Molecular epidemiology and the genetics of environmental cancer

Article Abstract:

In the past, many cancer risks could be determined only by epidemiological study. The observation of a number of individuals permitted the elucidation of tobacco snuff as a cause of oral cavity cancer in 1759, along with a host of other causes of cancer since that time. Today, however, scientists are learning more about the carcinogenesis on the molecular level. The process by which normal cells are transformed into malignant cancer cells is being studied by examining the molecular changes that occur at every step of the process. The first step in the development is initiation. It is at this point that some chemical carcinogen induces a mutation in a cell's DNA, which sets the stage for cancer. Some carcinogens damage DNA directly, while others are converted by cellular enzymes into the actual destructive molecule. After the cell is initiated, it may be affected by a tumor promotor. These are substances that do not cause cancer in their own right, but cause changes that promote the unregulated growth of the cell. As the cells multiply, they may induce the formation of new blood vessels to serve their growing need for nutrients and oxygen. During this growth, the cells become genetically unstable. More mutations may accumulate. Chromosomes may be lost, and others copied too often. If the right combination of genes and chromosomes results, a cancer has begun. Ultimately, the cancer may progress to the point that the cancer cells begin to disseminate and start metastatic disease in different parts of the body. Until now, the concept of cancer risk could only be applied to a population of people. However, as more is learned about the individual steps of carcinogenesis, it may be possible to identify the individual enzymes and cellular structures that make one person more susceptible to carcinogenesis than another. At that point, it may become possible to identify cancer risks on an individual basis. This may become feasible in as little as 10 years. (Consumer Summary produced by Reliance Medical Information, Inc.)

Causes of, Genetic aspects, Cancer, Molecular biology, Carcinogenesis

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Patterns in food use and their associations with nutrient intakes

Article Abstract:

Measures or indicators of dietary patterns were determined for use in studies of epidemiology, which involves the evaluation of factors that influence the frequency and distribution of disease. Frequency of food-use data were obtained from the Western New York Diet Study, which examined the relationship between diet and cancer. The frequency of food use data regarding 110 foods consumed by 1,475 men and 780 women (control subjects who did not have cancer) were analyzed, and nine dietary-pattern factors were determined for each gender. Dietary characteristics of interest to cancer researchers, such as intakes of energy, total fat, dietary fiber, and vitamins A and C, were assessed. The results showed that the standard measure for assessing dietary adequacy, the quantile of nutrient intake, indicates various dietary patterns that differ in their potential to increase the risk of cancer. Dietary patterns may also be influenced by age, ethnicity, and income, which also affect the risk of cancer. The analysis of patterns of food use and their relation to the intake of different nutrients may serve as a comprehensive measure of dietary effects in epidemiological research. (Consumer Summary produced by Reliance Medical Information, Inc.)

Analysis, Food habits

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Cigarette smoking, N-acetyltransferase 2 genetic polymorphisms, and breast cancer risk

Article Abstract:

Women who smoke and can not metabolize carcinogenic chemicals quickly may have a greater risk of breast cancer. Toxic chemicals typically found in cigarette smoke are metabolized by several enzymes, including one called N-acetyltransferase 2 (NAT2). Researchers used DNA analysis on 631 women to detect gene mutations in NAT2 that would cause women to detoxify carcinogens slowly or rapidly. Of the total group, 304 women had breast cancer. Slow metabolizers who were current or former smokers had a greater risk of breast cancer, but this result was only seen in postmenopausal women.

Health aspects, Risk factors, Smoking, Breast cancer, Acetylator status (Pharmacology)

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