and chemicals. The prolonged time interval and multiple factors involved complicate efforts by researchers to establish risk factors for cancer.
- 3. Continued exposure and changes in DNA result in a malignant tumor.
Risk Factors and Prevention
- Risk factors associated with geographic areas or ethnic groups may relate to environmental influences or diet as well as genetic variations.
- Some risk factors such as foods can be avoided.
- Other factors, such as genetic predisposition, cannot be avoided but can be addressed by encouraging frequent screening and therefore early diagnosis.
The list "Seven Steps to Health
1), includes some specific measures to reduce the common risk factors for cancer; for example, limiting sun exposure, ensuring regular medical and dental examinations and screening, or altering diet. For example, increasing fiber content in the diet and reducing fats decreases the risk of colorectal cancer. Many fresh fruits and vegetables provide antioxidants such as vitamins A and E, chemicals that protect cells against damaging substances called free radicals. Free radicals form in cells from exposure to radiation or certain products from metabolic processes. Foods containing antioxidants are now promoted to offset this problem. More information will be forthcoming as research continues in this area.
Host Defenses
As mentioned earlier, cancer suppressor genes present in the body can inhibit neoplastic growth. The immune system appears to offer protection by reacting to changes in the membranes of some tumor cells, which are seen as "foreign". The immune response includes both cell-mediated and humoral immunity. Cytotoxic T lymphocytes, natural killer cells (NK), and macrophages are involved in immune surveillance and the destruction of "foreign" or abnormal cells. Temporary or long-term immunodeficiency has been shown to increase the risk of cancer. For example, human immunodeficiency virus (HIV) infection or acquired immunodeficiency syndrome (AIDS) decreases the number of T lymphocytes. Cancers such as Kaposi's sarcoma and lymphomas occur frequently in AIDS patients.
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