Cancer is overtaking heart disease as the most frequent cause of death in the United States, accounting for 24 percent (approximately 520,000)
Among females the leading causes of cancer deaths are:
- lung, 25 percent;
- breast, 17 percent;
- colon and rectum, 10 percent;
- leukemia and lymphoma, 8 percent;
- and ovary, 6 percent
Although neoplasia is a disease of the genome with many common molecular pathways, human cancer may be envisioned as more than 100 distinct entities, each defined by the cell or tissue of origin and the appearance under the microscope.
For some, the initial inductive event is inherited, but, as demonstrated by Knudson, general belief is that more than one genetic or epigenetic event is necessary for promotion of human carcinogenesis.
Each site has a host-tumor interface and a subclinical growth phase, which might be measured in decades before emerging at a clinical threshold.
Screening policies for the prevention and early detection of cancer emerge from understanding the natural history of cancer at specific sites.
The hallmark of an effective screening policy is demonstration of a reduced mortality rate
This goal has been achieved by:
- the Pap smear for cervical cancer,
- mammography for breast cancer,
- and the fecal occult blood test and sigmoidoscopy for colorectal cancer.
For many decades breast cancer incidence has been increasing while mortality has remained stable, but now there is a decline in mortality, a result of widespread acceptance of mammography and detection of breast cancer in an earlier, curable stage.
Given that diet and nutrition may be characterized as an environmental factor, these differences incriminate environment-induced molecular events in human carcinogenesis.
The more frequent occurrence of cancer in older persons may reflect accumulation of environmentally based genetic events as well as molecular events associated with senescence
Acquired genetic or epigenetic events originating in physical, chemical, and viral etiologies are described in more detail below; initial insights were derived from observational studies.
Metabolic epidemiology encompasses other effects of the internal environment on carcinogenesis as well.
For example, breast cancer in women can be related to the lifetime duration of unprotected exposure to biologically active estrogens.
Early menarche, late menopause, and delayed or absent child bearing increase risk, whereas oophorectomy and estrogen antagonists reduce risk.
Recognition of internal and external environmental interactions in human carcinogenesis provides the means for risk reduction and the development of prevention strategies
- Elimination of exposure to asbestos or radiation, avoidance of occupational carcinogens, and reduction of cigarette smoking remove certain carcinogens from the environment and reduce risk.
- Sunscreens block the carcinogenic wavelength of ultraviolet light.
- Vaccination for hepatitis B virus reduces the risk of hepatocellular cancer.
Other measures to control environmental carcinogens may be directed to the internal environment by nutritional modification and chemoprevention.
A low-fat, high-fiber diet reduces risk of colorectal cancer and, possibly,breast and prostate cancer.
Oral vitamin A analogues reduce leukoplakia and second cancers in the aerodigestive epithelium
Oral nonsteroidal anti inflammatory drugs decrease rectal adenomas in patients with familial adenomatous polyposis.
Antiestrogens reduce second cancers in the breast.
